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Hepatocellular carcinoma (HCC) is a serious threat to human health and life due to its high morbidity and mortality. Ubiquitin-conjugating enzymes are players in the ubiquitin proteasome system and are responsible for a great number of physiological activities in cells. The action of ubiquitin-conjugating enzyme UBE2K in HCC has not been reported. Therefore, we studied the function and role of UBE2K in the malignant progression of HCC. An analysis of UBE2K expression in HCC cells was performed using RT-qPCR and protein immunoblotting. CCK-8, Transwell and sphere formation assays were used to identify the potential effects of UBE2K in HCC cell proliferation, migration and stemness property. RT-qPCR, and protein immunoblotting experiments was taken to explore the regulation between UBE2K and c-Myc. Here, we discovered that UBE2K expression was elevated in HCC cells, and elevated UBE2K predicts worse prognosis for HCC patients. Functionally, UBE2K promote, while UBE2K knockdown suppressed cell proliferation, migration and stemness property of HCC cells. Furthermore, c-Myc was identified as a downstream target of UBE2K. Moreover, functional rescue experiments finally proved that UBE2K facilitates the malignant progression of HCC cells by upregulating c-Myc. We clarified through in vivo experiments that UBE2K expression promotes tumor growth in HCC. Taken together, our study results proved the molecular regulation of UBE2K and c-Myc in HCC and the oncogenic role of UBE2K/c-Myc axis in HCC progression, thus it provides a promising molecular target for the diagnosis and treatment of HCC.

Abstract: Lenvatinib is a multikinase inhibitor which mainly hinders liver cancer proliferation by inhibiting angiogenesis. In 2018, Lenvatinib was approved for the first-line treatment of patients with advanced hepatocellular carcinoma [HCC] in the United States, the European Union, Japan, and China. Lenvatinib has been established as a sorafenib replacement drug with a higher objective response rate [ORR], longer progression-free survival [PFS], and time to progression [TTP]. Lenvatinib resistance during hepatocellular carcinoma treatment has become increasingly common in recent years. Accordingly, it is necessary to determine factors associated with Lenvatinib resistance and explore solutions. In this review, we sought to explore the drug resistance mechanisms of Lenvatinib in liver cancer and methods to reduce drug resistance and summarized the recent achievements of Lenvatinib in liver cancer treatment.

Long noncoding RNAs (lncRNAs) are confirmed as the key regulators of hepatocellular carcinoma (HCC) occurrence and progression, but the role of AlkB homologue 3 antisense RNA 1 (ALKBH3-AS1) in HCC is unclear. We revealed the overexpression of ALKBH3-AS1 in HCC tissues. The upregulated levels of ALKBH3-AS1 were observed in HCC cells. ALKBH3-AS1 was expressed in the nucleus and cytoplasm of HCC cells. The high ALKBH3-AS1 expression was markedly associated with a decreased survival rate of HCC patients. ALKBH3-AS1 knockdown repressed and ALKBH3-AS1 overexpression enhanced HCC cell invasion and proliferation. ALKBH3-AS1 silencing restricted HCC growth in vivo. A significant positive correlation between ALKBH3-AS1 and ALKBH3 mRNA levels was confirmed in HCC specimens. ALKBH3-AS1 silencing reduced ALKBH3 expression by stabilizing its mRNA stability in HCC cells. Notably, the impact of ALKBH3 silencing on HCC cells was similar to that of ALKBH3-AS1 knockdown. ALKBH3 restoration prominently attenuated the suppressive effects resulting from ALKBH3-AS1 silencing in HCCLM3 cells. Hypoxia-inducible factor-1α (HIF-1α) transcriptionally activated ALKBH3-AS1 expression in hypoxic HCC cells. ALKBH3-AS1 knockdown markedly attenuated cell proliferation and invasion in hypoxic Huh7 cells. Collectively, HIF-1α-activated ALKBH3-AS1 exerted an oncogenic role by enhancing ALKBH3 mRNA stability in HCC cells.

Splenic rupture is the most serious complication of infectious mononucleosis (IM) caused by Epstein-Barr virus (EBV) infection, with a mortality rate of over 1 in 10. We reported a case of spontaneous atraumatic splenic rupture secondary to IM in a young man. The patient presented with abdominal pain caused by splenic rupture as the initial symptom. The diagnosis and treatment process went through a series of twists and turns, including the emergency department, general surgery department, and infection department. This case suggests that clinicians should consider the possibility of EBV infection in young patients with spleen rupture without obvious cause to avoid misdiagnosis and missed diagnosis.

As an important relic of traditional Chinese culture, traditional villages have important cultural values. With the continuous deepening of modern urbanization and the development of rural tourism, the village landscape is also facing profound challenges. In the context of rural revitalization and tourism development, it is necessary to strengthen the landscape identity of traditional villages. Based on the background of rural revitalization, this article reviews and discusses the related concepts and research status of traditional village landscapes, the identity of village landscapes and existing problems in landscapes, and remodeling strategies by sorting out relevant research literature at home and abroad in recent years. People’s awareness of local landscape identity reshapes the landscape uniqueness of traditional villages so that the local culture and foreign culture can reach a state of balance and integration. The village landscape identity and the impact of digital technology and self-media platforms on landscape remodeling are reviewed and discussed. The study found that the landscape identity of traditional villages is reflected in the activity places with local regional cultural characteristics and relies on the spiritual emotions of the villagers. For the existing problems in the landscape, a landscape remodeling strategy is proposed to restore people’s awareness of local landscape identity and reshape the landscape uniqueness of traditional villages.

5-Fluorouracil (5-FU) has been applied to treat pancreatic cancer, which is one of the most common types of digestive system tumors. However, due to poor tumor selectivity, 5-FU's therapeutic effect has certain limitations. 5-FU's activity and selectivity against tumor cells can be improved by chitosan assisted drug delivery systems. Understanding the atomic interaction mechanism between chitosan and 5-FU is important. In this work, the interactions between 5-FU and different types of chitosan were systematically investigated by using molecular dynamics (MD) simulation. Based on the radial distribution function and the free energy calculation, our results demonstrate that the functional groups of chitosan could greatly regulate the interaction behavior between chitosan and 5-FU. Moreover, 5-FU could gradually release from chitosan at a more acidic pH (tumor tissues) environment. These results revealed the underlying atomic interaction mechanism between 5-FU and chitosan at various pH levels, and may be helpful in the design of chitosan-based drug delivery systems.

Background To summarize the characteristics and treatment, and analyze the prognosis of large number of infants with retinoblastoma (RB) in China through a multicenter, 10-year retrospective analysis. Methods The data of RB infants were collected from multiple centers. The characteristics and survival prognosis were analyzed. The overall survival (OS) rate was estimated by the Kaplan–Meier method. Multivariate Cox survival analysis was to evaluate the independent risk factors affecting the prognosis of RB infants. Results A total of 373 RB infants (202 boys and 171 girls) were included, the median age was 6.22 months (10 days to 11.93 months). The median follow-up time of RB infants was 18.4 (1.02–122.81 months). After excluding the lost to follow-up cases, the OS rate was 97.7% (345/353). Kaplan–Meier survival analysis indicated that 9 cases died and the median survival time was not reached. Univariate analysis of prognostic factors revealed eye affected, presenting signs, left eye stage and recurrence to be poor prognostic factors for OS rate in RB infants (all P P = 0.048) was an independent factor for prognosis of infants with RB. The median survival time of infants underwent chemotherapy + intra-arterial chemotherapy (IAC) + enucleation + vitrectomy was the longest than other treatments (n = 9, 47.64 months, OS = 100%, all P Conclusion Recurrence is an independent factor for prognosis of RB infants, which still needs attention after treatment. Early screening, comprehensive treatments and follow-up of patients may lead to improvements of prognosis of RB infants.

Purpose: This study was implemented to investigate the associations between SNP in mature microRNA (miRNA) sequence and lung cancer prognosis and to verify the function of those SNP.Experimental Design: Eight SNPs (rs3746444T>C in hsa-mir-499, rs4919510C>G in hsa-mir-608, rs13299349G>A in hsa-mir-3152, rs12220909G>C in hsa-mir-4293, rs2168518G>A in hsa-mir-4513, rs8078913T>C in hsa-mir-4520a, rs11237828T>C in hsa-mir-5579, and rs9295535T>C in hsa-mir-5689) were analyzed in a southern Chinese population with 576 patients with lung cancer, and the significant results were validated in two additional cohorts of 346 and 368 patients, respectively. A series of experiments were performed to evaluate the relevancies of those potentially functional SNPs.Results: We found that the microRNA-499 rs3746444T>C polymorphism exhibited a consistently poor prognosis for patients with lung cancer in the discovery set [HR, 1.24; 95% confidence interval (CI), 1.02–1.49; P = 0.028], in the validation set I (HR, 1.31; 95% CI, 1.01–1.71; P = 0.048) and in the validation set II (HR, 1.45; 95% CI, 1.12–1.86; P = 0.004). The adverse effect of CT/CC variants was more remarkable in patients receiving platinum-based chemotherapy. Further functional assays demonstrated that the rs3746444C variant allele influences the expression of several cancer-related genes and affects lung cancer cells' proliferation and tumor growth in vivo and in vitro via the cisplatinum resistance.Conclusion: Our findings suggested that the rs3746444T>C polymorphism in mature miR-499 sequence could contribute to poor prognosis by modulating cancer-related genes' expression and thus involve tumorigenesis and anti-chemotherapy, which may be a useful biomarker to predict lung cancer patients' prognosis. Clin Cancer Res; 21(7); 1602–13. ©2015 AACR.

File S1. Differentially expressed genes between A549-miRNA-499-T cells and A549-miRNA-499-C cells using microarray analysis. Column A. TargetID: Gene symbol in the genechip; Column B. DiffScore: Difference in the expression score of target gene between the A549-miRNA-499-T cells and A549-miRNA-499-C cells; Column C. DiffPval: P value of the difference calculated by the student's t test. Column D. DEFINITION: Full name of target genes based on the NCBI RefSeq (Build 36.2, Rel 22)database. Column E. ONTOLOGY_FUNCTION: Possible function of the target genes.

File S2. Validation of those differentially expressed genes between A549-miRNA-499-T and A549-miRNA-499-C cells by the quantitative real-time PCR method.

Table S1. All SNPs located in the mature miRNAs sequence.

Figure S2. The proliferation curves of A549 cells transfected with the miR-499-T vector, the miR-499-C vector and an "empty" vector without cisplatinum treatment during a week.

Figure S3. MicroRNA-499 expression levels in A549 cells transfected with the miR-499-T vector, the miR-499-C vector and an "empty" vector.

Table S2. Information on the TaqMan assay of SNPs in the microRNAs.

Table S3. Sequence of primers used in real time RT-PCR analysis.

BackgroundChronic Obstructive Pulmonary Disease (COPD) is a common and harmful disease that requires an effective tool to early screen high-risk individuals. Gansu has unique environments and customs, leading to the different prevalence and etiology of COPD from other regions. The association between altitude and COPD once attracted epidemiologists' attention. However, the prevalence in Gansu and the role of altitude are still unclarified.MethodsIn Gansu, a multistage stratified cluster sampling procedure was utilized to select a representative sample aged 40 years or older. The questionnaire and spirometry examination were implemented to collect participants' information. The diagnosis and assessment of COPD were identified by the Global Initiative for Chronic Obstructive Lung Disease (GOLD) criterion, while post-bronchodilator FEV1/FVC < LLN was for sensitivity analysis. Furthermore, the effect of high altitude on COPD was evaluated by the logistic regression model after propensity score matching (PSM). Finally, the participants were randomly divided into training and validation sets. The training set was used to screen the relative factors and construct a nomogram which was further assessed by the receiver operating characteristic (ROC) curve, calibration curve, and decision curve analysis (DCA) in the two sets.ResultsThere were 2,486 eligible participants in the final analysis, of which 1,584 lived in low altitudes and 902 lived in high altitudes. Based on the GOLD criterion, the crude and standardized prevalences in Gansu were 20.4% (18.7–22.0) and 19.7% (17.9–21.6). After PSM, the logistic regression model indicated that high altitude increased COPD risk [PSM OR: 1.516 (1.162–1.978)]. Altitude, age, sex, history of tuberculosis, coal as fuel, and smoking status were reserved for developing a nomogram that demonstrated excellent discrimination, calibration, and clinical benefit in the two sets.ConclusionsCOPD has become a serious public health problem in Gansu. High altitude is a risk factor for COPD. The nomogram has satisfactory efficiency in screening high-risk individuals.

Huali Gu,1 Yizhuo Wang,1 Dongsheng Huang,1 Xunda Ji,2 Yi Zhang,1 Jianmin Ma,3 Mei Li,4 Weiling Zhang,1 Huimin Hu,1 Jing Li,1 Pinwei Zhang1 1Department of Pediatrics, Beijing Tongren Hospital, Capital Medical University, Beijing, People’s Republic of China; 2Department of Ophthalmology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China; 3Department of Ophthalmic Oncology, Beijing Tongren Hospital, Capital Medical University, Beijing, People’s Republic of China; 4Department of Nuclear Medicine, Beijing Tongren Hospital, Capital Medical University, Beijing, People’s Republic of ChinaCorrespondence: Dongsheng Huang, Department of Pediatrics, Beijing Tongren Hospital, Capital Medical University, West South Road 2, Yizhuang Economic and Technological Development Zone, Daxing District, Beijing, 100176, People’s Republic of China, Tel +86 01058266032, Email hds5180@sina.com Xunda Ji, Department of Ophthalmology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Kong Jiang Road 1665, Shanghai, 200092, People’s Republic of China, Tel +86 15921670980, Email jixunda@xinhuamed.com.cnPurpose: Retinoblastoma (RB) is the most common intraocular malignancy in infancy and childhood. This study evaluated the clinical and imaging features, treatment, and prognosis of patients with recurrent RB with limb bone metastases and without central nervous system involvement.Patients and Methods: The clinical data of five patients with RB with limb bone metastases who were diagnosed at the Department of Pediatrics in Beijing Tongren Hospital between January 2015 and January 2021 were analyzed retrospectively.Results: Three males and two females were included (seven eyes: four group E and one each of group D, C, and B). The most common symptom was pain. Three patients had bone marrow and lymph node metastases. Three patients had single and two had multiple skeletal lesions. The main bones that were involved were the femur, humerus, talus, and ulna. The simultaneous involvement of the bone marrow and cortex was also observed. Serum neuron-specific enolase (NSE) levels were significantly elevated in four cases and slightly elevated in one case; primary intravenous chemotherapy resulted in a decrease in NSE levels and the gradual resolution of the bone lesions. Two patients died at the time of follow-up and three were in complete remission. The results of the statistical analysis showed that anterior chamber invasion was correlated with prognosis, and there was significant difference in the decrease in the serum NSE levels after intravenous chemotherapy.Conclusion: Regular lifelong follow-up of patients with RB is warranted to identify bone metastases earlier. Anterior chamber invasion may be a risk factor. The simultaneous involvement of the bone marrow and cortex is characteristic manifestations in images of RB with bone metastases. Multidisciplinary treatment especially intravenous chemotherapy is useful, at least at the beginning.Keywords: recurrent, NSE, SRE, pathological fracture, pamidronate, osteoclast inhibitors

Thermal performance assessment and optimization for energy conversion and utilization systems are of high significance in building energy efficiency. Generally speaking, the evaluation of actual thermodynamic system performance is mainly based on the First law of thermodynamics, with emphasis on the quantity of energy consumption, while ignoring the energy quality. Thus, it results in a one-sided evaluation in the analysis of system energy saving. In this paper, the electricity equivalent is used to analyse and evaluate the air source heat pump heating system under the different working conditions. Moreover, the dynamic thermal performances of three typical space heating devices (radiator, fan coil, and radiant floor) are investigated and compared by weighing both energy quantity and quality. The results show that the COP of radiator, fan coil, and radiant floor are 3.00, 3.82, and 4.76, and coefficient of energy quality are 48.32%, 51.43%, and 50.57%, respectively. However, the robustness of its thermal performance is lower than that of radiator and fan coil. This work can provide reference for energy systems assessment and guidance for practical design of building heating systems.

This study aimed to investigate the short-term efficacy and adverse reactions of irinotecan combined with first-line chemotherapeutics for the treatment of pediatric hepatoblastoma with pulmonary metastasis (HB-PM). Forty-one pediatric patients with HB-PM undergoing cisplatin + fluorouracil + vincristine + doxorubicin (C5VD) treatment with bad therapeutic effect or bad response were instead treated with two cycles of an irinotecan protocol (vincristine + irinotecan + cyclophosphamide + cisplatin). The changes in recent alpha-fetoprotein (AFP), efficacy and adverse reactions in these patients were statistically analyzed. Results showed that, the median level of AFP before chemotherapy was 56432 μg/L; however, it was significantly lower (749 μg/L) after two cycles of chemotherapy (rank sum test, P = 0.00). After two cycles of chemotherapy, three patients achieved a complete response and 32 patients achieved a partial response. The recent efficacy cases accounted for 85.36% of patients (35/41). The delayed diarrhea was the most common adverse reaction to irinotecan, with an incidence rate of 58.53% (24/41), which was improved after symptomatic treatment. In conclusion, the protocol of irinotecan combined with first-line chemotherapeutics can be used for the treatment of HB-PM that is not sensitive to the C5VD protocol, with good short-term curative effect and tolerable adverse reactions.

In most cancers, forkhead box N3 (FOXN3) acts as a transcriptional inhibitor to suppress tumor proliferation, but in pancreatic cancer, the opposite effect is observed. To confirm and investigate this phenomenon, FOXN3 expression in various carcinomas was determined using GEPIA2 and was found to be highly expressed in pancreatic cancer. Kaplan-Meier plotter was then used for survival analysis, revealing that high FOXN3 expression in pancreatic cancer might be associated with a poor prognosis. Similarly, clinical samples collected for immunohistochemical staining and survival analysis showed consistent results. The RNA-seq data of pancreatic cancer patients from the TCGA were then downloaded, and the differential expression gene set was obtained using R for gene set enrichment analysis (GSEA). The intersection of the above gene sets and FOXN3-related genes was defined as related differentially expressed gene sets (DEGs), and enrichment analysis was performed using Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG). Finally, we analyzed the relationship between FOXN3 and immune infiltration in pancreatic cancer. Collectively, our findings reveal that FOXN3 is involved in the occurrence and progression of pancreatic cancer and may be useful as a prognostic tool in pancreatic cancer immunotherapy.

This study aims to investigate the characteristics and related high risk factors of second neoplasms after chemotherapy and radiotherapy in children with solid tumors.The detailed clinical data of seven children with malignant solid tumors, who were treated in our department, were retrospectively analyzed, in order to summarize the clinical characteristics of the secondary onset of second neoplasms, and determined the risk factors related to the occurrence of second neoplasms.(1) Clinical characteristics: Among the seven children with malignant solid tumors, three children had rhabdomyosarcoma (3/132, 2.27%), two children had hepatoblastoma (2/313, 0.64%), one child had neuroblastoma (1/305, 0.33%), and one child had inflammatory myofibroblastoma (1/3, 33.33%). Furthermore, among these children, four children were boys and three children were girls, and their onset age ranged within 5-34 months, with a median onset age of 27 months. Moreover, among these children, three children were ≤1 year old. All second neoplasms exhibited symptoms, and the diagnosis was made after the complete remission of the first primary tumor. The time interval between these two tumors was within 17-78 months, and the median time was 38 months. Three of seven children with rhabdomyosarcoma were treated with chemotherapy in combination with radiotherapy, while four children only received the chemotherapy. The chemotherapy cycles were 6-39 times, and the median chemotherapy cycles were 10 times. Among these children, one child with relapsed stage IV rhabdomyosarcoma and one child with stage IV retroperitoneal neuroblastoma had 39 cycles and 33 cycles of chemotherapy respectively. (2) Characteristics of the accumulated doses of high-risk chemotherapy drugs: The accumulated dose of cyclophosphamide in six patients was within 2.47-44.45 g/m2, with a median of 6.14 g/m2. The accumulated dose of ifosfamide in five patients was within 13.63-96.41 mg/m2, with a median of 31.23g/m2. The accumulated dose of etoposide in six patients was within 1,237.35-3,754.95 mg/m2, with a median of 1,548.67 mg/m2. The accumulated dose of anthracyclines in seven patients was within 150.68-843.78 mg/m2, with a median of 329.73 mg/m2. The accumulated dose of vincristine in seven patients was within 3.11-18.89 mg/m2, with a median of 15.92 mg/m2. The accumulated dose of cisplatin in seven patients was within 271.23-1,681.59 mg/m2, with a median of 733.07 mg/m2. Children with abdominal inflammatory myofibroblastic tumors did not apply cyclophosphamide, ifosfamide and etoposide regimens. The main chemotherapy drugs consisted of methotrexate, pirarubicin, cisplatin and vincristine. (3) Radiotherapy doses. (4) Characteristics of second neoplasms: Among the seven children with second neoplasms, five children had leukemia, 3 patients with rhabdomyosarcoma were combined with radiotherapy. The doses of radiation were 40 and 45GY" after "(3) Radiotherapy doses (four children had acute myeloid leukemia and one children had acute B-lymphoblastic leukemia), one child had myelodysplastic syndrome, and one child had myeloid sarcoma. Furthermore, among these seven children, four children (4/7) had abnormal chromosomes, two children were normal, and one child gave up the treatment and underwent the chromosome test after the diagnosis of second neoplasms.The incidence of secondary onset of second neoplasms in children with malignant solid tumors is not high, considering that this is correlated to the use of alkylating agents, topoisomerase II inhibitors, platinum-based chemotherapy drugs and radiotherapy, and associated with the chromosomal abnormalities of children.Chemotherapy, Children, Radiotherapy, Second malignant neoplasm, Solid tumor.Questo studio ha lo scopo di studiare le caratteristiche e i relativi fattori ad alto rischio delle seconde neoplasie dopo chemioterapia e radioterapia nei bambini con tumori solidi. Sono stati analizzati retrospettivamente e dettagliatamente i dati clinici di sette bambini con tumori solidi maligni, che sono stati trattati nel nostro reparto, al fine di riassumere le caratteristiche cliniche all’inizio dell’insorgenza delle seconde neoplasie e determinare i fattori di rischio correlati al verificarsi di questa insorgenza. CARATTERISTICHE CLINICHE: tra i sette bambini con tumori solidi maligni, tre bambini avevano rabdomiosarcoma (3/132, 2,27%), due bambini avevano epatoblastoma (2/313, 0,64%), un bambino aveva neuroblastoma (1/305, 0,33%) e un bambino presentava miofibroblastoma infiammatorio (1/3, 33,33%). Inoltre si trattava di quattro bambini e tre bambine, e la loro epoca di insorgenza era compresa tra 5-34 mesi, con una mediana di 27 mesi; tre bambini avevano età non superiore ad 1 anno. Tutte le seconde neoplasie erano sintomatiche e la diagnosi era stata fatta dopo la completa remissione del primo tumore primario. L’intervallo di tempo tra questi due tumori era compreso tra 17 e 78 mesi e il tempo mediano era di 38 mesi. Tre su sette bambini con rabdomiosarcoma sono stati trattati con chemioterapia in combinazione con radioterapia, mentre quattro bambini hanno ricevuto solo la chemioterapia. I cicli di chemioterapia erano ripetuti da 6 a 39 volte e i cicli di chemioterapia in media 10 volte. Un bambino con rabdomiosarcoma in stadio IV recidivo e un bambino con neuroblastoma retroperitoneale in stadio IV hanno avuto rispettivamente 39 cicli e 33 cicli di chemioterapia. Caratteristiche delle dosi accumulate di farmaci chemioterapici ad alto rischio: la dose accumulata di ciclofosfamide in sei pazienti era compresa tra 2,47 e 44,45 g/m2, con una mediana di 6,14 g/m2. La dose accumulata di ifosfamide in cinque pazienti era compresa tra 13,63 e 96,41 mg/m2, con una mediana di 31,23 g/m2. La dose accumulata di etoposide in sei pazienti era compresa tra 1.237,35-3.754,95 mg/m2, con una mediana di 1.548,67 mg/m2. La dose accumulata di antracicline in sette pazienti era compresa tra 150,68- 843,78 mg/m2, con una mediana di 329,73 mg/m2. La dose accumulata di leurocristina in sette pazienti era compresa tra 3,11 e 18,89 mg/m2, con una mediana di 15,92 mg/m2. La dose accumulata di cisplatino in sette pazienti era compresa tra 271,23-1,681,59 mg/m2, con una mediana di 733,07 mg/m2. I bambini con tumori miofibroblastici infiammatori addominali non hanno ricevuto regimi di ciclofosfamide, ifosfamide ed etoposide. I principali farmaci chemioterapici sono stati il metotrexato, la pirarubicina, il cisplatino e la vincristina. Dosi di radioterapia. CARATTERISTICHE DELLE SECONDE NEOPLASIE: tra i sette bambini con seconde neoplasie, cinque bambini avevano la leucemia (quattro leucemia mieloide acuta e un bambino la leucemia linfoblastica B acuta), un bambino aveva la sindrome mielodisplastica e un bambino aveva sarcoma mieloide. Inoltre, tra questi sette bambini, quattro (4/7) avevano cromosomi anomali, due bambini erano normali e un bambino ha rinunciato al trattamento e ha subito il test cromosomico dopo la diagnosi di seconde neoplasie. CONCLUSIONE: L’incidenza dell’insorgenza secondaria di seconde neoplasie nei bambini con tumori solidi maligni non è elevata, considerando che ciò è correlato all’uso di agenti alchilanti, inibitori della topoisomerasi II, farmaci chemioterapici a base di platino e radioterapia e associati alle anomalie cromosomiche.

Long non-coding RNAs (lncRNAs) are essential drivers or suppressors in human hepatocellular carcinoma (HCC) by participating in controlling transcription, translation, mRNA stability, and protein degradation protein-protein interaction. TM4SF1-AS1 is recently identified as a tumor-promoting factor in lung cancer. Nevertheless, its function in HCC and related molecular mechanisms remain unknown. Here, our data indicated that either hypoxia or hypoxia-inducible factor (HIF) prolyl hydroxylase inhibitor (DMOG) induced the upregulation of TM4SF1-AS1 in HCC cells. HIF-1α knockdown rather than HIF-2α silencing remarkably abrogated hypoxia-upregulated TM4SF1-AS1 expression. Furthermore, we confirmed the elevated expression of TM4SF1-AS1 in HCC tissue samples and cell lines. The silencing of TM4SF1-AS1 prominently inhibited the proliferative, migratory, and invasive abilities of HCC cells. TM4SF1-AS1 depletion significantly blocked hypoxia-enhanced Hep3B cell proliferation and mobility. Interfering TM4SF1-AS1 remarkably reduced TM4SF1 mRNA and protein levels in HCC cells. But TM4SF1-AS1 knockdown did not impact the stability of TM4SF1 mRNA. Hypoxia enhanced the expression of TM4SF1 mRNA, which was subsequently decreased by TM4SF1-AS1 knockdown in HCC cells. We confirmed the positive correlation between TM4SF1 mRNA and TM4SF1-AS1 expression in HCC specimens. Finally, TM4SF1 prominently reversed the inhibitory role of TM4SF1-AS1 depletion in Hep3B cells. In summary, hypoxia-responsive TM4SF1-AS1 was overexpressed in human HCC and contributed to the malignant behaviors of tumor cells by enhancing TM4SF1-AS1 expression.

Objective To explore the surgical method, operation essentials and the clinical effect of the treatment of irreducible subtrochanteric femoral fractures by percutaneous cerclage wiring and Cephalomedullary nail. Method From February 2016 to October 2019, 17 cases of irreducible subtrochanteric femoral fractures (SFFs) treated via a minimally invasive wire system and intramedullary nail fixation were reviewed retrospectively. Ten male and seven female patients were involved. The average age was 59.88 ± 16.13 years, ranging from 41 to 94 years. Among the patients, seven were injured in traffic accidents, five fell from a standing height, and five injured themselves from falling. The cases were classified based on the Seinsheimer classification. Specifically, five cases were type IIIA, five cases were type IIIB, one case was type IV, and six cases were type V. According to the AO/OTA classification, 10 cases were 32B3, and seven cases were 32C3. During surgery, the patients were placed on a traction bed andattempted closed reduction. For those patients whose closed reduction failed confirmed by fluoroscopy, we performed a small anterolateral incision through which a self‐made minimally invasive percutaneous wire introducer (passer; patent Z: 2016 2 1002800.8) was employed for temporary fixation with a wire. A double‐stranded steel wire was introduced into a self‐made wire traction and lifting device (patent ZL 2020 2 0205658.7), the wire was pulled vertically and firmly fixed. Then an long InterTan nail was used for the fixation. The following information was recorded: (i) length of the invasive incision, (ii) blood loss on the third day after surgery, (iii) operation time; and (iv) maximum displacement and angulation of the fracture ends of the x‐rayed front and side fractures before and after surgery and the maximum displacement and formation of the three‐dimensional CT‐scanned fracture ends in the coronal plane, sagittal plane, and cross section before and after surgery. Result A total of 15 of the 17 patients were followed for 12 to 24 months. The 15 patients recovered, but one died from pulmonary infection 1 year after surgery. In the postoperative X‐ray and three‐dimensional CT observation reduction treatment, fracture displacement was less than 5 mm, each plane angle was less than 10 degrees, and postoperative fracture healing time was 3 to 14 months, with an average of 4.19 ± 4.04 months. The postoperative Harris hip function score ranged from 66 to 95 points, with an average of 80.81 ± 9.67 points. In terms of clinical outcomes, 11 cases were excellent, four cases were satisfactory, and one case was fair. Conclusion For refractory subtrochanteric fractures, percutaneous wiring combined with Cephalomedullary nail fixation is a minimally invasive, rapid, and effective method, which can achieve satisfactory results in clinical practice and is worth promoting., We designed and manufactured a wire minimally invasive system, including minimally invasive percutaneous wire introducer(Passer) and wire traction device. We used Passer to implant the double steel wire into the appropriate position of SFFs, and used a wire traction device to reduce the fracture distance and increase the quality of fracture reduction. The steeling traction device can provide the first compression fixation when pulled in the process of vertical fracture line and the second pressure fixation when it was tightened.

Intervertebral disc degenerative disease (IDD) is the most common degenerative spine disease, which leads to chronic low back pain and symptoms in the lower extremities. In this study, we found that RORα, a member of the retinoid-related orphan receptor family, is significantly elevated in nucleus pulposus tissue in IDD patients. The elevation of RORα is associated with increased apoptosis of nucleus pulposus (NP) cells. Therefore, we applicated a well-established inverse agonist of RORα, SR3335, to investigate its role in regulating NP cell metabolism and apoptosis. To further investigate the mechanism that SR3335 regulates the pathogenesis of IDD in vitro, tumor necrosis factor alpha (TNF-α) stimulation was used in human NP cells to mimic the hostile environment that leads to degeneration. We found that SR3335 treatment reversed the trend of increased apoptosis in NP cells induced by TNF-α treatment. Next, TNF-α treatment upregulated the expression of type II collagen and aggrecan and downregulated MMP13 (matrix-degrading enzyme matrix metalloproteinase 13) and ADAMTS4 (a disintegrin and metalloproteinase with thrombospondin motifs 4). However, these effects were reversed after SR3335 treatment. Furthermore, we find that SR3335 mediated the effect in NP cells by regulating the YAP signaling pathway, especially by affecting the phosphorylation state of YAP. In conclusion, the reduction of matrix degradation enzymes and apoptosis upon SR3335 treatment suggests that SR3335 is a promising drug in reversing the deleterious microenvironment in IDD patients.

Jing Li,* Weiling Zhang,* Huimin Hu, Yi Zhang, Yizhuo Wang, Huali Gu, Dongsheng Huang Department of Pediatrics, Beijing Tongren Hospital of China Capital Medical University, Beijing, 100176, People’s Republic of China*These authors contributed equally to this workCorrespondence: Dongsheng HuangDepartment of Pediatrics, Beijing Tongren Hospital of China Capital Medical University, No. 1 Dongjiao Lane, Dongcheng District, Beijing, 100730, People’s Republic of ChinaTel +86 10 5826 6032Email huamgdomgshemg@163.comObjective: This study aims to summarize the clinical features and prognoses of the malignant rhabdoid tumor of the kidney (MRTK) in children. It further aims to analyze the high-risk factors affecting MRTK prognosis.Methods: Clinical data from 14 children with MRTK treated in Paediatrics of Beijing Tongren Hospital from January 2010 to December 2019, along with the high-risk factors affecting prognosis, were retrospectively analyzed.Results: There were 14 children with MRTK included in the study, with a median onset age of 13 (3– 46) months. Thirteen patients had distant metastases, the most common site for metastases being inside the lung. A comprehensive treatment protocol combined with chemotherapy was mainly applied during the surgery. A surgical resection of primary tumors was performed on 13 (13/14) patients, and all 14 children received chemotherapy with ifosfamide + carboplatin + etoposide, ifosfamide + etoposide, and vincristine + pirarubicin + cyclophosphamide regimens, alternately. Three patients received radiotherapy and two received oral targeted drugs after partial response. The median follow-up was after 16.5 months (3– 53 months) and the four-year overall survival (OS) was 41.8%. In children aged ≤ 24 months and children aged > 24 months, the two-year OS was 67.2% and 100% (χ2 = 108.998, P< 0.05), respectively. In children with Ki 67 > 70% and children with Ki 67 < 70%, the two-year OS was 52.6% and 86.9% (χ2 = 8.544, P = 0.003), respectively. In children with distant metastases and children without distant metastasis, the two-year OS was 70% and 100% (χ2 = 14.239, P< 0.05), respectively.Conclusion: The most common MRTK distant metastasis site is the lung. Risk factors for poor MRTK prognoses include an age of < 24 months, Ki 67 > 70%, and distant metastases.Keywords: children, malignant rhabdoid tumor of the kidney, MRTK, treatment, prognosis

Mesenchymal stem cells (MSCs) are promising candidates for tissue regeneration and disease treatment. However, long-term

Cigarette smoke (CS) is a risk factor for chronic obstructive pulmonary disease (COPD), which can exacerbate inflammation and oxidative stress. Pristimerin (Pris) is a natural compound with antioxidant and anti-inflammatory effects. We managed to evaluate the protective effects of Pris on CS-induced COPD. The CS-induced COPD mice model and cell model were constructed. The effects of Pris treatment on lung function, inflammatory cell infiltration, myeloperoxidase (MPO), and pathological changes of lung tissues in mice model were evaluated. The impacts of Pris treatment on inflammatory factors, chemokines, and oxidative stress parameters in mice lung tissues and cells were determined by kits. The viability of human bronchial epithelial cells after Pris treatment was tested by CCK-8. The activation of NF-κB pathway was confirmed by Western blot and immunofluorescence. CS treatment impaired lung function, reduced weight of mice, and enhanced inflammatory cell infiltration, MPO, and lung tissue damage, but these effects of CS were reversed by Pris treatment. Furthermore, Pris treatment downregulated the levels of malondialdehyde, IL-6, IL-1β, TNF-α, CXCL1, and CXLC2, but upregulated superoxide dismutase and catalase levels. Pris treatment could overturn CS-induced activation of the NF-κB pathway. Pris alleviates CS-induced COPD by inactivating NF-κB pathway.

Immune rejection is the major limitation for porcine xenograft survival in primate recipients. Proinflammatory cytokines play important roles in immune rejection and have been found to mediate the pathological effects in various clinical and experimental transplantation trials. IL-17 and TNF-α play critical pathological roles in immune disorders, such as psoriasis and rheumatoid arthritis. However, the pathological roles of human IL-17 (hIL-17) and human TNF-α (hTNF-α) in xenotransplantation remain unclear. Here we found that hIL-17 and hTNF-α additively or synergistically regulate the expression of 697 genes in porcine aortic endothelial cells (PAECs). Overall, 415 genes were found to be synergistically regulated, while 282 genes were found to be additively regulated. Among these, 315 genes were upregulated and 382 genes were downregulated in PAECs. Furthermore, we found that hIL-17 and hTNF-α additively or synergistically induced the expression of various proinflammatory cytokines and chemokines (e.g., IL1α, IL6, and CXCL8) and decreased the expression of certain anti-inflammatory genes (e.g., IL10). Moreover, hIL-17 plus hTNF-α increased the expression of IL1R1 and IL6ST, receptors for IL1 and IL6, respectively, and decreased anti-inflammatory gene receptor expression (IL10R). hIL-17 and hTNF-α synergistically or additively induced CXCL8 and CCL2 expression and consequently promoted primary human neutrophil and human leukemia monocytic cell migration, respectively. In addition, hIL-17 and hTNF-α induced pro-coagulation gene (SERPINB2 and F3) expression and decreased anti-coagulation gene (TFPI, THBS1, and THBD) expression. Additionally, hIL-17 and hTNF-α synergistically decreased occludin expression and consequently promoted human antibody-mediated complement-dependent cytotoxicity. Interestingly, hTNF-α increased swine leukocyte antigen (SLA) class I expression; however, hIL-17 decreased TNF-α-mediated SLA-I upregulation. We concluded that hIL-17 and hTNF-α likely promote the inflammatory response, coagulation cascade, and xenoantibody-mediated cell injury. Thus, blockade of hIL-17 and hTNF-α together might be beneficial for xenograft survival in recipients.

The upstream regulators of microRNAs were rarely reported. Hydroquinone (HQ) is the main metabolite of benzene, one of the important environmental factors contributing to leukemia and lymphoma. In HQ-induced malignant transformed TK6 (TK6-HT) cells, the expression of PARP-1 and miR-223 were upregulated. When in PARP-1 silencing TK6-HT cells, miR-223 was downregulated and the apoptotic cell number correspondingly increased. In TK6 cells treated with HQ for different terms, the expression of miR-223 and PARP-1 were dynamically observed and found to be decreased and increased, respectively. Trichostatin A could increase the expression of miR-223, then the expression of HDAC1-2 and nuclear factor kappa B were found to be increased, but that of mH2A was decreased. PARP-1 silencing inhibited the protein expression of H3Ac, mH2A, and H3K27ac. By co-immunoprecipitation experiment, PARP-1 and HDAC2 were found to form a regulatory complex. In conclusion, we demonstrated that the upregulation of PARP-1 mediated activation of acetylation to promote the transcription of miR-223 possibly via coregulating with HDAC2, an epigenetic regulation mechanism involved in cell malignant transformation resulting from long-term exposure to HQ, in which course, H3K27ac might be a specific marker for the activation of histone H3, which also gives hints for benzene exposure research.

Unbalanced metabolism of an extracellular matrix (ECM) in nucleus pulposus cells (NPCs) is widely acknowledged as the primary cause of intervertebral disc degeneration (IDD). Irisin, a novel myokine, is cleaved from fibronectin type III domain-containing 5 (FNDC5) and has recently been proven to regulate the metabolism of ECM. However, little is known about its potential on NPCs and the development of IDD. Therefore, this study sought to examine the protective effects and molecular mechanism of irisin on IDD in vivo and in vitro. Decreased expression levels of FNDC5 and anabolism markers (COL2A1 and ACAN) but increased levels of catabolism markers (ADAMTS4) were found in degenerative nucleus pulposus (NP) tissues. In a punctured-induced rat IDD model, irisin treatment was found to significantly slow the development of IDD, and in TNF-α-stimulated NPCs, irisin treatment partly reversed the disorder of ECM metabolism. In mechanism, RNA-seq results suggested that irisin treatment affected the Hippo signaling pathway. Further studies revealed that with irisin treatment, the phosphorylation levels of key factors (LATS and YAP) were downregulated, while the expression level of CTGF was upregulated. Moreover, CTGF knockdown partially eliminated the protective effects of irisin on the metabolism of ECM in NPCs, including inhibiting the anabolism and promoting the catabolism. Taken together, this study demonstrated that the expression levels of FNDC5 were decreased in degenerative NP tissues, while irisin treatment promoted the anabolism, inhibited the catabolism of the ECM in NPCs, and delayed the progression of IDD via LATS/YAP/CTGF signaling. These results shed light on the protective actions of irisin on NPCs, leading to the development of a novel therapeutic target for treating IDD.

Neuroblastoma (NB) is the most common extracranial solid tumor in childhood, with 37% of patients diagnosed during infancy. This study is aimed at evaluating the survival outcome in infants diagnosed with neuroblastoma. This was a retrospective cohort study including patients under the age of 12 months with neuroblastoma from four tertiary referral centers in Beijing, China (Beijing Children's Hospital, Beijing Tongren Hospital, Peking University First Hospital, and Capital Institute of Pediatrics). Two hundred and forty-seven infants with neuroblastoma were included (male = 132 and female = 115). 91.1% (n = 225) patients were classified as having low-risk or intermediate-risk disease and 8.9% (n = 22) as having high-risk disease. The most common metastatic site is distant lymph node (n=89, 36.0%), followed by liver (n=57, 23.1%), bone (n=42, 17.0%), bone marrow (n=37, 15.0%), soft tissue (n=25, 10%), and central nervous system (n=4, 1.6%). MYCN amplification was present in 9.9% of tumor samples, chromosome 1p or 11q aberration in 14%. Treatment involved surgery alone in 9.7% of patients (n=24, all with low-risk disease), surgery followed by adjuvant chemotherapy in 50.2% (n=124), neoadjuvant chemotherapy followed by surgery in 40.1% (n=97), and chemotherapy alone in 0.8% (n=2). 4.9% (n=12) patients died, and the major cause of death is disease progression. Three-year event-free and overall survival were 91.6%±2.1% and 97.4%±1.1%, respectively, in patients with low- or intermediate-risk disease, and 58.7%±11.5% and 63.6%±11.2%, respectively, in those with high-risk disease.Conclusions: Infants with neuroblastoma achieve a reasonable clinical outcome when treated with surgery with or without chemotherapy using a risk-stratified approach in China. Such information will facilitate counseling, therapeutic decision-making, and development of adapted standard-of-care guidelines for future patients in the country. What is Known: • NB is a disease of infancy; 37% of patients are diagnosed as infants. • Most children younger than 12 months of age have a good prognosis even in the presence of metastatic disease. What is New: • Infants with neuroblastoma achieve reasonable clinical outcome when treated with surgery with or without chemotherapy using a risk-stratified approach in China. • CNS metastasis in infants with neuroblastoma is very rare at diagnosis and had a worse prognosis than those without metastasis.

Regulation of ubiquitination is involved in various processes in cancer occurrence and development, including cell cycle arrest, cell proliferation, apoptosis, invasion, metastasis, and immunity. Ubiquitination plays an important role not only at the transcriptional and post-translational levels but also at the protein level. When ubiquitination is in a pathological state, abnormally activated biological processes will not only induce cancer progression but also induce immune evasion. The main function of deubiquitinases (DUBs) is to remove ubiquitin chains from substrates, changing the biological activity of the substrates. It has great potential to improve the prognosis of cancer by targeting DUB to regulate proteome. Ubiquitin-specific peptidase 22 (USP22) belongs to the ubiquitin-specific protease (USP) family of DUBs and has been reported to be related to various physiological and pathological processes. USP22 is abnormally expressed in various malignant tumors such as prostate cancer, lung cancer, liver cancer, and colorectal cancer, which suggests that USP22 may play an important role in tumors. USP22 may stabilize programmed death ligand 1 (PD-L1) by deubiquitination while also regulating T-cell infiltration into tumors. Regulatory T cells (Tregs) are a unique class of immunosuppressive CD4+ T cells that primarily suppress the immune system by expressing the master transcription factor forkhead box protein 3 (FOXP3). USP22 was found to be a positive regulator of stable FOXP3 expression. Treg-specific ablation of USP22 leads to reduced tumor volume in multiple cancer models. This suggests that USP22 may regulate tumor resistance to immunotherapy. In this article, we review and summarize the biological functions of USP22 in multiple signal transduction pathways during tumorigenesis, immune evasion, and drug resistance. Furthermore, we propose a new possibility of combining USP22 with chemotherapeutic, targeted, and immunosuppressive drugs in the treatment of cancer.

Since bearing fault signal under complex running status is usually manifested as the characteristics of nonlinear and non-stationary, which implies it is difficult to extract accurate affluent features and achieve effective fault identification via conventional signal processing tools. In this article, a hybrid intelligent fault identification scheme, the combination of hierarchical dispersion entropy and improved Laplacian score, is proposed to address this problem, which is mainly composed of three procedures. First, the particle swarm optimization–based optimized hierarchical dispersion entropy is adopted to excavate multilevel fault symptoms from low-frequency and high-frequency components, which can both solve the shortcoming of missing of high-frequency feature information existing in the recently presented multiscale dispersion entropy and artificial parameter selection issue of hierarchical dispersion entropy. Second, an improved feature selection strategy based on improved Laplacian score is proposed to select the sensitive features to establish a low-dimensional feature data set by incorporating the weight coefficient into Laplacian score. Finally, the established low-dimensional feature data set is fed to a Softmax classifier to automatically identify different health conditions of rolling bearing. The efficacy of the proposed method is validated by two experimental cases. Results show that our approach is highly effective in recognizing different fault categories and severities of rolling bearing. Meanwhile, our approach exhibits higher accuracy and better identification performance than some similar entropy-based hybrid approaches and other identification methods reported in this article.

BACKGROUND Because of atypical clinical symptoms, lymphoma is easily confused with infectious diseases. Extranodal nasal-type natural killer/T-cell lymphoma (NKTL) is more common, and there are few cases of eyelid site onset and intracranial infiltration, which increases the difficulty of diagnosis. This disease usually has a very poor prognosis and there are few reports of recovery. CASE SUMMARY A 3-year-old boy was admitted to our hospital due to an initial misdiagnosis of "eyelid cellulitis" and failed antibiotic treatment. He was characterized by fever, right eyeball bulging, convulsions, and abnormal liver function. His blood Epstein-Barr virus (EBV) DNA was positive (8.798 × 104 copies/mL), and remained positive for about half a year. The cranial imaging examination suggested a space-occupying lesion in the right eyelid, with the right temporal lobe and meninges involved. The boy underwent ocular mass resection. The pathological diagnosis was NKTL. He was diagnosed as having NKTL with intracranial infiltration, combined with chronic active EBV infection (CAEBV). Then he underwent systemic chemotherapy and intrathecal injection. The boy suffered from abnormal blood coagulation, oral mucositis, diarrhea, liver damage, and severe bone marrow suppression but survived. Finally, the tumor was completely relieved and his blood EBV-DNA level turned negative. The current follow-up has been more than 2 years and his condition is stable. CONCLUSION This case suggests that chemotherapy combined with intrathecal injection may have a good effect on intracranial infiltrating lymphoma and CAEBV, which deserves further study and discussion.

TGFβ2 is an essential regulator of immune cell functionality, but the mechanisms whereby it drives immune infiltration in gastric cancer remain uncertain. The Oncomine and Tumor Immunoassay Resource (TIMER) databases were used for assessing the expression of TGFβ2, after which TIMER was used to explore the relationship between TGFβ2 and tumour immune infiltration. Finally, we assessed how TGFβ2 expression correlated with the expression of a set of marker genes associated with immune infiltration using TIMER and GEPIA. We determined TGFβ2 expression to be significantly correlated with outcome in multiple types of cancer in the Cancer Genome Atlas (TCGA), with the effect being particularly pronounced in gastric cancer. Furthermore, elevated TGFβ2 expression was found to be significantly correlated with gastric cancer N staging, and with the expression of a variety of immune markers associated with particular immune cell subsets. These results indicate that TGFΒ2 is associated with patient outcome and tumour immune cell infiltration in multiple cancer types. This suggests that TGFβ2 is a key factor which governs immune cell recruitment to gastric cancer tumours, potentially playing a vital role in governing immune cell infiltration and thus representing a valuable prognostic biomarker in gastric cancer patients.

An imbalance between matrix synthesis and degradation is the hallmark of intervertebral disc degeneration while inflammatory cytokines contribute to the imbalance. Bromodomain and extra-terminal domain (BET) family is associated with the pathogenesis of inflammation, and inhibition of BRD4, a vital member of BET family, plays an anti-inflammatory role in many diseases. However, it remains elusive whether BRD4 plays a similar role in nucleus pulposus (NP) cells and participates in the pathogenesis of intervertebral disc degeneration. The present study aims to observe whether BRD4 inhibition regulates matrix metabolism by controlling autophagy and NLRP3 inflammasome activity. Besides, the relationship was investigated among nuclear factor κB (NF-κB) signaling, autophagy and NLRP3 inflammasome in NP cells. Here, real-time polymerase chain reaction, western blot analysis and adenoviral GFP-LC3 vector transduction in vitro were used, and it was revealed that BRD4 inhibition alleviated the matrix degradation and increased autophagy in the presence or absence of tumor necrosis factor α. Moreover, p65 knockdown or treatment with JQ1 and Bay11-7082 demonstrated that BRD4 inhibition attenuated NLRP3 inflammasome activity through NF-κB signaling, while autophagy inhibition by bafilomycin A1 promoted matrix degradation and NLRP3 inflammasome activity in NP cells. In addition, analysis of BRD4 messenger RNA expression in human NP tissues further verified the destructive function of BRD4. Simply, BRD4 inhibition alleviates matrix degradation by enhancing autophagy and suppressing NLRP3 inflammasome activity through NF-κB signaling in NP cells.

Lnc-BMP1-1 is a lncRNA transcribed from SFTPC (surfactant associated protein C), a lung tissue specific gene encoding pulmonary-associated surfactant protein C (SPC) that is solely secreted by alveolar typeⅡ epithelial cells, among which the ones with SFTPC+ might be transformed into lung adenocarcinoma cells. Caveolin-1 (Cav-1) is a candidate tumor suppressor gene and is vital for coping with oxidative stress induced by cigarette smoke. When comparing lung cancer tissues with their adjacent normal tissues, the expression of lnc-BMP1-1 were decreased, especially in patients with cigarette smoking history (P=0.027), and positively associated with the expression of Cav-1 (P

Hepatocellular carcinoma (HCC), one of the main causes of cancer-related deaths globally, is characterized by rapid growth and high invasiveness. Accumulating evidence demonstrates that long noncoding RNAs (lncRNAs) play critical roles in the growth and metastasis of HCC. Recently, lncRNA LINC01123 has been found to contribute to cell proliferation and aerobic glycolysis in lung cancer. However, the function of LINC01123 in HCC, as well as the underlying mechanism of its action, remain unclear. Here, we found that the expression of LINC01123 was clearly upregulated in HCC tissues compared to nontumor tissues. Furthermore, expression of LINC01123 in HCC cells was significantly higher than in LO2 cells. Importantly, the upregulated level of LINC01123 was related to unfavorable clinical features and poor prognosis of HCC. Next, we demonstrated that LINC01123 knockdown suppressed the proliferation, migration and invasion of HCC cells in vitro. Depletion of LINC01123 inhibited HCC xenograft growth in vivo. Conversely, ectopic expression of LINC01123 facilitated HCC cell proliferation and invasion. Mechanistically, LINC01123 acted as a molecular sponge for miR-34a-5p in HCC cells. Tuftelin1 (TUFT1) was identified as the target gene of miR-34a-5p. LINC01123 positively regulated TUFT1 level by targeting of miR-34a-5p in HCC cells. Notably, TUFT1 restoration can abolish miR-34a-5p-induced inhibitory effects on HCC cell proliferation, migration and invasion. In conclusion, LINC01123 was overexpressed in HCC and accelerated cancer cell proliferation and invasion by regulating the miR-34a-5p/TUFT1 axis.