Search

c-Myc and E2F1 play critical roles in many human cancers. As long noncoding RNAs (lncRNA) are known to regulate various tumorigenic processes, elucidation of mechanisms of cross-talk between lncRNAs and c-Myc/E2F1-related signaling pathways could provide important insights into cancer biology. In this study, we used integrated bioinformatic analyses and found that the lncRNA MNX1-AS1 is upregulated in non–small cell lung cancer (NSCLC) via copy-number gain and c-Myc–mediated transcriptional activation. High levels of MNX1-AS1 were associated with poor clinical outcomes in patients with lung cancer. MNX1-AS1 promoted cell proliferation and colony formation in vitro and tumor growth in vivo. MNX1-AS1 bound and drove phase separation of IGF2BP1, which increased the interaction of IGF2BP1 with the 3′-UTR (untranslated region) of c-Myc and E2F1 mRNA to promote their stability. The c-Myc/MNX1-AS1/IGF2BP1 positive feedback loop accelerated cell-cycle progression and promoted continuous proliferation of lung cancer cells. In a lung cancer patient-derived xenograft model, inhibition of MNX1-AS1 suppressed cancer cell proliferation and tumor growth. These findings offer new insights into the regulation and function of c-Myc and E2F1 signaling in NSCLC tumorigenesis and suggest that the MNX1-AS1/IGF2BP1 axis may serve as a potential biomarker and therapeutic target in NSCLC. Significance: MNX1-AS1 drives phase separation of IGF2BP1 to increase c-Myc and E2F1 signaling and to activate cell-cycle progression to promote proliferation in NSCLC.

c-Myc and E2F1 play critical roles in many human cancers. As long noncoding RNAs (lncRNA) are known to regulate various tumorigenic processes, elucidation of mechanisms of cross-talk between lncRNAs and c-Myc/E2F1-related signaling pathways could provide important insights into cancer biology. In this study, we used integrated bioinformatic analyses and found that the lncRNA MNX1-AS1 is upregulated in non–small cell lung cancer (NSCLC) via copy-number gain and c-Myc–mediated transcriptional activation. High levels of MNX1-AS1 were associated with poor clinical outcomes in patients with lung cancer. MNX1-AS1 promoted cell proliferation and colony formation in vitro and tumor growth in vivo. MNX1-AS1 bound and drove phase separation of IGF2BP1, which increased the interaction of IGF2BP1 with the 3′-UTR (untranslated region) of c-Myc and E2F1 mRNA to promote their stability. The c-Myc/MNX1-AS1/IGF2BP1 positive feedback loop accelerated cell-cycle progression and promoted continuous proliferation of lung cancer cells. In a lung cancer patient-derived xenograft model, inhibition of MNX1-AS1 suppressed cancer cell proliferation and tumor growth. These findings offer new insights into the regulation and function of c-Myc and E2F1 signaling in NSCLC tumorigenesis and suggest that the MNX1-AS1/IGF2BP1 axis may serve as a potential biomarker and therapeutic target in NSCLC.Significance:MNX1-AS1 drives phase separation of IGF2BP1 to increase c-Myc and E2F1 signaling and to activate cell-cycle progression to promote proliferation in NSCLC.

Supplementary Materials and Methods

The quick rearrangement of IGF2BP1 droplets. A time-lapse movie of droplets formed by IGF2BP1 undergoes a fusion event.

Supplementary Figure S1-S5

Supplementary Table S1-S4

Long non-coding RNAs (lncRNAs) are reported to play key roles in tumorigenesis. However, the mechanisms underlying lncRNA-mediated regulation of RNA-binding protein phase separation in tumorigenesis have not been completely elucidated. In this study, an oncogenic lncRNA MELTF-AS1 was identified using systematic data analysis, screening, and verification. MELTF-AS1 was markedly upregulated in non-small cell lung cancer (NSCLC). High MELTF-AS1 levels were associated with advanced tumor-node-metastasis stage (TNM), high tumor size, and decreased survival time. Functionally, MELTF-AS1 regulated cell proliferation and metastasis in vitro and in vivo. RNA sequencing analysis revealed that MELTF-AS1 knockdown specifically modulated genes associated with cell proliferation, apoptosis, and migration. Mechanistically, at the genome level, copy number amplification promoted MELTF-AS1 expression. At the transcriptional level, the transcription factor SP1 directly activated MELTF-AS1 transcription by binding to its promoter. Furthermore, MELTF-AS1 could directly bind and drive the phase separation of YBX1, which was an RNA-binding protein and involved in tumorigenesis, thus activating ANXA8 transcription and promoting tumorigenesis of NSCLC. Aberrant activation of ANXA8 and promotion of tumorigenesis have been found in a variety of tumors. These novel findings demonstrated the critical role of MELTF-AS1-driven phase separation-mediated transcriptional regulation and provided a potential novel diagnostic and therapeutic target for NSCLC.

It was recently demonstrated that long noncoding RNAs (lncRNAs) have key regulation functions in the biology of human cancer. The current study aimed to determine the expression, clinicopathological characteristics and functional roles of lncRNA PCAT18 in gastric cancer (GC). By analysis of (Gene Expression Omnibus) GEO and TCGA data, following experimental verification, we identified the function role and molecular mechanism of PCAT18 in tumorigenesis of GC. We discovered that PCAT18 is significantly decreased in paired GC tissues and correlates with a poor outcome. Mechanistic studies found that suppression of the expression of EZH2 could prevent its binding to the PCAT18's promoter region and decrease H3K27's trimethylation modification. In addition, PCAT18 could adjust cell proliferation of GC in vitro as well as in vivo. Further mechanism research revealed that PCAT18 could regulate the expression of p16 by interacting with miR-570a-3p, thus inhibiting cell proliferation of GC. Our results have shown that the histone modification-mediated epigenetic suppression of PCAT18 and its essential role of PCAT18 in GC oncogenesis, which could provide a theoretical basis for GC therapy.

Numerous studies have reported that a variety of long noncoding RNAs (lncRNAs) can promote the proliferation, invasion, and migration of different tumor cells. However, different lncRNAs regulate cell functions in various forms, and the exact mechanisms are not clear. Here, we investigated the effect of the lncRNA ELF3‐AS1 on gastric cancer (GC) cell function and explored the exact mechanism. Quantitative real‐time polymerase chain reaction was used to detect the expression of ELF3‐AS1 in GC tissues and adjacent nontumor tissues. Knockdown and overexpression of ELF3‐AS1 was used to detect the effect of ELF3‐AS1 on cell function. Potential downstream target genes were identified using RNA transcriptome sequencing, while RNA immunoprecipitation, chromatin immunoprecipitation, and Western blotting were performed to explore the tumor promotion mechanisms of ELF3‐AS1. We observed that ELF3‐AS1 was highly expressed in GC tissues, and high ELF3‐AS1 expression predicted poor prognosis. The knockdown of ELF3‐AS1 significantly inhibited cell proliferation, migration, and epithelial‐mesenchymal transition and promoted apoptosis. Mechanistic investigations revealed that ELF3‐AS1 may regulate the downstream target gene, C‐C motif chemokine 20, by binding with the RNA‐binding protein hnRNPK. Additionally, we found that high ELF3‐AS1 expression was associated with thrombocytosis. Interleukin‐6 and thrombopoietin may be involved in ELF3‐AS1–induced paraneoplastic thrombocytosis. Together, our results demonstrate that aberrantly expressed ELF3‐AS1 in GC may play important roles in oncogenesis and progression and is expected to become a new target for the diagnosis and treatment of GC., ELF3‐AS1 regulates the downstream target gene CCL20 by binding with hnRNPK to play a role in promoting gastric cancer (GC) progression. ELF3‐AS1 promotes the expression of thrombopoietin (THPO) to increase the level of platelets in the peripheral blood.

Background Despite the increasing application of tolvaptan in cardiac surgery, there is no information on the use of tolvaptan in Stanford patients with type A aortic dissection. This study aimed to evaluate the postoperative clinical effects of tolvaptan in patients with type A aortic dissection after tafter surgery. Methods A retrospective analysis was performed on 45 patients treated for type A aortic dissection in our hospital from 2018 to 2020. These included 21 patients who were treated with tolvaptan (Group T) and 24 patients who received traditional diuretics (Group L). The hospital's electronic health records were used to obtain perioperative data. Results Group T did not differ significantly from Group L in terms of the duration of mechanical ventilation, postoperative blood required, length of catecholamine use, or the amount of intravenous diuretic drugs administered (all P > 0.05). The development of postoperative atrial fibrillation was significantly less in the tolvaptan group (P = 0.023). The urine volumes and change in body weight loss were slightly higher in group T than in group L but the differences were non-significant (P > 0.05). Serum potassium, creatinine, and urea nitrogen levels did not differ between the groups in the week after surgery, At the same time, sodium was significantly higher in the Group T group on day 7 after transfer from the ICU (P = 0.001). In Group L, sodium levels were also elevated by day 7 (P = 0.001). On days 3 and 7, serum creatinine and urea nitrogen levels increased in both groups (both P Conclusions Both tolvaptan and traditional diuretics were found to be effective and safe for patients with acute Stanford type A aortic dissection. Moreover, tolvaptan may be associated with reducing the incidence of postoperative atrial fibrillation.

Oncogene‐like effects of TMEM92‐AS1: LncRNA TMEM92‐AS1 regulates the expression of downstream target gene CCL5 by binding with YBX1 protein to play the role of oncogene and affects prognosis of patients with gastric cancer. TMEM92‐AS1 may also promote the secretion of G‐CSF by tumour cells to increase the level of neutrophils in the peripheral blood., Numerous studies have revealed that long noncoding RNAs (lncRNAs) with oncogene properties play vital roles in gastric cancer (GC). In this study, we aimed to elucidate the function of TMEM92‐AS1 in GC progression and to investigate its underlying mechanisms. TMEM92‐AS1 was filtered from the Gene Expression Omnibus database. GC tissues and adjacent normal tissues were used to detect the expression level of TMEM92‐AS1. MTT, colony‐formation assays, Edu, cell cycle, apoptosis and subcutaneous tumour formation assays were used to detect the role of TMEM92‐AS1 in cell function. RNA transcriptome sequencing was used to seek downstream target genes. Reverse transcription (RT)‐qPCR, western blot, RNA and chromatin immunoprecipitation assays were used to investigate the mechanisms involved. TMEM92‐AS1 was significantly overexpressed in GC tissues and correlated with poor overall survival and disease‐free survival. Furthermore, TMEM92‐AS1 promoted GC cell proliferation and migration in vitro and tumorigenic ability in vivo. RNA transcriptome sequence analysis revealed a potential downstream target gene, C‐C motif chemokine ligand 5 (CCL5), and a mechanistic study found that TMEM92‐AS1 regulated CCL5 by binding to the transcription factor Y‐box binding protein 1(YBX1), which has oncogene properties. In addition, TMEM92‐AS1 was found to be associated with peripheral blood leukocyte counts, especially neutrophils. Further investigation found that TMEM92‐AS1 may affect leukocytes via regulation of the expression of granulocyte colony‐stimulating factor in GC tissues. Our data provide an in‐depth insight into the mechanism behind the lncRNA TMEM92‐AS1, how it promotes GC progression and the possible mechanism in affecting peripheral leukocyte counts. Therefore, TMEM92‐AS1 is a potential target for GC individualized therapy and prognostic assessment.

MicroRNAs are crucial regulators in the phenotype switch of vascular smooth muscle cells (VSMCs). Nonetheless, the role of miR-146b-3p in VSMCs remains unclear. In the present study, platelet-derived growth factor-BB (PDGF-BB) at different concentrations was employed to stimulate VSMCs for different times, to establish the model of VSMC dysfunction. The relative expression of miR-146b-3p was quantified by quantitative real-time polymerase chain reaction (qRT-PCR). The proliferation of VSMCs was measured by BrdU assay. Flow cytometry analysis was employed for the analysis of cell cycle. VSMC migration was detected by Transwell assay. Phosphoinositide-3 kinase catalytic subunit-gamma (PIK3CG) and markers of VSMC differentiation, including α-SMA, SM-22α, SMMHC, and Calponin were examined employing Western blot. The targeting relationship between miR-146b-3p and PIK3CG 3ʹ-UTR was affirmed by dual-luciferase gene assay. We report that the reduction of miR-146b-3p expression was induced by PDGF-BB in a time-dependent and dose-dependent manner (P, Graphical Abstract

Gigantopterid plants share common traits of megaphyllous leaves with multi-ordered venation and have a stratigraphic distribution restricted to the Permian Period. They display a large variety of l...

In recent years, blockchain technology has been developing rapidly. More and more traditional industries are using blockchain as a platform for information storage and financial transactions, mainly because of its new characteristics of non-tamperability and decentralization compared with the traditional systems. As a representative of blockchain 2.0, Ethereum has gained popularity upon its introduction. However, because of the anonymity of blockchain, Ethereum has also attracted the attention of some unscrupulous people. Currently, millions of contracts are deployed on Ethereum, many of which are fraudulent contracts deployed by unscrupulous people for profit, and these contracts are causing huge losses to investors worldwide. Ponzi contracts are typical of these contracts, which mainly reward the funds invested by later investors to early investors, and later investors will have no gain. However, although there are some studies for identifying Ponzi contracts on Ethereum, there is some room for progress in the research. Therefore, we propose a method to detect Ponzi scheme contracts on Ethereum-CTRF. This method forms a dataset by extracting the word features and sequence features of the smart contract’s code and the features of transactions. The dataset is divided into a training set and a test set. Oversampling is performed on the training set to deal with the problem of positive and negative sample imbalance. Finally, the model is trained on the training set and tested on the test set. The experimental results show that the model has significantly improved recall compared with existing Ponzi contract detection methods.

Dysregulated expression of long non-coding RNAs (lncRNAs) has been reported in many types of cancers, indicating that it has important regulatory roles in human cancer biology. Recently, lncRNA urothelial cancer-associated 1 (UCA1) was shown to be dysregulated in many cancer types, but the detailed mechanisms remain largely unknown. In our study, we found that upregulated UCA1 is associated with poor prognosis in gastric cancer patients. Further experiments revealed that UCA1 knockdown significantly repressed the proliferation and migration both in vitro and in vivo. Moreover, RNA sequencing (RNA-seq) analysis revealed that UCA1 knockdown preferentially affected genes that are linked to cell proliferation, cell cycle, and cell migration. Mechanistically, UCA1 promotes cell proliferation progression through repressing p21 and Sprouty RTK signaling antagonist 1 (SPRY1) expression by binding to EZH2. We found that UCA1 could mediate the trimethylation of H3K27 in promoters of p21 and SPRY1. To our knowledge, this is the first report showing the global gene profile of downstream targets of UCA1 in the progression of gastric cancer. Collectively, our data reveal the important roles of UCA1 in gastric cancer (GC) oncogenesis. Keywords: UCA1, cell proliferation, cell migration, p21, SPRY1

Classifications and comparisons of petrified wood are currently based primarily on observable morphologies. The mineralogical characteristics of specimens collected from Qian Jiandian, Yanqing UNES...

Cholangiocarcinoma (CCA) is the most common biliary tract malignancy, with a low survival rate and limited treatment options. Long non-coding RNAs (lncRNAs) have recently been verified to have significant regulatory functions in many kinds of human cancers. It was discovered in this study that the lncRNA PVT1, whose expression is significantly elevated in CCA, could be a molecular marker of CCA. Experiments indicated that PVT1 knockdown greatly inhibited cell migration and proliferation in vitro and in vivo. According to RNA sequencing (RNA-seq) analysis, PVT1 knockdown dramatically influenced target genes associated with cell angiogenesis, cell proliferation, and the apoptotic process. RNA immunoprecipitation (RIP) analysis demonstrated that, by binding to epigenetic modification complexes (PRC2), PVT1 could adjust the histone methylation of the promoter of ANGPTL4 (angiopoietin-like 4) and, thus, promote cell growth, migration, and apoptosis progression. The data verified the significant functions of PVT1 in CCA oncogenesis, and they suggested that PVT1 could be a target for CCA intervention. Keywords: cholangiocarcinoma, lncRNA PVT1, ANGPTL4

Background: Recently, long non-coding RNAs (lncRNAs) have been verified to have significant regulatory roles in multiple human cancer processes. Long non-coding RNA LINC00152, located on chromosome 2p11.2, was identified as an oncogenic lncRNA in various cancers. However, the biological function and molecular mechanism of LINC00152 in cholangiocarcinoma (CCA) are still unknown.Methods: Bioinformatic analysis was performed to determine LINC00152 expression levels in the CCA and normal tissues by using raw microarray data downloaded from Gene Expression Omnibus (GSE76297) and The Cancer Genome Atlas (TCGA). Quantitative reverse transcription PCR (qRT-PCR) was used to validate LINC00152 expression in the CCA tissues compared with that in the paired normal tissues. CCK8, colony formation, Edu assays, transwell assays, flow cytometry, and in vivo tumor formation assays were performed to investigate the biological function of LINC00152 on CCA cell phenotypes. RNA-seq was carried out to identify the downstream target gene which was further examined by qRT-PCR, western bolt and rescue experiments. RNA immunoprecipitation (RIP) and Chromatin immunoprecipitation (ChIP) assays were performed to reveal the factors involved in the mechanism of LINC00152 functions in CCA.Results: LINC00152 is significantly upregulated in cholangiocarcinoma. LINC00152 regulated the proliferation and migration of cholangiocarcinoma cells both in vitro and in vivo. RNA-seq revealed that LINC00152 knockdown preferentially affected genes linked with cell proliferation, cell differentiation and cell adhesion. Furthermore, mechanistic investigation validated that LINC00152 could bind EZH2 and modulate the histone methylation of promoter of leucine rich repeats and immunoglobulin like domains 1 (LRIG1), thereby affecting cholangiocarcinoma cells growth and migration.Conclusion: Taken together, these results demonstrated the significant roles of LINC00152 in cholangiocarcinoma and suggested a new diagnostic and therapeutic direction of cholangiocarcinoma.

Background Recently, increasing evidence shows that long noncoding RNAs (lncRNAs) play a significant role in human tumorigenesis. However, the function of lncRNAs in human gastric cancer remains largely unknown. Results By using publicly available expression profiling data from gastric cancer and integrating bioinformatics analyses, we screen and identify a novel lncRNA, HOXC-AS3. HOXC-AS3 is significantly increased in gastric cancer tissues and is correlated with clinical outcomes of gastric cancer. In addition, HOXC-AS3 regulates cell proliferation and migration both in vitro and in vivo. RNA-seq analysis reveals that HOXC-AS3 knockdown preferentially affects genes that are linked to proliferation and migration. Mechanistically, we find that HOXC-AS3 is obviously activated by gain of H3K4me3 and H3K27ac, both in cells and in tissues. RNA pull-down mass spectrometry analysis identifies that YBX1 interacts with HOXC-AS3, and RNA-seq analysis finds a marked overlap in genes differentially expressed after YBX1 knockdown and those transcriptionally regulated by HOXC-AS3, suggesting that YBX1 participates in HOXC-AS3-mediated gene transcriptional regulation in the tumorigenesis of gastric cancer. Conclusions Together, our data demonstrate that abnormal histone modification-activated HOXC-AS3 may play important roles in gastric cancer oncogenesis and may serve as a target for gastric cancer diagnosis and therapy. Electronic supplementary material The online version of this article (10.1186/s13059-018-1523-0) contains supplementary material, which is available to authorized users.

Preeclampsia (PE) is a syndrome manifested by high blood pressure that could develop in the latter half of pregnancy; however, the underlying mechanisms are not understood. Recent evidence points to the function of noncoding RNAs (ncRNAs) as novel regulators of the invasion, migration, proliferation, and apoptosis of trophoblasts involved in the development of placental vasculature. Here, we investigated the role of long intergenic ncRNA 00473 (linc00473) in PE and the associated molecular mechanisms. The expression of linc00473 was downregulated in the placenta of patients with severe PE as revealed by qRT-PCR analysis. In vitro, linc00473 knockdown in trophoblast cell lines HTR-8/SVneo, JAR, and JEG3 significantly inhibited cell proliferation and promoted apoptosis, whereas linc00473 overexpression stimulated trophoblast proliferation. The mechanistic insights were provided by RNA-seq and qRT-PCR, which revealed that linc00473 could regulate the transcription of genes relevant to cell growth, migration, and apoptosis. In particular, linc00473 inhibited the expression of tissue factor pathway inhibitor 2 (TFPI2) through binding to lysine-specific demethylase 1 (LSD1). These results indicate that linc00473 could be involved in the pathogenesis and development of PE and may be a candidate biomarker as well as therapeutic target for this disease. Keywords: preeclampsia, linc00473, LSD1, proliferation

Substantial evidence shows that long non-coding RNAs (lncRNAs) participate in many biological mechanisms, and their dysregulation are also involved in the development and progression of cancers, including gastric cancer (GC). Long intergenic non-coding RNA 00324 (LINC00324), a 2115 bp ncRNA, is located on chromosome 17p13.1. The biological function and molecular mechanisms of LINC00324 in GC remains undiscovered. In this paper, we found that the expression level of LINC00324 was significantly upregulated in GC tissues compared with the corresponding normal tissues. The overexpression of LINC00324 was correlated with advanced TNM stage, larger tumor size, and lymph node metastasis as well as poor prognosis. Further experiments revealed that knockdown of LINC00324 could suppress the proliferation of GC cells. RNA transcriptome sequencing technology revealed that FAM83B may be a significant downstream target gene of LINC00324. LINC00324 could combine with the RNA-binding protein (RBP) human antigen R (HuR) and thus stabilize the expression of FAM83B. Moreover, rescue assays showed that the reduced FAM83B expression partially reversed the promotion of cell growth in GC induced by the overexpression of LINC00324. In conclusion, our study revealed that LINC00324 acted as an oncogene in tumorigenesis and progression, suggesting that it could be a new biomarker in diagnosis and prognosis of GC.

Background Mounting evidence indicates that long noncoding RNAs (lncRNAs) could play a pivotal role in cancer biology. However, the role and molecular mechanism and global genes that were mediated by lncRNA AFAP1-AS1 in non–small cell lung cancer (NSCLC) remain largely unknown. Methods Expression of AFAP1-AS1 was analyzed in 92 NSCLC tissues and cell lines by Quantitative real time polymerase chain reaction (qRT-PCR). The effect of AFAP1-AS1 on proliferation was evaluated by function assays both in in vitro and in vivo. RNA-seq assays were performed after knockdown AFAP1-AS1. RNA immunoprecipitation (RIP) was performed to confirm the interaction between AFAP1-AS1 and EZH2. Chromatin immunoprecipitation (ChIP) was used to study the promoter region of p21. Results AFAP1-AS1 expression was increased in NSCLC tissues and was correlated with clinical outcomes of NSCLC. Further experiments revealed that inhibition of its expression in NSCLC cells resulted in diminished cell growth in vitro and in vivo. RNA-seq revealed that knockdown of AFAP1-AS1 could induce the expression of p21. Mechanistic investigations found that AFAP1-AS1 could interact with EZH2 and recruit EZH2 to the promoter regions of p21, thus epigenetically repressing p21 expression. Conclusions Together, these results suggest that lncRNA AFAP1-AS1 may serve as a candidate prognostic biomarker and target for new therapies in human NSCLC. Electronic supplementary material The online version of this article (10.1186/s12943-018-0836-7) contains supplementary material, which is available to authorized users.

Background/Aims: Lung cancer (LC) is a serious disease with high morbidity and mortality. Long noncoding RNAs (lncRNAs) have garnered attention because they participate in diverse human disorders, including cancer. Our study examined the long intergenic noncoding RNA 00707 (LINC00707). The effects of LINC00707 on lung adenocarcinoma (LAD) and molecular mechanisms are unclear. This study is aimed to investigate the role of LINC00707 in the malignant processes of LAD. Methods: Quantitative reverse transcription PCR (qRT-PCR) was used to examine the expression level of LINC00707 in tissues and cell lines. The association of LINC00707 expression and postoperative prognosis was analyzed by the Kaplan-Meier method and log-rank test. Cell proliferation was evaluated in vitro and in vivo. Transwell assays were performed to examine cell migration. Cell cycle and apoptosis was determined by flow -cytometric and western blot analyses. Microarray analysis was conducted to screen for the downstream target gene Cdc42 of LINC00707, which was identified by qRT-PCR, functional analysis, and rescue experiment. Results: The expression level of LINC00707 was clearly upregulated in LAD tissues compared to that in corresponding normal tissues. Its overexpression was related to advanced TNM stage, larger tumor size, lymphatic metastasis, and poor prognosis. Functional assays revealed that LINC00707 knockdown repressed LAD cell proliferation both in vitro and in vivo. This process may involve the inducing of G1 arrest and apoptosis. Moreover, cell migration was impaired after LINC00707 inhibition. Microarray analysis and rescue assays suggested that Cdc42 is an important target gene involved in the carcinogenesis of LINC00707. Conclusions: In summary, LINC00707 is a noncoding oncogene that exerts important regulatory functions in LAD, suggesting its potential as a biomarker in the prognosis and treatment of LAD.

Foliage of a new peltaspermalean seed fern is described on the basis of a large collection of well-preserved plant adpressions with cuticle from the Upper Triassic Karamay Formation in Xinjiang Province, NW China. Pinnae are lanceolate with undulate-dentate margins and with fascicular lateral veins in lobes. Tertiary veins are simple as are interfascicular veins that occur between fascicular lateral veins. Cuticles are thick, amphistomatic, with abaxial and adaxial cuticles being similar to each other and having clear costal and intercostal areas. Stomata are sunken and randomly distributed on both the abaxial and the adaxial cuticle. The stomatal complex is monocyclic and comprises 4–7 subsidiary cells. Papillae are present on ordinary cells and on subsidiary cells surround the stomatal aperture. The adaxial leaf surface has a stomatal index of 3.27 and an average stomatal density of 15 per mm2, whereas the abaxial surface has a stomatal index of 5.25 and an average stomatal density of 30 per mm2. This is the first report of the cuticular structure of Scytophyllum from the Junggar Basin, which now enables detailed comparison with other species of the genus from Eurasia. Analysis of the sedimentary succession containing Scytophyllum suggests a humid or seasonally dry environment, but the thick cuticles with sunken stomata and abundant papillae indicate that the plant was adapted to living in water-stressed conditions.

An early Permian tuff bed between Coal 7 and Coal 6 of the Wuda Coalfield in Inner Mongolia bears T0 peat-forming vegetation preserved in situ. Documentation of the fossil record uncovered in an area of about 80 m2 shows 14 morphotaxa representing 11 whole-plant species with a wide variety of growth forms. The uncovered phytocoenosis is interpreted as a forest dominated by cordaites as the tallest trees, the remains of which covered over 50% of the excavated area. Marattialean tree ferns represent the lower canopy that was not taller than about 3 m. This storey fills gaps between cordaites and covers over 20% of the area. A rare element of lower canopy taxa was the cycadophyte genus Pterophyllum represented by a single plant. Poorly developed herbaceous groundcover includes Sphenophyllum oblongifolium, and four small fern species mostly with sphenopteroid type of foliage. Although members of the herbaceous layer covered only 7% of the excavated area, it was the most diverse storey of the peat-forming forest. Considering the small area excavated, along with the higher diversity known from the same tuff bed in the adjacent, former opencast mine, it appears that species richness in the forest was comparable to some of the less diverse Westphalian peat-forming floras in Euramerica.

The late Paleozoic genera Chansitheca Rege, Oligocarpia Goppert and Szea Z. Yao et T. N. Taylor are small ferns that represent putative early members of the Gleicheniaceae based on their morphology and the anatomy of their fertile organs. However, the rachis and cauline anatomy are unknown, rendering their systematic affinities controversial. Here we document rachides with partly preserved anatomical structure associated with compression/impression specimens of Chansitheca wudaensis from the Wuda Tuff Flora. The in situ preservation of the flora, occasional organic connection and close association, and matching size, proportions and xylem structure indicate that these rachides belonged to the same plant that produced fertile fronds of the Chansitheca wudaensis type and vegetative fronds of the Sphenopteris type co-occurring in this flora. The new details of the anatomy and morphology necessitate emendations to the diagnosis for this species. As the Wuda Tuff Flora has been dated to be 298.34 ± 0.09 million years ago (Asselian, Permian), this represents the oldest unequivocal evidence of Gleicheniaceae. Our results thus demonstrate that the Gleicheniaceae had already diverged from other ferns families, including the Osmundaceae, by this time.

A silicified gymnospermous wood, Yangquanoxylon miscellum gen. nov. et sp. nov., is described from the Upper Pennsylvanian-lower Permian Taiyuan Formation, Yangquan City, Shanxi Province, North China. The pycnoxylic wood is composed of thick-walled tracheids and thin-walled rays. It is characterized by mixed radial tracheid pits, uniseriate and homogeneous rays, occurrence of scalariform radial pitting, and various types of cross-field pitting. There are four types of cross-field pitting in Y. miscellum gen. nov. et sp. nov., including simple, taxodioid, phyllocladoid, and araucarioid. The absence of growth rings within fossil woods described here and reported previously from North China suggests a humid climate with minimal precipitation variations during the Late Pennsylvanian-early Permian.

Fungi today occur in great diversity on virtually every plant part, living and dead. Cordaitalean gymnosperms were important components of floral element in the late Palaeozoic palaeotropical floras. However, fungi associated with the stems of these plants are rarely documented. Basidiomycetes are one of the major groups of extant fungi, and may have played an important role in ancient continental ecosystems, but are rarely discovered in the upper Palaeozoic. A stem of the fossil cordaite Shanxioxylon sp. containing abundant ramifying and septate hyphae with clamp connections is preserved in the upper Taiyuan Formation (Cisuralian, lower Permian) in Shanxi Province, North China. The fungal remains described here are the first evidence of fungi associated with Permian cordaitalean stems from Cathaysia. Their association with Cathaysian cordaites expands knowledge of the ecology and plant substrates of basidiomycetous fungi in the Permian.

Background: In recent years, long non-coding RNAs (lncRNAs) have been shown to be a novel class of regulators of cancer biological processes. Although lncRNAs are dysregulated in numerous cancer types, limited data are available on the expression profiles and potential functions of lncRNAs in lung adenocarcinoma (LUAD). This study evaluated the expression and biological roles of lncRNA SOX21 antisense RNA 1 (SOX21-AS1) in LUAD. Methods: Quantitative reverse transcription PCR (qRT-PCR) was performed to detect the expression levels of SOX21-AS1 in 68 pairs of LUAD tissues and corresponding non-tumor tissues. The effect of SOX21-AS1 on proliferation was evaluated by MTT, colony formation, EdU assays, flow-cytometric analysis and in vivo tumor formation assays. Real-time PCR, western-blot and immunohistochemistry were used to evaluate the mRNA and protein expression of p57. Results: Higher expression levels of SOX21-AS1 positively correlated with tumor size and advanced tumor–node–metastasis (TNM) stage. Multivariate analyses indicated that SOX21-AS1 expression could serve as an independent prognostic factor for overall survival of LUAD. Furthermore, knockdown of SOX21-AS1 significantly inhibited LUAD cell proliferation both in vitro and in vivo and induced cell cycle phase arrest and cell apoptosis. Importantly, through qRT-PCR and western blot analysis, we found that inhibition of SOX21-AS1 remarkably induced p57 expression. Conclusions: Collectively, our study demonstrates that SOX21-AS1 is involved in the development and progression of LUAD and that SOX21-AS1 may be a potential diagnostic factor as well as a target for new therapies for patients with LUAD.