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Background: The molecular mechanisms underlying chemoresistance are still poorly understood in nasopharyngeal cancer; the protein expression of ERCC1 in DNA repair genes has been reported related t...

Hepatocellular carcinoma (HCC) belongs to the most frequent cancer with a high death rate worldwide. Thousands of long non-coding RNAs (lncRNAs) have been confirmed to influence the development of human cancers, including HCC. Nevertheless, the biological role of PRR34 antisense RNA 1 (PRR34-AS1) in HCC remains obscure. Here, we observed via quantitative real-time reverse transcriptase polymerase chain reaction (quantitative real-time RT-PCR) that PRR34-AS1 was highly expressed in HCC cells. Functional assays revealed that PRR34-AS1 promoted HCC cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) process in vitro and facilitated tumor growth in vivo. In addition, western blot analysis and TOP Flash/FOP Flash reporter assays verified that PRR34-AS1 stimulated Wnt/β-catenin pathway in HCC cells. Furthermore, RNA immunoprecipitation (RIP), RNA pull-down, and luciferase reporter assays uncovered that PRR34-AS1 sequestered microRNA-296-5p (miR-296-5p) to positively modulate E2F transcription factor 2 (E2F2) and SRY-box transcription factor 12 (SOX12) in HCC cells. Importantly, chromatin immunoprecipitation (ChIP) and luciferase reporter assays uncovered that E2F2 transcriptionally activated PRR34-AS1 in turn. Further, rescue experiments reflected that PRR34-AS1 affected HCC progression through targeting miR-296-5p/E2F2/SOX12/Wnt/β-catenin axis. Our findings found that PRR34-AS1 elicited oncogenic functions in HCC, which indicated that PRR34-AS1 might be a novel therapeutic target for HCC., Graphical abstract, Huang and colleagues unmasked that long non-coding RNA PRR34-AS1 sequesters miR-296-5p to elevate E2F2 and SOX12, therefore activating Wnt/β-catenin pathway and facilitating hepatocellular carcinoma development. The findings supported PRR34-AS1 as a possible novel target for hepatocellular carcinoma treatment.

Cyclin D1 (CCND1) has been identified as a metastatic promoter in various tumors including lung adenocarcinoma (LUAD), a subtype of non small cell lung cancer (NSCLC). The previous observation revealed that CCND1 was upregulated in NSCLC and predicted poor prognosis of LUAD patients. In this study, we examined a chaperonin containing TCP1 subunit 5 (CCT5) protein interacts with CCND1 in LUAD. Immunofluorescence demonstrated the co-localization of CCT5 and CCND1 protein in LUAD cells. CCT5 expression was detected with both immunohistochemistry (IHC) and bioinformatics analyses. Similar with the expression pattern of CCND1, CCT5 displayed a high level in LUAD tissues compared to non cancerous lung specimens. Patients with high CCT5 expression showed a significant shorter overall survival relative to those with low expression level. Furthermore, upregulated CCT5 exhibited significant positive correlation with TNM stage of LUAD patients in both IHC analyses and bioinformatics. Knocking down CCT5 remarkably inhibited LUAD cell migration and invasion in vitro by inactivating PI3K/AKT and its downstream EMT signals, which could abrogated the accelerated migration and invasion caused by CCND1 overexpression. In summary, our study discovered a highly expressed protein CCT5 in LUAD which interacted with CCND1 and promoted migration and invasion of LUAD cells by positively moderating PI3K/AKT-induced EMT pathway.

The purpose of this study was to explore the possible role and mechanism of LINC00538 in the pathogenesis of colon cancer.The expression levels of LINC00538 in 70 pairs of colon cancer tissue samples and adjacent ones were examined by qRT-PCR, and survival analysis of patients was performed according to the result. Meanwhile, colon cancer cell lines were screened. In addition, LINC00538 siRNA was transfected into colon cancer cells using liposome method, and then cell proliferation and cell cycle were examined by CCK8 and EDU assays, while cell apoptosis was detected by flow cytometry. Finally, the mechanism of LINC00538 in colon cancer was further explored by RNA-binding protein immunoprecipitation and chromatin immunoprecipitation.The expression of LINC00538 in colon cancer tissues was remarkably higher than that in normal ones, and the overall survival of patients with colon cancer was negatively correlated with the expression of LINC00538. After transfection of LINC00538 siRNA, the proliferation rate of colon cancer cell lines including HCT116 and RKO cells was weakened, the S phase of the cell cycle was shortened, while the cell apoptosis was elevated. In addition, further mechanism studies demonstrated that LINC00538 can bind to EZH2 and inhibit the expression of NKD2, thereby regulating the proliferation and apoptosis of colon cancer cells.This study demonstrated for the first time that LINC00538 was highly expressed in colon cancer and was associated with poor prognosis of patients. Knockdown of LINC00538 in colon cancer cell lines was able to inhibit the cell proliferation and cell cycle, while it promoted the apoptosis. It's mechanism of participating in the development of colon cancer may be through the down-regulation of NKD2 and the regulation of EZH2.

Background: The protein expression of ERCC1 in DNA repair genes was related to resistance platinum and predicting treatment outcomes in various malignant carcinoma ,the level of plasma Epstein-Barr virus（EBV）DNA concentrations is positively correlated with clinical stages of nasopharyngeal carcinoma(NPC), but the predictive value of ERCC1 mRNA and EBV-DNA level for stratified treatment with stage II NPC is unclear precisely. This study aimed to assess the predictive value of combined EBV-DNA and ERCC1 in stage II NPC patients treated with intensity-modulated radiotherapy (IMRT) with concurrent cisplatin and provide guidance for future stratified treatment.Methods: A total 78 stage II NPC patients who received IMRT and concurrent cisplatin-based chemotherapy had measurements of ERCC1 mRNA and pre-treatment EBV DNA levels by real-time PCR (RT-PCR) analysis were analyzed. Associations of ERCC1 mRNA and pre-treatment EBV DNA levels with clinical characteristics and survivals were evaluated.Results: Cut-off value of ERCC1 mRNA obtained from ROC curve was used and there were significant differences in progression-free survival (PFS) and overall survival (OS) between high expression group as compared to low expression group (P=0.021 and 0.030, respectively). Patients with pretreatment EBV-DNAP= 0.024) than those with pretreatment EBV-DNA≥2000 copies/ml, but there was no significant difference in OS (P= 0.062). Patients were divided into three groups by combination of ERCC1 mRNA and EBV-DNA level ERCC1 mRNA low expression/pre EBV-DNAP=0.038); 1-year, 3-year, 5‐year PFS were 100%, 100%, 100%; 97.1%, 91.2%, 84.8%; 95%, 85%, 71.4%, respectively (P=0.028). Multivariate analysis showed combination of ERCC1 mRNA and EBV-DNA levels remained independent prognostic factor but not ERCC1 mRNA and EBV-DNA alone. Conclusion: Combined ERCC1 mRNA and pre EBV-DNA is a better prognostic factor in stage II NPC patients treated with concurrent chemoradiation. Patients with ERCC1 mRNA high expression/pre EBV-DNA≥2000 copies/ml should be treated with more aggressive regimen.

Recent researches indicated Ddx5 and Ddx17 play crucial roles in tumorigenesis. However, the study of Ddx5 and Ddx17 in glioma remains a little. Our study investigated their expression in glioma and evaluated its association with clinical factors and prognostic significance. The expression of Ddx5 and Ddx17 were both upregulated in glioma tissues compared to normal brain tissues, and a significant positive correlation between Ddx5 and Ddx17 expression was identified by statistical analysis. Immunohistochemical staining verified the expression of Ddx5 and Ddx17 in peritumoral zone was lower than that in core zone but higher than normal brain tissues. Moreover, the increased expression of Ddx5 and Ddx17 was markedly correlated with WHO Grade and histological type, and high Ddx5 and Ddx17 were found to be significantly associated with the worse overall survival of glioma patients. In additional, higher expression of both Ddx5 and Ddx17 predicted shorter clinical survival time for high-grade glioma patients with radiotherapy or with chemotherapy. In conclusion, overexpressed Ddx5 and Ddx17 are involved in the clinical progression and poor prognosis of glioma patients, suggesting that their upregulation can be used as a reliable clinical predictor for tumor diagnosis and to predict survival in patients with glioma.