Xuzhou Medical College

About: Xuzhou Medical College is a education organization based out in Xuzhou, China. It is known for research contribution in the topics: Cancer & Cell growth. The organization has 12721 authors who have published 7802 publications receiving 102970 citations.

YAP Promotes Migration and Invasion of Human Glioma Cells.

Abstract: Previously, we have reported that Yes-associated protein (YAP) is upregulated in human glioma tissues and its level is positively correlated with patient prognosis. However, the role and mechanism of YAP in the highly invasive nature of human gliomas were largely unknown. In this study, examined by wound healing assay, transwell assay, or live-imaging, we found that YAP downregulation inhibited glioma cell migration and invasion, while YAP over-expression promoted them. Interestingly, the above effect of YAP on immortalized glioma cells was recapitulated in cultured primary glioma cells. In addition, the protein level of N-cadherin and Twist, two important proteins involved in tumor invasion, increased after YAP over-expression. Meanwhile, YAP over-expression significantly increased the F-actin level and changed the distribution of F-actin, leading to cytoskeletal reorganization, which plays an important role in cell motility. Furthermore, the promotion effect of YAP over-expression on glioma cell migration and invasion was partially abolished by Twist downregulation. Taken together, our findings show that YAP contributes to glioma cell migration and invasion by regulating N-cadherin and Twist, as well as cytoskeletal reorganization.

Lnc-PDZD7 contributes to stemness properties and chemosensitivity in hepatocellular carcinoma through EZH2-mediated ATOH8 transcriptional repression.

Abstract: Hepatocellular carcinoma (HCC) with stemness features are pivotal for tumorigenesis, chemoresistance, and progression. Long non-coding RNAs have been implicated in the regulation of HCC stemness features; however, their mechanisms remain largely unknown. Here, we found that Lnc-PDZD7 is a potential oncogene. We systematically analyzed the clinical significance and mechanism of Lnc-PDZD7 in stemness and chemosensitivity regulation. We analyzed the Lnc-PDZD7 expression levels in liver cancer tissues and cell line by qRT-PCR and In situ hybridization. Gain- and loss-of-function experiments were conducted to investigate the biological functions of Lnc-PDZD7 in stemness and chemosensitivity regulation. Bioinformatics analysis, dual-luciferase reporter assays were performed to validate that Lnc-PDZD7 competitively regulates EZH2, Moreover, chromatin immunoprecipitation assays, bisulfite genomic sequencing and Western blot were performed to evaluate the mechanisms of EZH2 repressing ATOH8. Lnc-PDZD7 is frequently upregulated in HCC tissues. Patients with high Lnc-PDZD7 expression had poorer prognoses and a poor response to adjuvant TACE therapy. Lnc-PDZD7 could promote stemness features and suppress the sensitivity of HCC cells to anticancer drugs in vitro and in vivo. Mechanistically, Lnc-PDZD7 functioned as a molecular sponge for miR-101, antagonizing its ability to repress EZH2 expression. Subsequently, EZH2 can further inhibit the expression of the stemness regulator ATOH8 via elevating its H3K27 trimethylation and DNA methylation. Lnc-PDZD7 promotes stemness properties and suppresses chemosensitivity though the miR-101/EZH2/ATOH8 pathway, providing new biomarkers for diagnosis and potential drug targets for HCC.