Glioblastoma multiforme (GBM) is among the most devastating types of cancer, with a median survival of <1 year. despite the development of new surgical and radiation techniques, and the use of multiple anti-neoplastic drugs, effective treatment strategies for malignant gliomas have not yet been developed. The limited efficacy of current treatments reflects the resistance of glioblastoma cells to cytotoxic agents. In this study, using western blot analysis, we found that Yin Yang 1 (YY1) expression was increased in cisplatin-resistant glioblastoma U87MG cells (U87MG-cR). We observed that the silencing of YY1 sensitized the U87MG-cR cells to cisplatin and that the overexpression of YY1 promoted the resistance of LN-229 glioblastoma cells to cisplatin, as shown by MTT assay. Using sphere formation assay, we also found that the silencing of YY1 inhibited the formation of the glioblastoma-initiating cell (GIc) phenotype in the U87MG-cR cells. In addition, the results of RT-qPcR revealed that miR-186 expression was decreased in U87MG-CR cells. Using RT-PCR and western blot analysis, we observed that overexpression of miR-186 inhibited YY1 expression in U87MG-CR cells. The overexpression of miR-186 also reversed cisplatin resistance and the formation of the GIc phenotype in glioblastoma cells. On the whole, the findings of this study demonstrate that miR-186 reverses cisplatin resistance and inhibits the formation of the GIc phenotype by degrading YY1 in glioblastoma.

No abstract

BackgroundGinkgo biloba extract EGb 761 is a putative antioxidant and has been used for thousands of years to treat a variety of ailments, including cancer. While it is known that cell behavior can be modulated by long non-coding RNAs (lncRNAs), the contributions of lncRNAs in EGb 761-induced anti-cancer effects are largely unknown.Material/MethodsColon cancer cell lines HT29 and HCT116 were used in this study. RT-qPCR was used to detect the relative expression of lincRNA-p21 in colon cancer cells. Wound-healing assay and Matrigel Transwell assay were performed to investigate the migration and invasion of colon cancer cells. Immunoprecipitation and Western blot experiments were used to verify ubiquitination and the interaction between lincRNA-p21 and E-cadherin, or E-cadherin and b-transducin repeat containing (BTRC) E3 ubiquitin protein ligase.ResultsCell function assay verified that treatment with EGb 761 suppressed the migratory and invasive abilities of colon cancer cells in a dose-dependent manner via the suppression of E-cadherin expression level. lincRNA-p21 was upregulated in colon cancer cells after treatment with EGb 761, and knockdown of lincRNA-p21 reversed the EGb 761-induced anti-metastatic effect. Furthermore, lincRNA-p21 was localized in cytoplasm of colon cells and regulated E-cadherin expression at a post-transcriptional level. Specifically, lincRNA-p21 promotes E-cadherin stability by preventing the interaction between BTRC and E-cadherin, which leads to the inhibition of E-cadherin ubiquitination.ConclusionsWe demonstrated that lincRNA-p21 mediates the anti-cancer effect of Ginkgo biloba extract EGb 761 by stabilizing E-cadherin protein in colon cancer, which may help define the functional role of EGb 761 in cancer treatment.

No abstract

SE translocation (SET) oncoprotein, an inhibitor of protein phosphatase 2A, is abnormally expressed in many cancers. In this study, SET was aberrantly upregulated in gastric cancer (GC) compared with control tissues. Clinicopathological analysis showed that SET expression was significantly correlated with pathological grade (p=0.002), lymph node stage (p=0.014), and invasive depth (p=0.022). Kaplan-Meier analysis indicated that patients with high SET expression showed poorer overall survival rates than those with low SET expression. Moreover, SET knockdown downregulated GC cell proliferation, colony formation, tumorigenesis, and metastasis. The biological effect of SET on proliferation and invasion was mediated by inhibition of protein phosphatase 2, which in turn, activated Akt. Taken together, our results suggested that SET overexpression is associated with GC progression, and it might be a potential diagnostic marker for GC, thereby a possible target for GC drug development.