查看更多>>摘要：This study was carried out to explore the role of the long noncoding RNA (IncRNA) SAMMSON in triple-negative breast cancer (TNBC). The research patients in this study included 68 TNBC patients. Cell Counting Kitcck-8 were utilized to determine cell proliferation abilities, respectively. Proteins and mRNAs were estimated by western blot and Methylation-specific polymerase chain reaction, respectively. We found that SAMMSON was upregulated, while p53 was downregulated in cancer (TNBC) tissues than in non-cancer tissues of TNBC patients. SAMMSON expression levels in TNBC tissues increased with the increase of clinical stages of TNBC patients. SAMMSON and p53 were inversely correlated in TNBC tissues. In TNBC cells, SAMMSON overexpression decreased p53 expression, while p53 overexpression failed to affect SAMMSON expression. In addition, SAMMSON overexpression increased TNBC cell proliferation, while p53 overexpression decreased the proliferation rates of TNBC cells. In addition, p53 overexpression attenuated the effects of SAMMSON overexpression. Therefore, overexpression of SAMMSON could promote TNBC cell proliferation by interacting with p53.
查看更多>>摘要：PCAT29 has reported to exert tumor suppressive roles. In this study, we investigated the function of PCAT29 in non-small-cell lung cancer (NSCLC). Expression levels of PCAT29, miR-494, and PTEN in non-tumor and NSCLC tumor tissue samples were measured by performing quantitative reverse transcription polymerase chain reaction. Cell apoptosis and proliferation analyses were formed to study the effects of overexpression of PCAT29, miR-494, and PTEN on apoptosis and proliferation of H23 cells. It was observed that PCAT29 was down-regulated in NSCLC and predicted poor survival. In NSCLC cells, miR-494 was inversely, while PTEN was positively correlated with PCAT29. In NSCLC cells, overexpression of PCAT29 led to down-regulated miR-494 and up-regulated PTEN. Overexpression of miR-494 resulted in down-regulated PTEN but did not affect the expression of PCAT29. Overexpression of PTEN affected neither PCAT29 nor miR-494. In addition, overexpression of PCAT29 and PTEN resulted in increased apop-totic rate and decreased proliferation of NSCLC cells. miR-494 played an opposite role and attenuated the effects of overexpression of PCAT29. Therefore, PCAT29 may up-regulate PTEN by down-regulating miR-494 to suppress the progression of NSCLC cells.
查看更多>>摘要：The oncogenic functions of circRNA circSEPT9 have been characterized in triple-negative breast cancer. We analyzed its role in laryngeal squamous cell carcinoma (LSCC). Quantitative reverse-transcription PCR (RT-qPCR) was used to analyze the expression of circSEPT9 and miR-10a in paired LSCC and nontumor tissues donated by 50 patients with LSCC. Methylation-specific PCR (MSP) was performed to analyze the role of circSEPT9 in miR-10a RNA gene methylation. circSEPT9 or miR-10a were overexpressed in LSCC cells to explore the interaction between them. The regulatory role of circSEPT9 and miR-10a in cell proliferation was studied with cell counting kit-8 (CCK-8) assay. CircSEPT9 was highly expressed in LSCC, whereas miR-10a was expressed at a lower level in LSCC. CircSEPT9 and miR-10a were closely correlated across LSCC tissue samples. In LSCC cells, circSEPT9 overexpression increased the methylation of the miR-10a gene and decreased the expression of miR-10a. CircSEPT9 overexpression increased LSCC cell proliferation, whereas miR-10a overexpression decreased cell proliferation. Co-transfection experiments showed that circSEPT9 overexpression attenuated the effects of miR-10a overexpression on cell proliferation. We conclude that circSEPT9 may increase miR-10a methylation to increase cell proliferation in LSCC.
查看更多>>摘要：Cell adhesion is the backbone of many events in the cancer cell life cycle, including proliferation, metastasis, migration, invasion and even cell survival. In a tumor, usually the cells in the core have high migratory potential though they constantly suffer from glucose starvation. Our study was aimed at understanding events such as attachment to the surfaces at one site and then mobility to the secondary sites during progression of cancer in the hormone sensitive breast cancer cells MCF7, following their exposure to different concentrations of glucose in the environment. We have shown that low glucose availability is detected within 3 h of shortage which is then translated into variable expression of genes for cell-to-cell adhesion such as cadherins and Ig-like cell adhesion molecules, and matrix-associated genes such as integrins and metalloproteases. We also found that low glucose concentrations induced cell adhesion, whereas higher concentrations stimulated cell migration. In addition, several regulatory molecules involved in mitochondrial metabolism, proliferation, and glucose uptake as demonstrated respectively by MTT assay, BrdU uptake, glucose uptake and pyruvate kinase activity showed varied expression during epithelial to mesenchymal transition. Cytoskeleton staining demonstrated development of lamellipodia in glucose starved medium indicating cascade of physiological and molecular events in the cells to find a more nutrient-rich environment for the development of secondary tumor. Further studies on protein markers with a 3D spheroid culturing approach arc likely to expand our understanding of onset of metastasis in tumor tissues.
查看更多>>摘要：Genome analyses using next-generation sequencing are providing more and more information on DNA sequences. However, there is a trend towards the return to RNA sequencing analyses, including both mRNAs and RNAs as simultaneous regulatory molecules. Consequently, enhancer RNA (eRNA) molecules are now extensively studied. The existence of eRNAs has been known for some time, but their roles are not yet fully understood. It turns out that the sequences of super-enhancers (hyperactive enhancers) have a significant and stimulating effect on the expression of oncogenes. Enhancers act at the level of transcription initiation and interact with many transcription factors that bind to DNA. Therapies targeting molecules that regulate gene expression may be effective cancer treatments, independent of tumor type, but relying on transcription factors and super-enhancers universally overexpressed in various types of cancer. This kind of treatment could become a new tissue-agnostic anticancer therapy.
查看更多>>摘要：Previous studies have demonstrated that miR-10b-3p is significantly downregulated in rats after cerebral ischemia injury, and this study aimed to investigate the effect of miR-10b-3p in cerebral ischemia/reperfusion (I/R) injury. The oxygen-glucose deprivation (OGD) induced SH-SY5Y cell model and middle cerebral artery occlusion model (MCAO) rats were constructed to investigate the role of miR-10b-3p and underline the regulatory mechanism of miR10b-3p/PDCD5 axis in cerebral I/R injury. The expression of miR-10b-3p and PDCD5 was evaluated by qRT-PCR and Western blot. The binding relationship between miR-10b-3p and PDCD5 was determined by bioinfoimatic analysis and luciferase reporter assay. Cell proliferation was evaluated by MTT assay and Edu staining assay. The apoptosis was assessed by TUNEL staining assay and flow cytometry. MiR-10b-3p was significantly downregulated and PDCD5 was upregulated both in OGD/R induced SII-SY5Y cells and the brain tissues of MCAO/R rats. Luciferase reporter assay determined that miR-10b-3p could directly bind to the 3' UTR of PDCD5 and negatively regulate its expression. MiRlOb-3p overexpression could efficiently inhibit cell viability and proliferation, induce apoptosis of OGD/R-induced SHSY5Y cells in vitro, and attenuate cerebral I/R injury of MCAO rats in vivo. Silencing of PDCD5 showed similar effect to miR-10b-3p mimics, while PDCD5 overexpression significantly reversed the protective effects of miR-10b-3p mimics on cerebral I/R injury. In summary, our results revealed that miR-10b-3p alleviated cerebral I/R injury partly through targeting PDCD5 and indicated that miR-10b-3p might be a potential target for ischemic stroke.
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