Background Synuclein-γ has been demonstrated to be highly expressed in various human cancers including cervical cancer, and has been shown to play a critical role in tumor aggressiveness. We aimed to investigate the role of Synuclein-γ in human cervical cancer in vitro and in vivo. Method Reverse transcription-quantitative polymerase chain reaction assay and Western blot assay were used to detect the mRNA and protein expression, respectively. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and colony formation assay were performed to measure the viabilities of cancer cells. Flow cytometry assay was used to detect the cell cycle and apoptosis. Moreover, an animal experiment was performed to evaluate the biological behavior of Synuclein-γ in vivo. Results In the current study, we found that Synuclein-γ was obviously over-expressed in cervical cancer tissues compared to the adjacent non-cancer tissues. Cervical cancer cells transfected with Synuclein-γ siRNA demonstrated significant inhibition of cancer proliferation ( P < 0.01), cell cycle arrest at G0/G1 phase, and cell apoptosis ( P < 0.05). Moreover, down-regulation of Synuclein-γ significantly inhibited cervical cancer growth in vivo. In addition, protein levels of AKT , c-Myc and Cyclin D1 were much lower in the Synuclein-γ siRNA-treated groups than that in the control group. Conclusions Synuclein-γ inhibition reduced cervical cancer tumor growth through the AKT pathway. This effect represented a therapeutic opportunity and provided a novel target for cervical cancer treatment.
IntroductionWe also investigated the Carpachromene in the cytotoxicity studies against common human ovarian cancer cell line i.e., SW 626, in-vitro.Material and methodsCell viability of Carpachromene was very low against common human ovarian cancer cell line i.e. SW 626 without any cytotoxicity on normal cell line. To compare the biological activities of molecules, the enzymes used are α-glucosidase, acetylcholinesterase, respectively. Finally, calculations were made using the molecular docking method to compare the biological activity of the carpachromene molecule. We then examined whether the release of Smac is necessary for apoptosis in ovarian cancer cells using the SW 626 cell line. We first examined mitochondrial and cytosolic Smac levels after Carpachromene treatment. ResultsFollowing the docking calculations, the properties of the carpachromene molecule were examined by ADME/T analysis in order to be used as a drug in the future. In addition, the anti-oxidant properties of the molecules were examined in both gas and water phase with the HF/6-31g basis set with the Gaussian software program. As shown, exposure of ovarian cancer cells to Carpachromene decreased mitochondrial Smac and increased cytosolic Smac levels in a time-dependent fashion. As depicted in results, a decrease in Smac expression was confirmed by Western blot. Silencing of Smac significantly inhibited Carpachromene-induced caspase-3 cleavage and attenuated apoptosis in these cells Moreover, overexpression of a Smac heptapeptide (Smac-N7) enhanced Carpachromene-induced cell deathConclusionsAccording to the above findings, the Carpachromene may be administrated for the treatment of several types of human ovarian cancer in humans.
Background RNA binding motif protein 15 (RBM15), a writer of N6-methyladenosine (m6A) methylation, contributes significantly to the development of various tumors. However, the function of RBM15 in cervical cancer (CC) has not been determined. Methods Based on the GSE9750, GSE63514, and m6A datasets, m6A-related differentially expressed genes (DEGs) were screened out. The hub genes were identified by generating a Protein-Protein Interaction (PPI) network. RT-qPCR was conducted to assess the mRNA expression of hub genes. CCK8, scratch wound healing, and transwell assays were utilized to examine the influence of RBM15 on HeLa and SiHa cells. Tumor xenograft models were used to assess the effects of RBM15 on tumorigenesis. A mechanistic analysis of RBM15 in CC tumors was conducted using the GeneCards and Coxpresdb databases, followed by a Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, and the pathway-related genes were subsequently validated using Western blotting. Results Five DEGs were screened, including WTAP, RBM15, CBLL1, and YTHDC2. Among them, WTAP, RBM15, CBLL1, and YTHDC2 were hub genes and can be used as biomarkers for CC. RBM15 expression was considerably increased, while WTAP, CBLL1, and YTHDC2 were significantly downregulated. Knockdown of RBM15 significantly suppressed the proliferation, invasion, and migration of CC cells and tumorigenesis. Moreover, knockdown of RBM15 significantly reduced the expression levels of proteins related to the JAK-STAT pathway. Conclusions Knockdown of RBM15 inhibited the progression of CC cells, which probably by inhibiting the JAK-STAT pathway pathway.
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