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Cell proliferation was detected by CCK-8 method, cell apoptosis was detected by flow cytometry, and cell invasion by transwell invasion experiment.<br /><br /> miR-423 and miR-548c-3p showed low expression in osteosarcoma, and the overexpression of miR-432 and miR-548c-3p in osteosarcoma cells could inhibit the proliferation of tumor cells and promote their apoptosis. miR-432 and miR-548c-3p might be tumor suppressors of osteosarcoma, and their expression levels could be used as important reference indexes to evaluate the benign and malignant levels of osteosarcoma.<br /><br /> These results suggested that the abnormal expressions of miR-432 and miR-548c-3p may be key factors of the occurrence and development of osteosarcoma.<br /><br />These results suggested that the abnormal expressions of miR-432 and miR-548c-3p may be key factors of the occurrence and development of osteosarcoma.<br /><br /> Previous studies have shown that MEX3C is an oncogene; however, its role in osteosarcoma (OS) development has not been reported. We aimed at investigating whether MEX3C could be engaged in the malignant progression of OS through regulating FGF14.<br /><br /> MEX3C levels in tumor tissues and adjacent ones of 52 OS patients were studied by quantitative real-time polymerase chain reaction (qRT-PCR), and the relationship between MEX3C expression and clinicopathological characteristics of OS patients was analyzed. At the same time, qRT-PCR further verified the MEX3C level in OS cell lines, and HOS and MG63 OS cell lines were selected to construct MEX3C overexpression and knockdown cell model, respectively. The impact of MEX3C on OS cell functions were determined by cell wound healing and transwell assay. In addition, the interaction between MEX3C and FGF14 was further determined by luciferase assay, western blot and recovery experiments.<br /><br /> MEX3C had increased expression both in OS tissue samples and in OS cell lines. High expression of MEX3C was predictive of high incidence of nodal involvement or distant metastasis. Silencing MEX3C remarkably attenuated the migration ability of OS cells, while, conversely, overexpression enhanced that. Bioinformatics analysis and luciferase assay confirmed that MEX3C bind to FGF14 directly, and the expression of FGF14 was significantly reduced in OS tumor tissue specimens, and was negatively correlated with MEX3C. Overexpression of FGF14 was able to reverse the promoting effect of MEX3C on the crawling ability and invasiveness of OS cells.<br /><br /> MEX3C was remarkably increased in OS tissues and was remarkably correlated with the incidence of metastasis of OS patients. In addition, MEX3C accelerated the malignant progression of OS through negatively modulating FGF14.<br /><br />MEX3C was remarkably increased in OS tissues and was remarkably correlated with the incidence of metastasis of OS patients. In addition, MEX3C accelerated the malignant progression of OS through negatively modulating FGF14.<br /><br /> Cervical cancer is a global health issue in women accounting for huge morbidity and mortality. Lack of effective chemotherapy and harmful side-effects of the current chemotherapeutics creates an urgent need for the development of safer and efficient chemotherapy to curb cervical cancer. Hence, the current study was designed to investigate the in vitro anticancer potency of Eremanthin against human HeLa cervical cancer cells.<br /><br /> Cell cytotoxicity was examined by MTT cell proliferation assay and clonogenic assay was performed for cell colony analysis. Eremanthin-induced necrotic cell death was assessed through phase contrast microscopy. [https://www.selleckchem.com/products/myci361.html MYCi361 manufacturer] Flow cytometric analysis was performed for estimation of cell cycle phase distributions. Reactive oxygen species (ROS) production was detected via DCF fluorescence and mitochondrial membrane potential (MMP) loss was monitored by flow cytometry. ENLITEN ATP assay system bioluminescence detection kit was used for quantification of complete intracellular ATP. Caspase-3 activity alphosphorylated PI3K and AKT diminished.<br /><br /> Eremanthin molecule is a potent anticancer agent against human cervical cancer and may be included as lead molecule in cervical cancer treatment provided further in vitro and in vivo investigations are performed.<br /><br />Eremanthin molecule is a potent anticancer agent against human cervical cancer and may be included as lead molecule in cervical cancer treatment provided further in vitro and in vivo investigations are performed.<br /><br /> The treatment options of endometrial hyperplasia consist of surgical, interventional and medical therapies including apoptosis-inducing agents. The purpose of the study was to evaluate the effects of ultraviolet (UV) radiation on the viability and the type of cell death on the human endometrial stromal cells (ThESC) line.<br /><br /> We investigated the effect of UV exposure on human endometrial stromal cell line (ThESC) on cell viability using MTT assay as well as changes in cell morphology using phase microscopy and acridine orange (AO)/ethidium bromide (EB) cell staining.<br /><br /> UV treatment significantly decreased the percentage of the viable ThESC cells compared to the viability of untreated control cells using MTT assay (p&lt;0.05). In addition, UV treatment of ThESC cells for 60 and 90 min induced high level of cell morphology disruption, followed with loss of both the cell shape and the presence of defragmented debris and stained with intense red color.<br /><br /> The obtained results suggest the potential role of UV light application as additional treatment option of benign endometrium hyperplasia alone or in combination with other treatment modalities.<br /><br />The obtained results suggest the potential role of UV light application as additional treatment option of benign endometrium hyperplasia alone or in combination with other treatment modalities.<br /><br /> To explore the efficacy of metformin in the treatment of estrogen-dependent endometrial carcinoma (EC) complicated with type 2 diabetes mellitus (T2DM), and the influencing factors for the prognosis of such patients.<br /><br /> The clinical data of 68 patients histopathologically diagnosed with estrogen-dependent EC complicated with T2DM in our hospital from April 2013 to March 2016, and 132 estrogen-dependent EC patients with normal blood glucose during the same period were retrospectively analyzed. The clinical and pathological features were compared between diabetic patients and non-diabetic patients. The diabetic patients were divided into the metformin group and the non-metformin group according to whether metformin was taken. The survival curves were plotted and analyzed using the Kaplan-Meier method, and the overall survival (OS) and progression-free survival (PFS) were compared among the three groups. Moreover, the multivariate analysis was performed using the COX regression model, so as to analyze the influencing factors for the prognosis of patients with estrogen-dependent EC complicated with T2DM.