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The efficient therapeutic targets which could be utilized for gastric cancer are limited. In this context, this study was undertaken to evaluate possible anticancer activity of miR-23 against gastric cancer.

The normal GES-1 and human AGS, SNU-1 and SNU-5 gastric cancer cells were used in this study. qRT-PCR was used for the determination of miR-23 expression. MTT assay was used for cell viability and acridine orange (AO)/ethidium bromide (EB) assay was used for detection of apoptosis. The experiments were performed in triplicate.

The microRNA (miR)-23 was downregulated in gastric cancer cells and showed inhibitory effect on cell growth which was manifested as decline in cell survival. Additionally, the chemosensitivity of gastric cancer cells to cisplatin was enhanced with miR-23 overexpression. Furthermore, miR-23 also inhibited the migration and invasion of cancer cells. MAP3K9 was shown to be the target gene of miR-23 and silencing of MAP3K9 was seen to mimic the growth inhibitory effect of miR-23. Overexpression of MAP3K9 reversed the growth inhibition in miR-23 mimics transfected gastric cancer cells.

miR-23 exerts growth inhibitory effect against gastric cancer cells and negatively regulates the cell migration and invasion along with enhancement of chemosensitivity of cancer cells.

miR-23 exerts growth inhibitory effect against gastric cancer cells and negatively regulates the cell migration and invasion along with enhancement of chemosensitivity of cancer cells.

Gastric carcinoma is the fourth principal cause of cancer-related deaths throughout the globe. There are inadequate clinical therapies for gastric cancer due to lack of operational drugs and ambiguity in molecular mechanisms. As such there is a persistent requirement for novel and effective anticancer drugs for gastric cancer. The main purpose of the current study was to investigate the antitumor effects of a plant diterpenoid, namely Oridonin, against SGC-7901 human gastric cancer cells along with examining its effects on cellular apoptosis, cell autophagy and cell cycle phase distribution.

WST-1 cell proliferation assay was used to evaluate cell viability of SGC-7901 human gastric cancer cells. Apoptosis was evaluated by using DAPI and comet assays using fluorescence microscopy. Autophagy was evaluated by transmission electron microscopy (TEM) and western blot method. Effects on cell cycle phase distribution were studied by flow cytometry.

Oridonin molecule led to considerable and dose-dependent antipncer cells by triggering apoptosis and autophagy, and targeting cell cycle at G2/M phase.

The current study was undertaken to examine the anticancer potential of davanone against human ovarian cancer cells along with evaluating its effects on cell apoptosis, PI3K/AKT/MAPK signaling pathway and cell migration and invasion.

CCK-8 assay was performed for cell viability and clonogenic potential was examined through clonogenic assay. Acridine orange (AO)/Ethidium bromide (EB) dual staining assay was performed to detect apoptosis and quantification of apoptosis was achieved through annexin V-FITC/propidium iodide (PI) staining assay. Mitochondrial membrane potential (MMP) was studied via flow cytometric analysis of ovarian cancer cells. Cell migration and invasion potential of ovarian cancer cells was monitored via transwell assay. Western blotting technique was used to study PI3K/AKT/MAPK pathway.

The results indicated that davanone induced dose as well as time dependent inhibition in cell viability of OVACAR-3 cells. Next, AO/EB staining suggested that the antiproliferative effects of davanone are apoptosis-mediated. There was a remarkable increase in apoptotic cell percentage with the molecule dose. Caspase-3, -8 and -9 activity along with Bax activity were observed to be increasing with davanone doses and Bcl-2 activity decreased with increasing molecule concentration. Transwell assay indicated potential inhibition of invasive and migratory ability of OVACAR-3 cells after davanone exposure. Finally, western blotting analysis revealed that davanone resulted in blocking of PI3K/AKT/MAPK signaling pathway in OVACAR-3 cells.

The results indicate that davanone is a potential anticancer agent against human ovarian cancer mediated via caspase-dependent apoptosis, loss of MMP, inhibition of cell migration and invasion and targeting PI3K/AKT/MAPK signaling pathway.

The results indicate that davanone is a potential anticancer agent against human ovarian cancer mediated via caspase-dependent apoptosis, loss of MMP, inhibition of cell migration and invasion and targeting PI3K/AKT/MAPK signaling pathway.

α-mangostin belongs to xanthone class of natural products, showing a great biological and pharmacological potential. α-mangostin has shown remarkable anticancer potential against different cancer cell lines. Herein, α-mangostin was tested for its anticancer potential against human ovarian cancer cell line (OVACAR-3). Its effects on reactive oxygen species (ROS), mitochondrial-mediated apoptosis, cell migration and invasion and m-TOR/PI3K/AKT signaling pathway, was also determined.

MTT assay was performed to evaluate the rate of proliferation and clonogenic assay was used to assess the effects of α-mangostin on OVACAR-3 cell colonies. Phase contrast microscopy was implemented to evaluate cellular morphology. Acridine orange (AO) and ethidium bromine (EB) staining was used to check apoptosis along with western blotting. JC-1 and DCFH-DA staining assays were performed for the determination of mitochondrial membrane potential (MMP) and ROS, respectively. Cell migration and invasion analysis was performed witht.

α-Mangostin could induce antiproliferative effects against OVACAR-3 cells mediated via ROS production, mitochondrial-mediated apoptosis and inhibition of m-TOR/PI3K/AKT signalling. Therefore, it may prove a lead molecule in ovarian cancer treatment.

To investigate the changes in tumor markers (TMs), coagulation function and vascular endothelial growth factor (VEGF) in patients with ovarian cancer (OC) and benign ovarian disease (BOD).

A total of 68 OC patients admitted to and treated in our hospital were selected (OC group), and another 68 BOD patients in the same time period were enrolled (BOD group). The variations in TMs, coagulation function and VEGF in OC and BOD patients were explored by analyzing the TMs, coagulation function and expression levels of serum VEGF and D-dimer in OC group and BOD group as well as the differences in TMs and coagulation function in patients in different stages.

The values of TMs such as cancer antigen 125 (CA125), carbohydrate antigen 19.9 (CA19.9) and human epididymis protein 4 (HE4) in OC group were remarkably higher than those in BOD group, with significant differences (p<0.05). The values of those TMs were relatively low in the patients in stage I-II but relatively high in the patients in stage III-IV, and are highly expressed in OC patients, and the combined detection of TMs, coagulation function and serum VEGF can serve as an important method of diagnosing OC.

TMs, coagulation function indexes and serum VEGF and D-dimer are highly expressed in OC patients, and the combined detection of TMs, coagulation function and serum VEGF can serve as an important method of diagnosing OC.

Ovarian cancer has a difficult diagnosis and high mortality rate. Cisplatin, a platinum compound agent which has been widely used in the clinical treatment of ovarian cancer. selleckchem However, development of chemoresistance is a major obstacle that limits the therapeutic efficacy. The precise roles and molecular mechanisms of cisplatin resistance in ovarian cancer remain unclear.

The expressions of microRNA (miR)-182-5p and CDK6 mRNA from ovarian tumors and cell lines were detected by qRT-PCR. link2 MiR and siRNA were transfected into ovarian cancer cells using Lipofectamine 2000 transfection reagent. Cisplatin resistant ovarian cancer cell line was established by exposing parental cells to gradually increased cisplatin doses. The binding of miR-182-5p on CDK6 3'UTR was predicted from Targetscan.org and validated by Western blot and dual luciferase reporter assay. link3 The cell viability was determined by MTT assay.

miR-182-5p is downregulated in ovarian cancer tissues and cells. Overexpression of miR-182-5p significantly erapeutic target against chemoresistant ovarian cancer.

To evaluate the efficacy and safety of the sequential chemoradiotherapy mode of chemotherapy-radiotherapy-consolidation chemotherapy and the concurrent chemoradiotherapy after operation for advanced (stage III-IV) endometrial cancer.

A total of 116 patients with stage III-IV endometrial cancer were divided into the Sequential group (n=58) and the Concurrent group (n=58) according to the different modes of postoperative adjunctive therapy. The levels of tumor markers in the serum and the occurrence of adverse reactions were compared between the two groups, and the survival and progression of the patients were followed up and recorded. Moreover, the factors influencing the tumor progression in patients were analyzed.

The levels of serum carcino-embryonic antigen (CEA), cancer antigen (CA) 125, CA19-9 and adiponectin (APN) declined markedly after treatment with chemoradiotherapy in both groups compared with those before treatment (p<0.05). The median survival was 49.4±4.5 months and 47.9±4.0 months, andactions and has good tolerance. Low surgical-pathological stage and postoperative sequential chemoradiotherapy are independent protective factors against tumor progression.

Compared with the concurrent chemoradiotherapy, the sequential chemoradiotherapy can prominently delay the progression of advanced endometrial cancer, induce no apparent adverse reactions and has good tolerance. Low surgical-pathological stage and postoperative sequential chemoradiotherapy are independent protective factors against tumor progression.

Hypofractionated post mastectomy radiotherapy (PMRT) is commonly given using conventional radiotherapy technique. Volumetric modulated arc therapy (VMAT) and Intensity modulated radiation therapy (IMRT) are better sparing heart and lungs. This study was conducted to assess the toxicity profile and dosimetry outcomes of patients receiving PMRT using IMRT or VMAT.

67 biopsy-proven patients with carcinoma of the breast who had undergone modified radical mastectomy (MRM) were included in the study. They were treated using VMAT or IMRT to a dose of 42.56 Gy in 16 fractions. Acute and late toxicities were graded using RTOG toxicity grading scale. Toxicities and recurrences were summarized as proportions with 95% confidence intervals. Spearman's correlation was used to find association between the dose received by the organs at risk (OARs) and the grade of toxicities.

The mean age of the study population was 48±9.5 years. The incidence of acute grade 2 and above radiation dermatitis and pneumonitis were 11.9% rable in planning target volume (PTV) coverage and OAR doses, but VMAT had less number of monitor units and shorter treatment time.

Of all breast cancers, triple-negative and HER-2 positive are the most aggressive breast cancer subtypes with a high risk of recurrence and worse prognosis. The study's purpose was to further assess the molecular mechanisms underlying aggression of breast cancer.

The microarray gene expression datasets of GSE29431 and GSE53752 were obtained from the GEO (Gene Expression Omnibus) database, which include HER-2 positive breast cancer, triple-negative breast cancer (TNBC) and normal breast tissue samples. Differentially expressed genes (DEGs) were determined using the LIMMA package of R software and subsequently functional enrichment analysis were performed by the ClusterProfiler package in the R platform. The STRING database was used to construct a protein-protein interaction (PPI) network. The most significant module and key genes were identified by Cytoscape software. Utilizing the Kaplan-Meier plotter and UALCAN database, we defined the key genes associated with prognotic values and molecular subtypes as invasive genes.