ANXA3 deletion inhibits the resistance of lung cancer cells to oxaliplatin.

OBJECTIVE: The purpose of this study was to explore the role of ANXA3 in lung cancer cell resistance to oxaliplatin (OXA). MATERIALS AND METHODS: After adding different concentrations of Ox, A549, and A549/Ox cell viability were examined using cell counting kit-8 (CCK-8) assay, and the mRNA and protein expressions of ANXA3 were analyzed by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) and Western blot, respectively. After treating cells with 5 µg/mL and 15 µg/mL Ox for 24 hours and knocking down ANXA3, qRT-PCR, CCK8, flow cytometry, transwell, and BrdU assays were performed to examine ANXA3 expression level, cell viability, apoptosis, migration, and proliferative capacities, respectively. In addition, Western blot was performed to detect the protein expression of c-caspase 3. RESULTS: The higher the concentration of Ox added, the worse the cell viability. Meanwhile, ANXA3 expression in A549/Ox cells was found remarkably higher than that in normal A549 cells. After treated with different concentrations of Ox for 24 hours, the cell viability, migration capacity and cell proliferation of A549 cells were found remarkably decreased, while the opposite results were observed in cell apoptosis and C-caspase 3 protein expression, and the Ox treatment group was evidently lower than control group. CONCLUSIONS: Knockdown of ANXA3 may be able to inhibit the resistance of LCa cells to OXA.

PCAT6 participates in the development of gastric cancer through endogenously competition with microRNA-30.

OBJECTIVE: To investigate the role of lncRNA PCAT6 in the progression of gastric cancer and its underlying mechanism. PATIENTS AND METHODS: Expression levels of PCAT6 in 72 gastric cancer tissues and paracancerous tissues were detected by qRT-PCR (Quantitative Real-Time Polymerase Chain Reaction). The correlation between PCAT6 expression and clinical data of gastric cancer patients was analyzed by the chi-square test. After lentivirus transfection of PCAT6 in gastric cancer cells, proliferation, apoptosis, and invasion were detected by CCK-8 (cell counting kit-8), flow cytometry, and transwell assay, respectively. Western blot was utilized to detect protein expressions of apoptosis-related and EMT-related (epithelial-mesenchymal transition) genes in gastric cancer cells. Furthermore, target genes of PCAT6 were predicted via bioinformatics method and verified by luciferase reporter gene assay. The effects of target genes on biological functions of gastric cancer cells were determined as well. RESULTS: PCAT6 was overexpressed in gastric cancer tissues than those of paracancerous tissues. PCAT6 expression was negatively correlated to prognosis, tumor size, TNM (tumor node metastasis) stage and metastasis of gastric cancer. For in vitro experiments, overexpression of PCAT6 increased proliferation, migration, and invasion, whereas decreased apoptosis of gastric cancer cells. MicroRNA-30 was predicted as the target gene of TCAT6. Furthermore, microRNA-30 was found to bind to TCAT6 via targeting MKRN3. Either microRNA-30 knockdown or PCAT6 overexpression could remarkably promote MKRN3 expression. CONCLUSIONS: PCAT6 is overexpressed in gastric cancer, which promotes the development of gastric cancer by endogenously competition with microRNA-30 via targeting MKRN3.

[Bilateral laryngocele:a case report].

A 71 years old male with throat discomfort, shortness of breath, irritating cough admission. Fiberoptic laryngoscope: bilateral glottis ventricular zone with about quail egg size smooth cystic masses. Throat enhanced CT: infrahyoid margin level about bilateral aryepiglottic fold inside have package containing gas shadow, communicated with the laryngeal chamber. Support laryngoscope under coblation radiofrequency ablation assisted laryngeal cyst excision were done and postoperative pathology consistent with laryngocele.