PurposeTo explore the relationship between retinoic acid receptor gamma (RARG) and ovarian cancer (OC) cell proliferation and the prognosis of patients.MethodsThe transcriptome and clinical information of 379 OC and 88 normal ovarian samples were downloaded from the Cancer Genome Atlas (TCGA) database and the Genotype Tissue Expression (GTEx) database. We compared the mRNA level of RARG between ovrian normal and tumor tissues with the Wilcoxon rank sum test.The R package “limma” was used to analyze the differences in RARG expression between different clinical subgroups. Kaplan−Meier analysis was applied to evaluate the correlation between RARG and prognosis of patients. A nomogram was established to predict the effect of RARG on prognosis of OC patients. Immunohistochemistry and qRT−PCR experiments were conducted to determine the differential expression of RARG between ovarian normal and tumor tissues. Finally, we altered RARG expression using specific siRNA and lentiviral expression vectors to explore the function of RARG by CCK-8, cell cycle, colony formation, and xenograft assays in nude mice.ResultsRARG was highly expressed in ovarian tumors and was an independent predictor of poor overall survival outcomes. Subgroup analysis showed the high expression of RARG was related to FIGO stage III-IV (P=0.027), overall survival time <5 years (P=0.013) and dead status (P=0.041). The Kaplan-Meier curve indicated that patients with high RARG expression level had poor prognosis. The area under the curve (AUC) of RAGR expression for predicting patient survival rates at 1, 5 and 9 years were 0.659, 0.616 and 0.627, respectively. The GSEA enrichment analysis revealed that RARG was involved in ovarian cancer progression through multiple pathways. In cellular experiments in vitro, downregulation of RARG expression significantly suppressed the proliferation and colony formation capacity of OC cells. In cellular experiments in vivo, knockdown of RARG significantly reduced tumor growth in nude mice, decreased expression levels of Ki-67 and proliferation cell nuclear antigen (PCNA).ConclusionsHigh expression of RARG could promote OC cell proliferation and was an independent predictor of poor prognosis. RARG might work as a potential molecular target and biomarker for individualized diagnosis and treatment in OC patients.

Introduction To date, the role of deficient mismatch repair (dMMR) remains to be proven in gastric cancer, and it is difficult to judge its value in clinical application. Our study aimed to investigate how MMR status affected the prognosis in patients with gastrectomy, as well as the efficacy of neoadjuvant chemotherapy and adjuvant chemotherapy in patients with dMMR with gastric cancer. Materials and Methods Patients with gastric cancer with certain pathologic diagnosis of dMMR or proficient MMR (pMMR) using immunohistochemistry from 4 high-volume hospitals in China were included. Propensity score matching was used to match patients with dMMR or pMMR in 1:2 ratios. Overall survival (OS) and progression-free survival (PFS) curves were plotted using the Kaplan-Meier method and compared statistically using the log-rank test. Univariate and multivariate Cox proportional hazards models based on hazard ratios (HRs) and 95% confidence intervals (CIs) were used to determine the risk factors for survival. Results In total, data from 6176 patients with gastric cancer were ultimately analyzed, and loss of expression of one or more MMR proteins was observed in 293 patients (293/6176, 4.74%). Compared to patients with pMMR, patients with dMMR are more likely to be older (≥66, 45.70% vs. 27.94%, P < .001), distal location (83.51% vs. 64.19%, P < .001), intestinal type (42.21% vs. 34.46%, P < .001), and in the earlier pTNM stage (pTNM I, 32.79% vs. 29.09%, P = .009). Patients with gastric cancer with dMMR showed better OS than those with pMMR before PSM (P = .002); however, this survival advantage was not observed for patients with dMMR after PSM (P = .467). As for perioperative chemotherapy, results of multivariable Cox regression analysis showed that perioperative chemotherapy was not an independent prognostic factor for PFS and OS in patients with dMMR with gastric cancer (HR = 0.558, 95% CI, 0.270-1.152, P = .186 and HR = 0.912, 95% CI, 0.464-1.793, P = .822, respectively). Conclusion In conclusion, perioperative chemotherapy could not prolong the OS and PFS of patients with dMMR with gastric cancer.

Purpose: To study the expression levels of apoptotic factors in corticosteroid-mediated femoral head necrosis (FHN) in rats. Methods: Sprague-Dawley (SD) rats (n = 60) bred adaptively for one week were randomly assigned to control and model groups (30 rats/group). A rat model of corticosteroid-induced femoral head necrosis was established. Then, 3 mL of blood drawn from the inferior vena cava of each rat was used for the assay of the expression levels of osteoprotegerin (OPG) and osteoclast differentiation factor (RANKL) in each group using enzyme-linked immunosorbent assay (ELISA). The caspase-3- and Bcl-2-+ve cells in each group were determined with immunohistochemical method. Results: Relative to control, serum OPG level of model group was significantly decreased, while the RANKL level was markedly raised (p < 0.05). The degree of empty lacunae in the model rats was markedly increased, relative to control. Caspase-3-+ve cells were more numerous in the model group than in control, while Bcl-2-positive cells were markedly decreased compared to control (p < 0.05). Conclusion: Apoptosis occurs in the rat model of femoral head necrosis. Glucocorticoids may regulate the apoptotic process by  upregulating caspase-3 and inhibiting Bcl-2. This provides a novel lead for FHN therapy. Keywords: Femoral head necrosis, Corticosteroid, Glucocorticoid, Apoptosis