MOB1A regulates glucose deprivation-induced autophagy via IL6-STAT3 pathway in gallbladder carcinoma

MOB kinase activator 1A (MOB1A) plays an important role in many diseases and cancers. Here, we observed that MOB1A was substantially overexpressed in gallbladder carcinoma (GBC) tissues compared with nontumor tissues. The high expression of MOB1A was closely associated with poor survival in patients with GBC at advanced TNM stages. Furthermore, our study indicated that MOB1A promoted autophagy by activating the IL6/STAT3 signaling pathway and regulating the chemosensitivity to gemcitabine under glucose deprivation conditions both in vitro and in vivo. In conclusion, these findings suggested that MOB1A is critical for the development of GBC via the MOB1A-IL6/STAT3-autophagy axis.     

Reliability of Sonoelastography in Ductal Carcinoma

The objective of the study was to evaluate the reliability of sonoelastography in ductal carcinoma in patients in primary and secondary health care settings. Google Scholar, PubMed, Medline, Medscape, Wikipedia and NCBI were searched in January 2018 for all original research and review articles to identify relevant studies. Two reviewers selected the articles independently for based on the title and abstract. The selection criteria were sonoelastography accuracy for diagnosing ductal carcinoma as index text, B-mode sonography, and micropure imaging; surgery and histologic findings were used as reference text; and benign and malignant breast abnormalities and ductal carcinoma were used as target conditions. Two reviewers extracted the data on selected study characteristics, and the results were used to construct the tables and figures. Fifteen studies on ductal carcinoma were found. The overall sensitivity of sonoelastography in diagnosing ductal carcinoma was 85.7%, and the specificity, 79.8%. On the basis of the literature review, it was concluded that sonoelastography has high sensitivity and specificity in diagnosing ductal carcinoma.     

a-1, 2岩藻糖基转移酶II在肺鳞癌组织中的表达及对肺鳞癌细胞增殖的影响

目的：探讨a-1，2岩藻糖基转移酶II（FUT2）在肺鳞癌中的表达情况及其对肺鳞癌细胞增殖的影响。方法：应用UALCAN数据库分析FUT2在临床肺鳞癌患者组织中的差异表达及其与肺鳞癌患者临床TNM分期、年龄及性别因素的相关性；采用瞬时转染技术，将FUT2的shRNA质粒转染进H226细胞株中构建FUT2低表达的肺鳞癌细胞模型；利用CCK-8、平板克隆及Western blot实验检测FUT2对肺鳞癌细胞的生长、单克隆细胞团形成及PCNA蛋白表达的影响。结果：FUT2在肺鳞癌尤其是肺鳞癌TNM早中期呈现高表达趋势（P＜0.05），而与年龄和性别无关。低表达FUT2可以抑制肺鳞癌细胞的生长速率和单克隆细胞团的形成数，同时，可以抑制肺鳞癌细胞PCNA蛋白的表达水平，差异均有统计学意义（P＜0.05）。结论：FUT2在肺鳞癌中高表达且促进肺鳞癌细胞的增殖能力，有望成为肺鳞癌的早期诊断指标。     

Pharmacological evaluation and mechanistic study of compound Xishu Granule in hepatocellular carcinoma

ObjectiveIn this study, we used HepG2 human hepatocellular carcinoma cells to study the effects of Compound Xishu Granule (CXG) on cell proliferation, apoptosis, and the cell cycle in vitro. We also used a xenograft tumor model to study the anti-tumor effects of CXG and related mechanisms in vivo.MethodsThe effect of CXG on cell viability was measured using Cell Counting Kit-8 and a colony formation assay. The effect of CXG on apoptosis and the cell cycle was analyzed using flow cytometry. The in vivo anti-tumor effect of CXG was assessed by measuring the volume change in xenograft tumors after drug administration. The CXG anti-tumor mechanism was studied using western blotting assay to detect cell cycle and apoptotic associated proteins.ResultsCXG suppressed HepG2 cell proliferation in a time- and dose-dependent manner in vitro. Colony formation experiments showed that CXG administration for 24 h significantly reduced HepG2 cell formations (P < .01). Flow cytometric analysis showed that CXG treatment for 48 h promoted apoptosis and blocked HepG2 cells in the G2/M phase. Western blotting results showed that Bax was significantly up-regulated and Bcl-2 was down-regulated in graft tumor tissues and HepG2 cells after CXG administration, which increased the Bax/Bcl-2 ratio. PLK1, CDC25C, CDK1, and Cyclin B1 expression were up-regulated. CXG had a good inhibitory effect on graft tumor growth in vivo.ConclusionCXG has good anti-tumor effects in vitro and in vivo. In vitro, CXG promoted HepG2 cell apoptosis and induced G2/M phase arrest. In vivo, CXG significantly inhibited graft tumor growth. The CXG mechanism in treating hepatocellular carcinoma may be that CXG can induce abnormal apoptotic and cell cycle associated protein expression, leading to mitotic catastrophe and apoptosis.     

Pulmonary Carcinosarcoma: A Surveillance,Epidemiology, and End Results (SEER) Analysis

IntroductionPulmonary carcinosarcoma (PC) is a rare malignant neoplasm composed of epithelial and mesenchymal components. It accounts for < 1% of thoracic cancers and is not fully understood. This study examined Surveillance, Epidemiology, and End Results (SEER) data to describe demographic and clinical characteristics of patients with PC and assessed survival outcomes by treatment modality and stage.Patients and MethodsSEER data were reviewed to identify patients diagnosed with primary PC (1973-2012). Overall survival (OS) and disease-specific survival (DSS) were analyzed by univariate/multivariable Cox proportional hazards models and Kaplan-Meier methods.ResultsA total of 411 patients were included. Median age was 67 (range, 24-96) years. Disease stage at the time of initial diagnosis was known for 74.7% of the identified patients (307/411). Of these patients, 23.1% had localized disease. Survival was significantly better for patients with localized disease (OS: 31 vs. 6 months, P < .001; DSS: 54 vs. 8 months, P < .001). Additionally, patients who received surgery alone had significantly improved OS (20 months; P < .001) and DSS (32 months; P < .001) compared to patients who received combined surgery and radiotherapy (OS: 7 months; DSS: 8 months) or radiotherapy alone (OS: 4 months; DSS: 4 months).ConclusionTreatment with surgery alone resulted in superior survival outcomes compared to other treatment modality combinations, regardless of patient age and disease stage. Within the limitations of this study, providers may wish to consider these findings when devising patient treatment plans.