Gastric cancer is one of the most common cancers and the second leading cause of cancer-associated mortality worldwide. Recurrence, metastasis and resistance to drug treatment are the main barrier to survival of patients with advanced stage gastric cancer. Further study of the molecular mechanisms involved will improve the therapeutic options for gastric cancer. In a previous study, c-Maf was discovered as an oncogene transduced in the avian AS42 retrovirus, and was found to be overexpressed in multiple myeloma and angioimmunoblastic T-cell lymphoma. c-Maf inducing protein (CMIP) is involved in the c-Maf signaling pathway, which was reported to serve an important role in human minimal change nephrotic syndrome and in human reading and language related behavior. However, the relationship between CMIP and human gastric cancer has not yet been reported. In the present study, CMIP protein levels in gastric cancer tissues and cells were measured using immunohistochemistry and western blot analysis; the expression of CMIP protein was significantly higher in gastric cancer tissues compared with normal gastric tissues. Expression was positively associated with poorer clinical parameters, relapse-free survival and overall survival. Furthermore, using cell counting, Cell Counting Kit-8, colony formation, wound healing and Transwell assays, together with flow cytometry, CMIP depletion by RNA interference was observed to reduce the capacity of gastric cancer cells to proliferate and migrate in vitro. Furthermore, the upstream and downstream genes of CMIP were analyzed by luciferase reporter assay and reverse transcription quantitative polymerase chain reaction, which indicated that CMIP was a direct target of miR-101-3p. In addition, CMIP knockdown was observed to result in the downregulation of MDM2 and mitogen activated protein kinase (MAPK) expression at the mRNA level. In conclusion, CMIP demonstrated an oncogenic role in human gastric cancer cells. Furthermore, microRNA-101-3p, MDM2 and MAPK were involved in the CMIP signaling pathway in gastric cancer. CMIP could be a novel target for further investigation in the clinical therapeutic management of gastric cancer.

Introduction The molecular pathogenesis of liver cancer remains unclear; some ncRNAs have been considered as potential drug targets for cancer treatment. LncRNA PSMG3‑AS1 has been reported to promote breast cancer, while its role in hepatocellular carcinoma (HCC) is unknown. Methods Bioinformatics analysis was conducted to investigate the relationship between miR-143-3p and PSMG3-AS1. RT-qPCR was used to detect the expression levels of miR-143-3p and PSMG3-AS1 and the correlation between them in HCC. The survival curve was used to analyze the effect of PSMG3-AS1 on the prognosis of liver cancer. RT-qPCR was used to detect the effect of different concentration gradients of miR-143-3p on PSMG3-AS1. CCK8 and clone formation experiments were used to examine the role of miR-143-3p and PSMG3-AS1 in regulating the proliferation of SNU-182 and SNU-398 cells. Results Our preliminary bioinformatics analysis showed that miR-143-3p can target PSMG3-AS1. We, therefore, analyzed the interaction between PSMG3-AS1 and miR-143-3p in HCC. We found that PSMG3-AS1 was upregulated, while miR-143-3p was downregulated in HCC. The expression levels of PSMG3‑AS1 and miR-143-3p were closely and inversely correlated with each other. High expression levels of PSMG3‑AS1 predicted poor survival. In HCC cells, overexpression of PSMG3-AS1 led to increased proliferation rates. Overexpression of miR-143-3p played an opposite role and reversed the effect of overexpression of PSMG3‑AS1. Discussions miR-143-3p may target PSMG3‑AS1 to inhibit the proliferation of HCC cells.

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The study aimed to evaluate the prognostic value of CD169 expression in tumorinfiltrating macrophages from regional lymph nodes(RLN) in various tumors. In order to identify eligible articles, PubMed, EMBASE, Web of Science, and Cochrane Library were used to conduct a systematic search. Pooled hazard ratios (HRs) or odds ratios (ORs) with corresponding 95% confidence intervals (CIs) were adopted to assess the relationship between CD169 expression and overall survival (OS) and clinicopathological characteristics. Ten studies, including eleven cohorts with 1699 patients, were enrolled. We found that high CD169 + expression in tumor-infiltrating macrophages from RLN was associated with a favorable OS (HR=0.56, 95%CI: 0.39-0.79, P=0.001).Subgroup analysis showed that high CD169+ expression had more predictive power in digestive system tumors ((HR=0.52, 95%CI: 0.42-0.67, <0.001).In addition, high CD169 expression was significantly linked with lymph node metastasis (OR=0.66, 95%CI: 0.47-0.94, P=0.020) and TNM stage (OR=0.62, 95%CI: 0.48-0.80, P<0.001). High CD169 expression in tumor-infiltrating macrophages from RLN was correlated with favorable survival outcome in patients with malignancies. CD169 may be a novel and effective prognostic marker, especially for digestive system tumors.