Genome-wide association studies and meta-analyses indicate that the polymorphism of rs266729 in adiponectin gene increases the risk of type 2 diabetes mellitus (T2DM); however, these study methods have not been able to identify the underlying genetic effect on the development of T2DM. A genetic model-free approach was conducted to determine the underlying genetic model of inheritance of T2DM because of rs266729 in adiponectin gene.We searched available studies on the association between the rs266729 in adiponectin gene and T2DM in accordance with the inclusion and exclusion criteria. Based on the information extracted from the studies, generalized odds ratio value (GOR) was used to evaluate whether the rs266729 polymorphism was a risk factor for T2DM. The parameter λ was calculated to estimate the genetic model, which was defined as the quotient of natural logarithm odds ratio of GC to CC divided by the natural logarithm odds ratio of GG to CC. Finally, binary logistic regression analysis was used to calculate the genetic effect of rs266729 on T2DM.Data from 7 studies were included in this meta-analysis. The total number of subjects was 12,323, comprising 5,948 cases and 6,395 controls. Mean (standard deviation) age of cases was 59.50 (11.53), and that of the controls was 53.80 (11.65), whereas the proportion of male was 40.9 and 50.0%, respectively. GOR was 1.13 (1.02, 1.25) and λ was 0.47 (0.29, 0.64). The result of logistic regression indicated that the G allele influenced the development of T2DM in the additive model, whereas the genetic effect was 1.13 (1.06, 1.19). Sources of control populations were the cause of between-study heterogeneity; nonetheless, there was no publication bias among studies.The G allele of rs266729 in adiponectin gene increases the risk of T2DM through an additive genetic model with an effect of 1.13 (1.06, 1.19).

Esophageal cancer (EC) is the eighth most common type of cancer and the sixth leading cause of cancer-related deaths worldwide. At present, the clinical treatment for EC is based mainly on radical surgery, chemotherapy, and radiotherapy. However, due to the limited efficacy of conventional treatments and the serious adverse reactions, the outcome is still unsatisfactory (the 5-year survival rate for patients is less than 25%). Thus, it is extremely important and urgent to identify new therapeutic targets. The concept of tumor microenvironment (TME) has attracted increased attention since it was proposed. Recent studies have shown that TME is an important therapeutic target for EC. Microenvironment-targeting therapies such as immunotherapy and antiangiogenic therapy have played an indispensable role in prolonging survival and improving the prognosis of patients with EC. In addition, many new drugs and therapies that have been developed to target microenvironment may become treatment options in the future. We summarize the microenvironment of EC and the latest advances in microenvironment-targeting therapies in this review.

Development of chemoresistance remains a major challenge in treating patients suffering from esophageal squamous cell carcinoma (ESCC), despite treatment advances. MicroRNAs (miRNAs) have been shown to play critical roles in the regulation of ESCC cell chemoresistance. Here, we aimed to investigate the role of miR-624 in ESCC and its molecular mechanism in mediating the resistance of ESCC cells to two common chemotherapeutic drugs, cisplatin (CIS) and paclitaxel (PT). Expression patterns of miR-624, arrestin domain-containing 3 (ARRDC3), Yes-associated protein (YAP), and hypoxia-inducible factor-1α (HIF1α) in ESCC tissues and cell lines were identified using RT-qPCR and Western blot analysis. The binding affinities with the miR-624/ARRDC3/YAP/HIF1α axis were characterized. The chemotherapy-sensitive cell line KYSE150 and chemotherapy-resistant cell line KYSE410 were transfected with an overexpression plasmid or shRNA to study the effect of miR-624/ARRDC3/YAP/HIF1α axis on ESCC cell resistance to CIS and PT. Their in vivo effects on resistance to PT were assessed in tumor-bearing nude mice. High expression of miR-624, YAP and HIF1α, and low expression of ARRDC3 were observed in ESCC tissues and cell lines. miR-624 presented with higher expression in KYSE410 than in KYSE150 cells. miR-624 downregulated ARRDC3 to increase YAP and HIF1α expression so as to enhance ESCC cell resistance to CIS and PT in vitro and in vivo . Taken together, these data indicate an important role for miR-624 in promoting the chemoresistance of ESCC cells, highlighting a potential strategy to overcome drug resistance in ESCC treatment. miR-624 targets ARRDC3 to inhibit its expression, and consequently upregulates YAP expression by inhibiting degradation of YAP. By this mechanism, HIF1α expression is upregulated and the HIF1α signaling pathway is activated. ESCC cell chemotherapy resistance is eventually increased.

Gastric cancer (GC) is one of the most frequently diagnosed types of cancer worldwide, and exploring its potential therapeutic targets is particularly important for improving the prognosis of patients with GC. The aim of the present study was to investigate the association between serine/threonine kinase 17a (STK17A) expression and GC prognosis. STK17A expression was measured by quantitative real-time PCR, western blotting and immunohistochemical staining. Standard stable transfection technology was also used to construct overexpression and knockdown cell lines. Wound healing, Transwell, Cell Counting Kit-8 and colony formation assays, as well as other methods, were used to explore the function and underlying molecular mechanism of STK17A in GC. The results indicated that STK17A overexpression significantly promoted the proliferation and migration of GC cells. The clinical significance of STK17A in a cohort of 102 cases of GC was assessed by clinical correlation and Kaplan-Meier analyses. Overexpression of STK17A was demonstrated to be associated with tumor invasion depth (P<0.001), lymph node metastasis (P<0.001) and poor prognosis in terms of 5-year survival (P<0.001). In addition, Cox multivariate analysis revealed that STK17A expression was an independent risk factor for overall and progress-free survival (P<0.001). Therefore, STK17A may be a valuable biomarker for the prognosis of patients with GC.