Objective To investigate the expression and prognostic value of microRNA-29b-2-5p(miR-29b-2-5p)and syntaxin 16(STX16)in hepatocellular carcinoma(HCC).Methods The cancer tissues and adjacent tissues of 88 HCC patients diagnosed in Nantong Tumor Hospital from January 2013 to September 2020 were collected.The expressions of miR-29b-2-5p and STX16 in cancer tissues and adjacent tissues were analyzed by real-time fluorescent quantitative PCR.The expression of STX16 protein in cancer tissues and adjacent tissues were analyzed by immunohistochemistry.Pearson correlation analysis was used to analyze the correlation be-tween miR-29b-2-5p and STX16.Non-parametric χ2 test was used to analyze the relationship between the ex-pression of the two proteins and clinicopathological parameters,and Kaplan-Meier survival curve was used to analyze the relationship between the expression of the two proteins and prognosis.Results The relative ex-pression level of miR-29b-2-5p was 0.780(0.351,1.708)in cancer tissues and 1.014(0.458,3.124)in adja-cent tissues in 88 HCC patients.The relative expression level of miR-29b-2-5p in cancer tissues was signifi-cantly lower than that in adjacent tissues(P=0.012).The relative expression level of STX16 mRNA was 0.775(0.406,0.946)in cancer tissues and 0.368(0.080,1.301)in adjacent tissues in 88 HCC patients.The relative expression level of STX16 mRNA in cancer tissues was significantly higer than that in adjacent tissues(P<0.01).Immunohistochemical results showed that STX16 was expressed in the cytoplasm,and the expres-sion of STX16 in cancer tissues was higher than that in adjacent tissues(P<0.05).The expression of miR-29b-2-5p in cancer tissues was related to cancer stage(P<0.05),and the expression of STX16 was related to cancer stage and alpha-fetoprotein(P<0.05).Patients with low miR-29b-2-5p expression had a shorter over-all survival(OS)than those with high miR-29b-2-5p expression,and patients with high STX16 expression had a shorter OS than those with low STX16 expression(P<0.05).Conclusion The expression of miR-29b-2-5p is low and STX16 is high in HCC tissues.The combined detection of miR-29b-2-5p and STX16 can effectively evaluate the prognosis of HCC patients.

Objective: To analyze the effects of miR-138 on the expression of small glutamine-rich TPR-containing protein A (SGTA) and cell adhesion-mediated drug resistance (CAM-DR) phenotype in non-Hodgkin's lymphoma (NHL). Methods: The adhesion model was constructed using fibronectin (FN) or bone marrow stromal cells HS-5. The effect of miR-138 on the expression of SGTA was analyzed by Western blotting and RQ-PCR. Dual-luciferase assays were performed to probe the effects of miR-138 on SGTA 3' UTR activities. Subsequently, we investigated the effect of miR-138 on cell cycle, adhesion ability and CAM-DR. Moreover, the correlation between miR-138 expression and therapeutic response was analyzed in 35 paraffin-embedded diffuse large B cell lymphoma samples. Results: Our data showed that adhesion of NHL cells to FN or HS-5 cells significantly increased miR-138 expression (P<0.05). Knockdown of miR-138 markedly increased the protein (all P<0.05) but not for mRNA (all P>0.05) levels of SGTA in NHL cell. The luciferase activity of SGTA 3' UTR was significantly suppressed by miR-138 transfected cells (0.73±0.03 vs 1.00±0.02, t=0.914, P=0.002). No change in terms of reporter activity was observed in SGTA 3'UTR mutant transfected cells (0.93±0.04 vs 1.00±0.02, t=1.375, P=0.241). Also we found that ectopic expression of miR-138 significantly induced cell cycle arrest at G₁ phase in both suspension and adherent cells (all P<0.05). Knockdown of miR-138 had no effect on cell adhesion ability (all P>0.05). More importantly, in suspension cells, knockdown of miR-138 significantly decreased the percentage of doxorubicin-induced cell death. However, knockdown of miR-138 dramatically increased the percentage of doxorubicin-induced cell death in FN/HS-5-adherent cells. Furthermore, the miR-138 expression was significantly higher in patients with progression of disease/stable disease than those experiencing complete response/partial response (9.72±1.11 vs 3.06±0.22, t=9.144, P<0.001). Conclusion MiR-138 promoted CAM-DR phenotype through cell adhesion-mediated SGTA down-regulation and cell cycle arrest.