MiRNAs play important roles in tumorigenesis. This study focused on exploring the effects and regulation mechanism of miRNA-137 on the biological behaviors of gastric cancer. Total RNA was extracted from tissues of 100 patients with gastric cancer and from four gastric cancer cell lines. Expression of miR-137 was detected by real-time PCR from 100 patients. The effects of miR-137 overexpression on gastric cancer cells’ proliferation, apoptosis, migration and invasion ability were investigated in vitro and in vivo. The target gene of miR-137 was predicted by Targetscan on line software, screened by dual luciferase reporter gene assay and demonstrated by western blot. As a result, the expression of miR-137 was significant reduced in gastric cancer cell line HGC-27, HGC-803, SGC-7901 and MKN-45 as well as in gastric cancer tissues compared with GES-1 cell or matched adjacent non-neoplastic tissues (p<0.001). The re-introduction of miR-137 into gastric cancer cells was able to inhibit cell proliferation, migration and invasion. The in vivo experiments demonstrated that the miR-137 overexpression can reduce the gastric cancer cell proliferation and metastasis. Bioinformatic and western blot analysis indicated that the miR-137 acted as tumor suppressor roles on gastric cancer cells through targeting AKT2 and further affecting the Bad and GSK-3β. In conclusion, the miR-137 which is frequently down-regulated in gastric cancer is potentially involved in gastric cancer tumorigenesis and metastasis by regulating AKT2 related signal pathways.

Background: Aberrant expression of up-regulated long non-coding RNA [LncRNA highly upregulated in liver cancer (HULC)] has been observed to play an important regulatory role in the development of multiple human diseases. However, the molecular mechanism underlying the role of HULC and miR-377-5p in HCC needs to be urgently explored. Methods:The mRNA and protein expression levels of HULC were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot in hepatocellular carcinoma (HCC) cell line HB611, HepG2 and H22, respectively. HULC-shRNA was transfected into HepG-2 cells, which were randomly divided into the control, shRNA-NC, and sh-HULC groups. The correlation between HULC and miR-377-5p was analyzed by performing a luciferase reporter assay. The targeting relationship between miR-377-5p and hypoxia-inhibitory factor-1α (HIF-1α) was also investigated using a luciferase reporter assay.Sh-HULC and miR-377-5p inhibitors were transfected either alone or together into HepG2 cells, and which were divided into the control group, the sh-HULC group, the miR-377-5p inhibitor, and the sh-HULC + inhibitor group for subsequent experiments. HepG2 cell proliferation and invasion were measured by 5-Ethynyl-2-Deoxyuridine (EdU) staining and Transwell invasion assay, respectively. Western plot was carried out to detect the protein expression levels of Ki67, PCNA, E-cadherin, and N-cadherin.Tumor xenograft mouse models were established to confirm the effect of HULC down-regulation on the development of HCC in vivo.Results: The mRNA and protein expression levels of HULC were markedly increased, whereas the mRNA expression levels of miR-377-5p were decreased in HCC cell lines. HepG2 cell proliferation and invasion were suppressed in the Sh-HULC group, while miR-377-5p showed the opposite. Further experiments exhibited that miR-377-5p was targeted by HULC, and an negative correlation between HULC and miR-377-5p was observed. Importantly, the in vivo experiments indicated that down-regulation of HULC could inhibit tumor growth. Taken together, our research demonstrated that down-regulation of HULC plays an anti-cancer role through restrainingHepG2 cell proliferation and invasion.Conclusions: In summary, our in vitro and in vivo findings confirmed HULC to play a role in the progression of HCC, with the underlying mechanism possibly involving the miR-377-5p/HIF-1α pathway.

Cytotoxic T lymphocytes (CTLs) are important for the recognition of the hepatitis B virus (HBV), mediating immunoprotective mechanisms and determining the clinical outcome following HBV infection. CTLs recognize the invading virus via the T cell receptor (TCR). The aim of the current study was to investigate the variability of TCR in lymphocytes from patients with chronic hepatitis B and whether TCR genomic recombination is regulated by the current treatment strategies. Peripheral blood mononuclear cells (PBMCs) were isolated from patients with chronic hepatitis B and high-throughput sequencing was performed to analyze the gene expression diversity of β chain complementarity determining region. High-throughput sequencing produced ~380,000 reads. The sequences of V and J family mRNAs of the β chain V area were analyzed and databases were created for all 30 V family and J family genes. Using the Basic Local Alignment Search Tool, 15 genes were identified to be upregulated in the samples following treatment. Among them, the expression of T cell receptor β variable 28 (TRBV28)_T cell receptor β joining 1–5 (TRBJ1.5) and TRBV6_TRBJ2.10 were significantly different in the treated samples compared with samples taken prior to treatment. Genomic recombination patterns of TRBV and TRBJ of the β chain V area were observed to be different in the samples following treatment. The data of the current study demonstrated that the genomic rearrangement of the V and J segments of TCR β chain V area may be associated with the chronic progression of HBV and impact on treatment efficacy.