Overexpressed circ-RPL15 predicts poor survival and promotes the progression of gastric cancer via regulating miR-502-3p/OLFM4/STAT3 pathway.

BACKGROUND: Increasing studies have revealed that circular RNAs (circRNAs) contribute to gastric cancer (GC) progression. The circular RNA ribosomal protein L15 (circ-RPL15) is involved in chronic lymphocytic leukemia. However, its expression and functions in GC remain elusive. METHODS: The expression of circ-RPL15 in human GC tissues and adjacent normal tissues, human gastric cancer cell lines (MGC-803, BGC-823, MGN-28, SGC-7901, AGS) and normal gastric mucosal epithelial cell line (GES-1) were detected by RT-PCR. The relationship between circ-RPL15 level and clinical-pathological indicators were also analyzed. Gain- of function experiments of circ-RPL15 and miR-502-3p were conducted to verify their roles in mediating GC cell proliferation, apoptosis and metastasis. Also, the downstream mechanisms of circ-RPL15 were predicted by bioinformatics analysis, and the interactions between circ-RPL15 and miR-502-3p, miR-502-3p and OLFM4 were verified by dual luciferase reporter gene assay and RNA FISH. RESULTS: circ-RPL15 was upregulated in GC tissues and cell lines, and the overexpressed circ-RPL15 was correlated with poorer survival of GC patients. Functionally, circ-RPL15 upregulation distinctly promoted the proliferation, migration and invasion of GC cells and inhibited apoptosis. Mechanistically, circ-RPL15 functioned as a competitive endogenous RNA via sponging miR-502-3p and activated OLFM4/STAT3 pathway. CONCLUSION: circ-RPL15 promotes GC progression and predicts poor prognosis of GC patients, and regulates the malignant phenotypes of GC cells by mediating the miR-502-3p/OLFM4/STAT3 axis.

miR-625 reverses multidrug resistance in gastric cancer cells by directly targeting ALDH1A1.

Background: microRNAs (miRNAs) are emerging as critical regulators of multidrug resistance (MDR) in gastric cancer, a major cause of chemotherapy failure. miR-625 is downregulated in gastric cancer and negatively associated with metastasis. In the current study, we aimed to investigate whether miR-625 regulates MDR in gastric cancer. Methods: The level of miR-625 in gastric cancer cells with or without MDR was quantified by quantitative reverse transcription PCR (qRT-PCR) analysis. The sensitivity of gastric cancer cells to chemotherapeutic agents was assessed by MTT assay. The protein expression was determined by Western blot analysis, and the luciferase reporter assay was applied to confirm miR-625 regulation of the potential target. Results: miR-625 is downregulated in MDR gastric cancer cells compared with chemosensitive counterparts. In addition, miR-625 increases the sensitivity and promotes apoptosis of gastric cancer cells when treated with different chemotherapeutic agents. Moreover, miR-625 directly targets the aldehyde dehydrogenase 1A1 (ALDH1A1), and importantly, the restoration of ALDH1A1 expression rescues miR-625 effects on MDR in gastric cancer cells. Conclusion: miR-625 reverses MDR in gastric cancer cells by targeting ALDH1A1. Hence, our study identifies miR-625 as a novel regulator of MDR in gastric cancer cells, and implicates its potential application for overcoming MDR in gastric cancer chemotherapy.

Silencing of DLEU2 suppresses pancreatic cancer cell proliferation and invasion by upregulating microRNA-455.

Long noncoding RNA (lncRNA) DLEU2 has been shown to be dysregulated in several type of tumor. However, the potential biological roles and molecular mechanisms of DLEU2 in pancreatic cancer (PC) progression are poorly understood. In this study, we found that the DLEU2 level was substantially upregulated in PC tissues and PC cell lines, and significantly associated with poor clinical outcomes in PC patients. Overexpression of DLEU2 significantly induced PC cell proliferation and invasion, whereas knockdown of DLEU2 impaired cell proliferation and invasion in vitro. Furthermore, bioinformatics analysis, luciferase reporter assay, and RNA immunoprecipitation assay revealed that DLEU2 directly bond to microRNA-455 (miR-455) and functioned as an endogenous sponge for miR-455, which could remarkably suppress cell growth and invasion. We also determined that SMAD2 was a direct target of miR-455, and the restoration of SMAD2 rescued cell growth and invasion that were reduced by DLEU2 knockdown or miR-455 overexpression. In addition, low miR-455 expression and high SMAD2 expression was correlated with poor patient survival. These results indicate that DLEU2 is an important promoter of PC development, and targeting the DLEU2/miR-455/SMAD2 pathway could be a promising therapeutic approach in the treatment of PC.

Effect of azithromycin and pefloxacin in treatment of acute enteritis based on clinical efficacy comparison.

This paper aims to compare and analyze clinical efficacy of azithromycin and pefloxacin in treatment of acute enteritis. The 160 patients with acute enteritis were randomly divided into a study group (n=80) treated with azithromycin, and a reference group (n=80) treated with pefloxacin. We compared overall treatment efficiency (markedly, effective, invalid), clinical symptoms and signs remission time (antipyretic time, antidiarrheal time, symptoms and signs disappearance time), interleukin-6 and C-reactive protein concentration before and after treatment, adverse reactions rate (nausea, abdominal pain, headache, etc.). In comparison of overall treatment efficiency of the two groups, the results showed that the study group was significantly superior to the reference group (P<0.05). In comparison of clinical symptoms and signs remission time of the two groups, the study group were significantly shorter than the reference group (P<0.05). At the same time, in comparison of levels of interleukin-6 and C-reactive protein concentration after treatment, the study group was significantly superior to the reference group (P<0.05). There was no significant difference between the two groups in incidence of adverse reactions (P<0.05). The efficacy of azithromycin for acute enteritis is better than that of pefloxacin, and it can significantly reduce clinical symptom remission time. Moreover, safe and reliable, it has great value in clinical application.