Circular RNA circ-PRKCI functions as a competitive endogenous RNA to regulate AKT3 expression by sponging miR-3680-3p in esophageal squamous cell carcinoma.

Circular RNA (circRNA) is a new noncoding RNAs and plays an important role in many pathological processes. Recently, studies have shown that circular RNA_PRKCI (circ-PRKCI) regulates cell proliferation and cell migration of tumor cells. Esophageal carcinoma is a highly malignant digestive tract tumor, which is divided into esophageal adenocarcinoma and esophageal squamous cell carcinoma. In this study, we studied whether circ-PRKCI might influence cell proliferation and cell migration in esophageal squamous cell carcinoma. Quantitative reverse transcription PCR was performed to detect the relative expression of circ-PRKCI in five cases of esophageal squamous cell carcinoma and five cases of paired adjacent normal tissues. RNA immunoprecipitation assay and Luciferase assay confirm the direct interaction between miR-3680-3p and AKT3 or circ-PRKCI. Ethynyldeoxyuridine assays and cell counting Kit-8 were performed to evaluate the effect of miR-3680-3p or circ-PRKCI on cell proliferation, transwell assays were also performed to detect migration in vitro. We found circ-PRKCI is obviously upregulated in esophageal squamous cell carcinoma and upregulation of circ-PRKCI stimulated cell migration and proliferation of ESCC cells. In the mechanism, we confirm that circ-PRKCI, as a molecular sponge of miR-3680-3p, upregulates the expression of AKT. In conclusion, our current studies have been revealing that circ-PRKCI/miR-3680-3p/AKT3 regulatory network plays an important role in esophageal squamous cell carcinoma and that provide new insights into the pathogenesis of esophageal squamous cell carcinoma.

TUSC8 enhances cisplatin sensitivity of NSCLC cells through regulating VEGFA.

PURPOSE: We aimed at studying LncRNA TUSC8 expression in non-small cell lung cancer (NSCLC) cells and its sensitivity to cisplatin chemotherapy, and explore its role in the occurrence, development and treatment of NSCLC. METHODS: NSCLC tissues and adjacent normal ones were randomly selected from 45 patients in our hospital who were pathologically diagnosed as NSCLC. Then H358 and H1299 cells were treated with cisplatin at different concentrations (0 µM, 2 µM, 4 µM, 8 µM, 16 µM) for 24 hours. RESULTS: Our data showed that long non-coding RNA (LncRNA) TUSC8 mRNA expression in NSCLC tissue specimens was remarkably lower than that in adjacent ones. A great link was found between LncRNA TUSC8 and tumor size, TNM stage and overall survival rates of patients with Lung cancer (LCa). The proliferation of NSCLC cells remarkably reduced after overexpression of LncRNA TUSC8 compared with the control group pcDNA3.1-NC, while cell apoptosis indicated an opposite trend. A binding relationship between LncRNA TUSC8 and its downstream target gene VEGFA was verified by luciferase assay. The proliferation rate of NSCLC cells decreased with the increase of cisplatin concentration, and the inhibition rate of LncRNA TUSC8 overexpression group was higher than that of the control group pcDNA3.1-NC under different concentrations of cisplatin. CONCLUSIONS: Lowly expressed LncRNA TUSC8 in NSCLC is related to pathological parameters and prognosis of NSCLC patients. It may negatively regulate VEGFA by targeting its 3'UTR, thereby increasing the sensitivity of NSCLC cell lines to cisplatin, inhibiting the proliferation of NSCLC cells and promoting their apoptosis.