Long noncoding RNA GHET1 promotes cell proliferation through oxidative stress in prostate cancer

Abstract

AbstractGastric carcinoma high expressed transcript 1 (GHET1) is an oncogenic Long noncoding RNA. GHET1 expression promotes multiple levels of developing a complex molecular network. The main purpose of the study was to investigate the mechanism by which long noncoding RNA (lncRNA) GHET1 promotes prostate cancer cell proliferation and related metabolism. In vitro study, lncRNA GHET1 was overexpressed in LN‐cap, PC‐3, 22RV1, and C4‐2 cells. The cell viability was measured by MTT and trans‐well assay. A flow cytometer was also used to detect cell cycles and apoptosis. Western blot analysis was used for protein expression validation. mRNA expression was detected by real‐time PCR. lncRNA GHET1 enhanced cell proliferation, migration, and could resist paclitaxel‐induced apoptosis and cell cycle arrest GHET1 expression stimulates reactive oxygen species (ROS) level upregulated in prostate cancer cells, increased the expression of HIFα, IL‐1B and IL‐6, and activated ROS/STAT‐3/Twsit1 signaling pathway. Knockdown GHET1 could reduce cell proliferation and migration due to the overexpression of GHET1. lncRNA GHET1 promotes prostate cancer growth through oxidative stress signaling pathways and resists the antineoplastic drug paclitaxel, which can be used as a target for antineoplastic therapy and drug resistance therapy in the future in clinics.