The journal of gene medicine · 2021
Long non-coding RNA SNHG8 promotes prostate cancer progression through repressing miR-384 and up-regulating HOXB7.
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Shi Zhenfeng, Zhang Hao, Jie Situ, Yang Xiaojian, Huang Qunxiong, Mao Yunhua, Zhang Yan
Аннотация
BACKGROUND: Multiple long non-coding RNAs (lncRNAs) have been demonstrated to function as vital regulators in the progression of prostate cancer (PCa). In the present study, we aimed to probe the function of lncRNA small nucleolar RNA host gene 8 (SNHG8) in PCa progression.
METHODS: A quantitative real-time polymerase chain reaction and western blotting were utilized to measure SNHG8, microRNA-384 (miR-384) and homeobox B7 (HOXB7) expression. Call-couting kit-8 and bromodeoxyuridine experiments were employed to evaluate PCa cell proliferation. Transwell experiments were performed to detect PCa cell migration and invasion. Dual-luciferase reporter experiments and RNA immunoprecipitation experiments were conducted to determine the targeting relationships among miR-384, SNHG8 and HOXB7.
RESULTS: SNHG8 was up-regulated in PCa tissues and cells. Silencing of SNHG8 suppressed the proliferation, migration and invasion of PCa cells. SNHG8 functioned as a molecular sponge to repress miR-384. The effects of SNHG8 knockdown on PCa cell proliferation, migration and invasion were counteracted by miR-384 inhibition. HOXB7 was confirmed to be a target gene of miR-384. SNHG8 knockdown repressed HOXB7 expression via targeting miR-384.
CONCLUSIONS: SNHG8 promotes PCa cell proliferation, migration and invasion via decoying miR-384 and up-regulating HOXB7.
METHODS: A quantitative real-time polymerase chain reaction and western blotting were utilized to measure SNHG8, microRNA-384 (miR-384) and homeobox B7 (HOXB7) expression. Call-couting kit-8 and bromodeoxyuridine experiments were employed to evaluate PCa cell proliferation. Transwell experiments were performed to detect PCa cell migration and invasion. Dual-luciferase reporter experiments and RNA immunoprecipitation experiments were conducted to determine the targeting relationships among miR-384, SNHG8 and HOXB7.
RESULTS: SNHG8 was up-regulated in PCa tissues and cells. Silencing of SNHG8 suppressed the proliferation, migration and invasion of PCa cells. SNHG8 functioned as a molecular sponge to repress miR-384. The effects of SNHG8 knockdown on PCa cell proliferation, migration and invasion were counteracted by miR-384 inhibition. HOXB7 was confirmed to be a target gene of miR-384. SNHG8 knockdown repressed HOXB7 expression via targeting miR-384.
CONCLUSIONS: SNHG8 promotes PCa cell proliferation, migration and invasion via decoying miR-384 and up-regulating HOXB7.