Eur Rev Med Pharmacol Sci 2018; 22 (15): 4812-4819
DOI: 10.26355/eurrev_201808_15616

LncRNA HCP5 promotes the development of cervical cancer by regulating MACC1 via suppression of microRNA-15a

Y. Yu, H.-M. Shen, D.-M. Fang, Q.-J. Meng, Y.-H. Xin

Department of Reproductive, The Children and Women’s Healthcare of Laiwu City, Laiwu, China. xlbyixue@163.com


OBJECTIVE: To explore the role of long non-coding RNA (lncRNA) HCP5 in the development of cervical cancer and its underlying mechanism.

PATIENTS AND METHODS: Expression levels of HCP5, MACC1 and microRNA-15a in cervical cancer tissues and paracancerous tissues were detected. The relationship between HCP5 expression and prognosis of patients with cervical cancer was analyzed by Kaplan-Meier. Cell proliferation was detected by Cell Counting Kit-8 (CCK-8) assay after altering expressions of HCP5 and microRNA-15a by plasmids transfection. The binding condition of HCP5, MACC1 and microRNA-15a was evaluated by luciferase reporter gene assay. The regulatory effect of microRNA-15a on MACC1 expression was determined by Western blot.

RESULTS: HCP5 and MACC1 were overexpressed in cervical cancer tissues than those of paracancerous tissues. The survival rate of patients with cervical cancer was negatively correlated to HCP5 expression, but positively correlated to microRNA-15a expression. Luciferase reporter gene assay showed that microRNA-15a was directly bound to HCP5 and MACC1. Besides, overexpression of microRNA-15a could remarkably inhibited MACC1 expression. In vitro experiments showed that HCP5 promoted proliferation of cervical cancer cells, which was reversed by microRNA-15a knockdown.

CONCLUSIONS: Overexpressed HCP5 promoted the development of cervical cancer through increasing MACC1 expression by microRNA-15a adsorption.

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To cite this article

Y. Yu, H.-M. Shen, D.-M. Fang, Q.-J. Meng, Y.-H. Xin
LncRNA HCP5 promotes the development of cervical cancer by regulating MACC1 via suppression of microRNA-15a

Eur Rev Med Pharmacol Sci
Year: 2018
Vol. 22 - N. 15
Pages: 4812-4819
DOI: 10.26355/eurrev_201808_15616