Open Access

ARTICLE

Silencing of long non-coding RNA CCHE1 inhibits the ovarian cancer SKOV3 cell invasion and migration and inactivates the p38-MAPK signaling pathway

by HONGWEI CHEN, XUAN SONG, HEMEI LI

Department of Gynecology and Obstetrics, the Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430014, China

* Address correspondence to: Hemei Li,
# These authors contributed equally to this work

BIOCELL 2020, 44(3), 345-351. https://doi.org/10.32604/biocell.2020.08944

Received 27 October 2019; Accepted 25 January 2020; Issue published 22 September 2020

Abstract

Ovarian cancer (OC) is a major cause of cancer-related deaths among gynaecological malignancies. Emerging studies suggest that the long non-coding RNA (lncRNA) may be the potential biomarker for the diagnosis and prognosis of the cancer. The current study was carried out to investigate the role of lncRNA CCHE1 silencing in OC cell invasion and migration. Expression of lncRNA CCHE1 in normal ovarian cell Hose and OC cell lines HO 8910, A2780 and SKOV3 was detected. LncRNA were transfected with siRNA, and then the proliferation of cells was detected by using MTT assay. Cell invasion and migration was measured by using Transwell assay and scratch test, respectively. The protein levels of E-cadherin, N-cadherin, ERK, p38-MAPK and the phosphorylation of ERK and p38-MAPK in cells after siRNA transfection were detected by using Western blot analysis. Consequently, lncRNA CCHE1 expression was highly expressed in OC cell lines, especially in SKOV3 cells. siRNA1, siRNA2 and siRNA3 all decreased. lncRNA CCHE1 expression in SKOV3 cells and siRNA2 showed the best silencing efficacy. Silencing of lncRNA CCHE1 decreased proliferation, invasion and migration, and reduced the protein levels of N-cadherin, ERK, p38-MAPK and the phosphorylation of ERK and p38-MAPK, while reducing the protein level of E-cadherin in SKOV3 cells. Collectively, our study proved that the silencing of lncRNA CCHE1 could inhibit SKOV3 cell invasion and migration via inactivating the p38-MAPK signaling pathway.

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