Long Noncoding RNA loc285194 Expression in Human Papillomavirus-Positive and -Negative Cervical Squamous Cell Carcinoma, C33A, and SiHa Cells and Transforming Growth Factor-β1

长链非编码 RNA loc285194 在人乳头瘤病毒阳性和阴性宫颈鳞状细胞癌、C33A 和 SiHa 细胞以及转化生长因子-β1 中的表达

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作者:Jian Wang, Yi Zhang, Ru Lin, Baohong Mao, Wendi Wang, Yan Bai, Wenhua He, Qing Liu

Abstract

BACKGROUND This study aimed to investigate the expression of long noncoding RNA (lncRNA) loc285194 in cervical squamous cell carcinoma (CSCC) biopsies that were positive and negative for human papillomavirus (HPV) and in human CSCC cell lines SiHa and C33A and to investigate the overexpression of lncRNA loc285194. MATERIAL AND METHODS Cervical biopsy tissue and plasma samples from 66 patients with histologically confirmed CSCC, that were HPV16-positive (N=22), HPV18-positive (N=27), and HPV-negative (N=17), and healthy controls (N=20) and human CSCC cell lines SiHa (HPV16-positive) and C33A (HPV-negative) were studied. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was used to measure the expression of lncRNA loc285194 in cervical biopsies and plasma. Enzyme-linked immunosorbent assay (ELISA) and Western blot were used to measure levels of transforming growth factor-ß1 (TGF-ß1). A lncRNA loc285194 expression vector was constructed and transfected into SiHa and C33A cells that underwent a transwell assay for cell migration. RESULTS Expression of lncRNA loc285194 was downregulated in HPV-positive and HPV-negative tissue samples and plasma from patients with CSCC and distinguished between patients and healthy controls. Plasma levels of loc285194 and TGF-ß1 were significantly correlated with the presence of CSCC. In SiHa and C33A cells, TGF-ß1 expression was downregulated, and cell migration was inhibited following lncRNA loc285194 overexpression. Although lncRNA loc285194 expression was not affected by TGF-ß1 treatment, its effects on cell migration were reduced by TGF-ß1. CONCLUSIONS The expression of lncRNA loc285194 inhibited the migration of CSCC cells in vitro through the inactivation of TGF-ß1.

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