LncRNA WT1-AS up-regulates p53 to inhibit the proliferation of cervical squamous carcinoma cells

• Published in: BMC cancer Vol. 19; no. 1; p. 1052
• Main Authors: Zhang, Yunxia, Na, Renhua, Wang, Xinling
• Format: Journal Article
• Language: English
• Published: England BioMed Central Ltd 06.11.2019; BioMed Central; BMC
• Subjects: Adult; Analysis; Anopheles; Cancer research; Carcinoma; Carcinoma, Squamous Cell - complications; Carcinoma, Squamous Cell - genetics; Carcinoma, Squamous Cell - metabolism; Cell Line, Tumor; Cell Proliferation - genetics; Cervical squamous cell carcinoma; Female; Gene Expression Regulation, Neoplastic; Health aspects; Humans; Medical schools; Middle Aged; p53; Papillomavirus infections; Papillomavirus Infections - complications; Papillomavirus Infections - genetics; Papillomavirus Infections - virology; Prognosis; Proliferation; RNA, Long Noncoding - genetics; Squamous cell carcinoma; Stomach cancer; Survival Analysis; Tumor proteins; Tumor Suppressor Protein p53 - genetics; Tumor Suppressor Protein p53 - metabolism; Tumors; Up-Regulation; Uterine Cervical Neoplasms - complications; Uterine Cervical Neoplasms - genetics; Uterine Cervical Neoplasms - metabolism; WT1-AS; Young Adult; Cervical squamous cell carcinoma; Prognosis; Proliferation; WT1-AS; p53
• ISSN: 1471-2407; 1471-2407
• DOI: 10.1186/s12885-019-6264-2

It has been reported that the development of cervical squamous cell carcinoma (CSCC) requires the involvement of a large number of lncRNAs. In a recent study lncRNA, WT1-AS was been characterized as a tumor-suppressive lncRNA in gastric cancer. In our study we aim to explore the involvement of WT1-AS in CSCC. Seventy-six CSCC patients (20 to 63 years, 40.1 ± 6.1 year) from the 233 CSCC patients who were admitted by the Affiliated Tumour Hospital of Xinjiang Medical University between august 2010 and January 2014. RT-qPCR, cell proliferation rate measurement, cell transfection, and western blot were carried out to analyze the samples. We found that HPV infection failed to affect WT1-AS expression in CSCC tissues, while WT1-AS was down-regulated in CSCC tissues compared with non-cancer tissues. P53 was also down-regulated in CSCC tissues and positively correlated with WT1-AS. Analysis of the survival of CSCC patients revealed that low levels of WT1-AS were accompanied by poor survival. Significantly up-regulated p53 was observed after WT1-AS over-expression in CSCC cells, while p53 over-expression failed to affect WT1-AS. P53 and WT1-AS over-expression resulted in the inhibited proliferation of CSCC cells. Therefore, WT1-AS is down-regulated in CSCC and it may inhibit CSCC cell proliferation at least partially by up-regulating p53.