Long non-coding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) promote cell proliferation in colorectal cancer by affecting P53

Y. Zhao, Z.-S. Qin, Y. Feng, X.-J. Tang, T. Zhang, L. Yang

Department of General Surgery, Huai’an First People’s Hospital, Nanjing Medical University, Huai’an, Jiangsu Province, P.R. China. 1163785088@qq.com

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• Oncology

OBJECTIVE: Colorectal cancer (CRC) is one of the most frequent malignant tumors worldwide. The connection between lncRNAs expression and CRC development has not been well identified in the recent literature. This study focuses on the role of lncRNA-SNHG1 on CRC progression and development. The quantitative Real-time PCR (qRT-PCR) assay was conducted to identify the expression level of small nucleolar RNA host gene 1 (SNHG1).

PATIENTS AND METHODS: Cell proliferation and viability were examined by 3-(4,5)-dimethylthiazol(-z-y1)-3,5-diphenyl tetrazoliumbromide (MTT assay) and colony formation assay. Cell apoptosis and cell cycle distribution were detected by flow cytometry.

RESULTS: Expressions of p53, p21, BAX were assessed by Western blotting. CRC cells transfected with lncRNA-shRNA were injected into nude mice to identify the role of SNHG1 on tumorigenesis in vivo. SNHG1 expression level was elevated in CRC tissues when compared to adjacent tissues (n=86). SNHG1 knockdown significantly suppressed cell proliferation and viability, while SNHG1 overexpression had the opposite effect. Decreased SNHG1 expression enhanced cell apoptosis and triggered cell cycle arrest in G0/G1 phase, while elevated SNHG1 expression done the opposite. Besides, downregulation of SNHG1 impeded tumorigenesis in vivo. Protein levels of p53 and p53 target genes were affected by SNHG1 in vitro.

CONCLUSIONS: Our research demonstrated that SNHG1 may participate in controlling CRC proliferation, viability, and apoptosis via modulating p53 partially, which provides potential therapeutic targets for CRC.

 

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