LncRNA TTN‑AS1 promotes endometrial cancer by sponging miR‑376a‑3p

• Published in: Oncology reports Vol. 44; no. 4; pp. 1343 - 1354
• Main Authors: Shen, Longde, Wu, Yinyin, Li, Ailu, Li, Lichun, Shen, Longyuan, Jiang, Qiuxia, Li, Qiuxia, Wu, Zhifen, Yu, Liji, Zhang, Xiaohong
• Format: Journal Article
• Language: English
• Published: Greece Spandidos Publications 01.10.2020; Spandidos Publications UK Ltd; D.A. Spandidos
• Subjects: Antibodies; Apoptosis; Apoptosis - genetics; Biotechnology; Cancer; Cancer therapies; Cell Line, Tumor; Cell Movement - genetics; Cell Proliferation - genetics; Connectin - genetics; Development and progression; Endometrial cancer; Endometrial Neoplasms - genetics; Endometrial Neoplasms - pathology; Female; Gene expression; Gene Expression Regulation, Neoplastic - genetics; Hospitals; Humans; MicroRNAs; MicroRNAs - genetics; Plasmids; RNA, Long Noncoding - genetics; RNA-Binding Proteins - genetics; Software; China; endometrial cancer; miR-376a-3p; cell proliferation; lncRNA TTN-AS1; PUM2
• ISSN: 1021-335X; 1791-2431; 1791-2431
• DOI: 10.3892/or.2020.7691

Increasing research has demonstrated that lncRNAs participate in the development of multiple cancer types. However, the role of TTN‑AS1 in endometrial cancer (EC) remains unknown. The present study aimed to explore the function of titin‑antisense RNA1 (TTN‑AS1) in EC progression and the underlying mechanisms. qRT‑PCR was performed to assess the TTN‑AS1 expression patterns in EC tissues and cell lines. Loss of function experiments were carried out to estimate the effects of TTN‑AS1 on EC cell proliferation, migration and invasion. To reveal the underlying mechanisms, informatics tools were used to predict the targets. Rescue experiments were performed to investigate the TTN‑AS1‑regulated miR‑376a‑3p/pumilio homolog 2 (PUM2) axis involved. The results of the present study revealed that TTN‑AS1 was highly expressed in both EC tissues and cell lines, and TTN‑AS1 knockdown inhibited EC cell proliferation, migration and invasion. With respect to the mechanisms, miR‑376a‑3p was revealed to be targeted by TTN‑AS1, and reversed the effects on EC development induced by TTN‑AS1. In addition, PUM2 was positively regulated by TTN‑AS1, and miR‑376a‑3p mediated the regulation between them. Furtherly, in vivo experiments confirmed the results. Collectively, TTN‑AS1 enhanced EC cell proliferation and metastasis by targeting the miR‑376a‑3p/PUM2 axis, which may shed light on EC diagnosis and treatment.