Jump to Main Content
Long non-coding RNA TP73‑AS1 promotes colorectal cancer proliferation by acting as a ceRNA for miR‑103 to regulate PTEN expression
- Jia, Zeming, Peng, Jian, Yang, Zhi, Chen, Jie, Liu, Ling, Luo, Dongren, He, Panxiang
- Gene 2019 v.685 pp. 222-229
- antisense RNA, apoptosis, carcinogenesis, caspase-3, cell growth, cell proliferation, colorectal neoplasms, disease course, non-coding RNA, patients, prognosis, tissues
- There is an increasing evidence that long non-coding RNAs (lncRNAs) play an important role in tumorigenesis and cancer progression. This study focused on the functional role of P73 antisense RNA 1T (TP73‑AS1), a lncRNA, in colorectal cancer (CRC). We found that TP73‑AS1 expression was significantly low in CRC tissues and cells, and high TP73‑AS1 expression was negatively associated with TNM stage, prognosis, overall survival, and disease-free survival in the CRC patients. Moreover, TP73‑AS1 overexpression dramatically inhibited CRC cell growth, promoted apoptosis, downregulated Bcl‑2 levels, and increased caspase‑3 expression. Furthermore, TP73‑AS1 expression levels were positively associated with PTEN levels in clinical CRC samples. As expected, TP73‑AS1 could upregulate PTEN expression in CRC cells. Mechanistically, PTEN was shown to be the target of miR‑103. Interestingly, TP73‑AS1 overexpression could increase PTEN expression through competitive binding to miR‑103. Functionally, our data show that such TP73‑AS1-induced PTEN expression through binding to miR‑103 facilitated CRC cell proliferation. Thus, we showed that TP73‑AS1 inhibits CRC cell growth by functioning as a ceRNA (competing endogenous RNAs) to regulate PTEN levels. Our findings provide new insights into the underlying molecular mechanisms of TP73‑AS1-mediated CRC.