Long non-coding RNA TP73-AS1 promotes colorectal cancer proliferation by acting as a ceRNA for miR-103 to regulate PTEN expression

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.