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Basic Information

Classification Information

Regulatory Mechanism		Biological Function		Clinical Application
TF		Immune		Survival
Enhancer		Apoptosis	apoptosis	Drug
Variant		Cell Growth		Circulating
MiRNA		EMT		Metastasis
Methylation		Coding Ability		Recurrence

Cancer&Entry Information

Cancer Name	colorectal cancer
ICD-0-3	C19.9
Methods	qPCR, Western blot, Luciferase reporter assay, RIP, etc.
Sample	CRC tissues, CRC cell lines (HCT116, HT-29, LoVo, SW480, and SW620) and the normal colon epithelial cell line NCM460
Expression Pattern	down-regulated
Function Description	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.
Pubmed ID	30472379
Year	2018
Title	Long non-coding RNA TP73-AS1 promotes colorectal cancer proliferation by acting as a ceRNA for miR-103 to regulate PTEN expression

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