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Basic Information

Classification Information

Regulatory Mechanism		Biological Function		Clinical Application
TF		Immune		Survival
Enhancer		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 etc.
Sample	CRC tissues, cell lines(HCT-116/HCT-8)
Expression Pattern	up-regulated
Function Description	The effect of lnc CCAT1 on human HCT-116/HCT-8 cells and its potential mechanism were investigated. In present study, differential expression of CCAT1, miR-410 and ITPKB were detected in colon cancer tissues and adjacent parts. Then the prediction programs were applied to predict the target genes of miR-410. The complementary bindings of miR-410 with lnc CCAT1 and ITPKB were assessed by luciferase assays. The interaction between LncRNA CCAT1 and miR-410 was analyzed. In addition, the mRNA and protein of ITPKB and apoptosis factors were examined in cells after miR-410 overexpression or silencing. Meanwhile, MTT and flow cytometer were used to detect the cells proliferation and apoptosis level. Results showed that CCAT1 and miR-410 were up-regulated in colon cancer tissues, but ITPKB was down-regulated. Lnc CCAT1 and ITPKB were predicted to be the targets of miR-410 and the prediction were verified by luciferase assays. The expression of lnc CCAT1 and ITPKB were inhibited by miR-410 in human HCT-116/ HCT-8 cells. Meanwhile, lnc CCAT1 could lead to a decrease of miR-410. Furthermore, miR-410 overexpression could promote cell proliferation and reduce apoptosis. In summary, these data demonstrated that miR-410 could promote cell proliferation and reduce apoptosis by inhibiting ITPKB expression and the expression of lnc CCAT1 antagonized the effect of miR-410.
Pubmed ID	29190961
Year	2017
Title	Long noncoding RNA CCAT1 functions as a ceRNA to antagonize the effect of miR-410 on the down-regulation of ITPKB in human HCT-116 and HCT-8 cells

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