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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Bo Li1, Chong Shi2, Jingming Zhao2 and Bai Li3
1Department of Gastrointestinal Colorectal and Anal Surgery, China-Japan Union Hospital of Jilin University, Changchun, P.R. China
2Department of Anorectal Surgery, The Afflicted Hospital to Changchun University of Chinese Medicine, Changchun, P.R. China
3Department of Colorectal and Anal Surgery, The First Affiliated Hospital of Jilin University, Changchun, P.R. China
Bai Li, email: [email protected]
Keywords: colon cancer, miRNA-410, CCAT1, ITPKB
Received: April 13, 2017 Accepted: August 26, 2017 Published: October 07, 2017
Colorectal cancer is one of the most common malignancies, which has seriously affected people’s health. Abnormal expression of long non-coding RNAs and microRNAs are closely related to the process of occurrence, development, invasion and metastasis of colorectal cancer. However, 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.
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