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Upregulation of miR?598 promotes cell proliferation and cell cycle progression in human colorectal carcinoma by suppressing INPP5E expression.


ABSTRACT: Colorectal cancer (CRC) is one of the most common types of cancer worldwide. Recently, microRNAs (miRs) have been considered as novel therapeutic targets for the treatment of cancer. miR?598 is a poorly investigated miR. The underlying mechanism of miR?598 in CRC cells remains to be elucidated. In the present study, miR?598 was demonstrated to be significantly upregulated in CRC tissue by analyzing data from The Cancer Genome Atlas and the Gene Expression Omnibus. The results of a polymerase chain reaction demonstrated that miR?598 expression was significantly upregulated in CRC tissues and cells. Gain of function and loss of function assays demonstrated that miR?598 significantly promoted cell proliferation and cell cycle progression. miR?598 was demonstrated to modulate cell functions by regulating 72 kDa inositol polyphosphate?5?phosphatase (INPP5E). In addition, knockdown of INPP5E counteracted the growth arrest caused by an miR?598?inhibitor. In conclusion, the present study demonstrated that miR?598 contributed to cell proliferation and cell cycle progression in CRC by targeting INPP5E.

SUBMITTER: Li KP 

PROVIDER: S-EPMC5783518 | biostudies-literature | 2018 Feb

REPOSITORIES: biostudies-literature

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Upregulation of miR‑598 promotes cell proliferation and cell cycle progression in human colorectal carcinoma by suppressing INPP5E expression.

Li Kun-Ping KP   Fang Yong-Ping YP   Liao Jin-Qi JQ   Duan Jin-Dong JD   Feng Li-Guang LG   Luo Xiao-Zai XZ   Liang Zhi-Jian ZJ  

Molecular medicine reports 20171206 2


Colorectal cancer (CRC) is one of the most common types of cancer worldwide. Recently, microRNAs (miRs) have been considered as novel therapeutic targets for the treatment of cancer. miR‑598 is a poorly investigated miR. The underlying mechanism of miR‑598 in CRC cells remains to be elucidated. In the present study, miR‑598 was demonstrated to be significantly upregulated in CRC tissue by analyzing data from The Cancer Genome Atlas and the Gene Expression Omnibus. The results of a polymerase cha  ...[more]

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