@Article{096504017X15051741798389,
AUTHOR = {Qingzhu Ma, Yan Wang, Hualing Zhang, Fengqiang Wang},
TITLE = {miR-1290 Contributes to Colorectal Cancer Cell Proliferation  by Targeting INPP4B},
JOURNAL = {Oncology Research},
VOLUME = {26},
YEAR = {2018},
NUMBER = {8},
PAGES = {1167--1174},
URL = {http://www.techscience.com/or/v26n8/56731},
ISSN = {1555-3906},
ABSTRACT = {Colorectal cancer (CRC) is one of the most common oncological conditions worldwide, to date. MicroRNA-
1290 (miR-1290) has been demonstrated to regulate its progression. We studied the role of miR-1290 in CRC 
progression. The gene was upregulated in CRC tissues and cells. Its overexpression promoted CRC cell proliferation analyzed by MTT assay, colony formation assay, and soft agar growth assay. In addition, miR-1290 
knockdown inhibited CRC cell proliferation. We also found that miR-1290 overexpression reduced the p27 
level and increased cyclin D1 at both the mRNA and protein levels, whereas miR-1290 knockdown increased 
p27 and reduced cyclin D1, confirming miR-1290 promoted CRC cell proliferation. Inositol polyphosphate 
4-phosphatase B (INPP4B) was the target of miR-1290. Luciferase reporter assay revealed that miR-1290 
directly bound to the 3'-UTR of INPP4B; the mutated seed sites in miR-1290 abrogated this effect. Double 
knockdown of INPP4B and miR-1290 promoted CRC cell proliferation, suggesting miR-1290 promoted CRC 
cell proliferation by targeting INPP4B.},
DOI = {10.3727/096504017X15051741798389}
}