Open AccessRegulation of NCAPG by miR‐99a‐3p (passenger strand) inhibits cancer cell aggressiveness and is involved in CRPC
Author(s) -
Arai Takayuki,
Okato Atsushi,
Yamada Yasutaka,
Sugawara Sho,
Kurozumi Akira,
Kojima Satoko,
Yamazaki Kazuto,
Naya Yukio,
Ichikawa Tomohiko,
Seki Naohiko
Publication year - 2018
Publication title -
cancer medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 53
ISSN - 2045-7634
DOI - 10.1002/cam4.1455
Subject(s) - gene knockdown , microrna , biology , prostate cancer , ectopic expression , cancer , cancer research , cell growth , pathogenesis , cell , gene , genetics , immunology
Effective treatments for patients with castration‐resistant prostate cancer ( CRPC ) have not yet been established. Novel approaches for identification of putative therapeutic targets for CRPC are needed. Analyses of RNA sequencing of micro RNA (mi RNA ) expression revealed that miR‐99a‐3p (passenger strand) is significantly downregulated in several types of cancers. Here, we aimed to identify novel miR‐99a‐3p regulatory networks and therapeutic targets for CRPC . Ectopic expression of miR‐99a‐3p significantly inhibited cancer cell proliferation, migration, and invasion in PC a cells. Non‐ SMC condensin I complex subunit G ( NCAPG ) was a direct target of miR‐99a‐3p in PC a cells. Overexpression of NCAPG was detected in CRPC clinical specimens and was significantly associated with shorter disease‐free survival and advanced clinical stage. Knockdown of NCAPG inhibited cancer cell aggressiveness. The passenger strand miR‐99a‐3p acted as an antitumor mi RNA in naïve PC a and CRPC . NCAPG was regulated by miR‐99a‐3p , and its overexpression was involved in CRPC pathogenesis. Involvement of passenger strand of mi RNA in cancer pathogenesis is novel concept, and identification of antitumor mi RNA regulatory networks in CRPC might be provided novel prognostic markers and therapeutic targets for this disease.