TRIM44 promotes cell proliferation and migration by inhibiting FRK in renal cell carcinoma

Yuta Yamada, Naoki Kimura, Ken ichi Takayama, Yusuke Sato, Takashi Suzuki, Kotaro Azuma, Tetsuya Fujimura, Kazuhiro Ikeda, Haruki Kume, Satoshi Inoue

研究成果: Article査読

12 被引用数 (Scopus)

抄録

TRIM44 has oncogenic roles in various cancers. However, TRIM44 expression and its function in renal cell carcinoma (RCC) are still unknown. Here in this study, we investigated the clinical significance of TRIM44 and its biological function in RCC. TRIM44 overexpression was significantly associated with clinical M stage, histologic type (clear cell) and presence of lymphatic invasion (P =.047, P =.005, and P =.028, respectively). Moreover, TRIM44 overexpression was significantly associated with poor prognosis in terms of cancer-specific survival (P =.019). Gain-of-function and loss-of-function studies using TRIM44 and siTRIM44 transfection showed that TRIM44 promotes cell proliferation and cell migration in two RCC cell lines, Caki1 and 769P. To further investigate the role of TRIM44 in RCC, we performed integrated microarray analysis in Caki1 and 769P cells and explored the data in the Oncomine database. Interestingly, FRK was identified as a promising candidate target gene of TRIM44, which was downregulated in RCC compared with normal renal tissues. We found that cell proliferation was inhibited by TRIM44 knockdown and then recovered by siFRK treatment. Taken together, the present study revealed the association between high expression of TRIM44 and poor prognosis in RCC patients and that TRIM44 promotes cell proliferation by regulating FRK.

本文言語English
ページ(範囲)881-890
ページ数10
ジャーナルCancer science
111
3
DOI
出版ステータスPublished - 2020 3 1
外部発表はい

ASJC Scopus subject areas

  • 腫瘍学
  • 癌研究

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