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LINC01426 contributes to clear cell renal cell carcinoma progression by modulating CTBP1/miR‐423‐5p/FOXM1 axis via interacting with IGF2BP1
Author(s) -
Jiang YuFeng,
Zhang HaiMin,
Li Wei,
Yan Yang,
Yao XuDong,
Gu WenYu
Publication year - 2021
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.29871
Subject(s) - clear cell renal cell carcinoma , foxm1 , carcinogenesis , biology , cancer research , cell growth , downregulation and upregulation , transcription factor , cell , microbiology and biotechnology , cell cycle , cancer , genetics , renal cell carcinoma , pathology , gene , medicine
Increasing evidence suggests that long noncoding RNAs (lncRNAs) are pivotal regulators in oncogenesis. However, the role of numerous lncRNAs has never been unmasked in clear cell renal cell carcinoma (ccRCC). Presently, we investigated the function of long intergenic nonprotein coding RNA 1426 (LINC01426) in ccRCC, as The Cancer Genome Atlas data indicated that LINC01426 was highly expressed in ccRCC tissues and its overexpression was correlated with disappointing prognosis. First, we verified that LINC01426 was indeed upregulated in ccRCC cell lines and its depletion restrained ccRCC cell proliferation and migration. Besides, we proved that LINC01426 facilitated ccRCC tumorigenesis via forkhead box M1 (FOXM1). Moreover, it was revealed that miR‐423‐5p was downregulated and directly targeted FOXM1 in ccRCC, and that LINC01426 positively regulated FOXM1 via its inhibition on miR‐423‐5p. Notably, we also uncovered that miR‐423‐5p was transcriptionally silenced by CTBP1 and HDAC2. Of importance, LINC01426 was certified to distribute both in the cytoplasm and the nucleus of ccRCC cells, and it increased CTBP1 expression through recruiting insulin like growth factor 2 mRNA binding protein 1 (IGF2BP1) in cytoplasm whereas interacted with CTBP1 protein to improve the transcriptional repression on miR‐423‐5p in nucleus. Jointly, our observations unveiled that LINC01426 aggravates ccRCC progression via IGF2BP1/CTBP1/HDAC2/miR‐423‐5p/FOXM1 axis, highlighting LINC01426 as a novel promising target for ccRCC treatment.