Bidirectional Regulation of c-Myc and TRB1 Establishes Oncogenic Reciprocal Regulation.

Authors

Yuya Suzuki, Mai Nagasaka, Chiharu Miyajima, Kaori Tsuzuki, Mau Suzuka, Koh Yoshida, Daisuke Morishita, Kohki Toriuchi, Hiromasa Aoki, Mineyoshi Aoyama, Hidetoshi Hayashi, Yasumichi Inoue

Published in

Biological & pharmaceutical bulletin. Volume 49. Issue 8. Pages 1320-1328.

Abstract

The transcription factor c-Myc is frequently upregulated in human cancers through multiple mechanisms, including chromosomal translocation and gene amplification. Since the human TRIB1 gene is located on chromosome 8q24 in close proximity to the MYC oncogene, the MYC and TRIB1 genes may be co-amplified in a large percentage of human cancers. We herein demonstrate molecular crosstalk between TRB1 and c-Myc. Bioinformatic analyses reveal a positive correlation between MYC and TRIB1 expression across multiple cancer types. In prostate cancer cells, the knockdown of c-Myc reduces TRB1 expression. Mechanistically, c-Myc directly binds to the proximal promoter region of the TRIB1 gene and activates its transcription. Conversely, the depletion of TRB1 decreases c-Myc levels and affects the expression of c-Myc target genes. These results indicate that TRB1 contributes to the oncogenic functions of c-Myc and suggest the potential of the TRB1-c-Myc axis as a therapeutic target for cancer treatment.

PMID:
42669521
Bibliographic data and abstract were imported from PubMed on 31 Aug 2026.

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