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Peer-reviewedCC BY-NCBiological and Pharmaceutical Bulletin

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

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.

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BibTeX
@article{suzuki2026bidirectional,
  title = {{Bidirectional Regulation of c-Myc and TRB1 Establishes Oncogenic Reciprocal Regulation}},
  author = {Yuya Suzuki and Mai Nagasaka and Chiharu Miyajima and Kaori Tsuzuki and Mau Suzuka and Koh Yoshida and Daisuke Morishita and Kohki Toriuchi and Hiromasa Aoki and Mineyoshi Aoyama and Hidetoshi Hayashi and Yasumichi Inoue},
  journal = {Biological and Pharmaceutical Bulletin},
  year = {2026},
  month = aug,
  doi = {10.1248/bpb.b26-00037},
  url = {https://www.jstage.jst.go.jp/article/bpb/49/8/49_b26-00037/_article},
  note = {CC BY-NC},
}
RIS
TY  - JOUR
TI  - Bidirectional Regulation of c-Myc and TRB1 Establishes Oncogenic Reciprocal Regulation
AU  - Yuya Suzuki
AU  - Mai Nagasaka
AU  - Chiharu Miyajima
AU  - Kaori Tsuzuki
AU  - Mau Suzuka
AU  - Koh Yoshida
AU  - Daisuke Morishita
AU  - Kohki Toriuchi
AU  - Hiromasa Aoki
AU  - Mineyoshi Aoyama
AU  - Hidetoshi Hayashi
AU  - Yasumichi Inoue
PY  - 2026
DA  - 2026/08/28
JO  - Biological and Pharmaceutical Bulletin
DO  - 10.1248/bpb.b26-00037
UR  - https://www.jstage.jst.go.jp/article/bpb/49/8/49_b26-00037/_article
AB  - 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.
SN  - 1347-5215
SN  - 0918-6158
ER  -