Gunma University Initiative for Advanced Research > News > Research > High KPNA2 expression predicts poor prognosis in pathological T4 colorectal cancer by importing c-Myc into the nucleus to suppress p53-dependent p21 expression (Division of Gene Therapy Science, Dr. Yokobori Laboratory)

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High KPNA2 expression predicts poor prognosis in pathological T4 colorectal cancer by importing c-Myc into the nucleus to suppress p53-dependent p21 expression (Division of Gene Therapy Science, Dr. Yokobori Laboratory)

A collaborative research team consisting of Associate Professor Takehiko Yokobori of the Division of Gene Therapy Science, Gunma University Initiative for Advanced Research (GIAR), Professor Hiroshi Saeki and Professor Ken Shirabe from the Department of General Surgical Science, Gunma University Graduate School of Medicine, and Professor Atsushi Shibata from the Faculty of Pharmacy, Keio University, has been conducting research aimed at identifying novel prognostic biomarkers and therapeutic targets for locally advanced colorectal cancer (pathological T4 colorectal cancer). The study was led by graduate student Gendensuren Dorjkhorloo and Assistant Professor Takuya Shiraishi from the Department of General Surgical Science.

In this study, the team focused on Karyopherin alpha 2 (KPNA2), a nuclear transport protein, and demonstrated that high KPNA2 expression is associated with increased distant metastasis, higher postoperative recurrence rates, and poor clinical outcomes. Furthermore, they elucidated the molecular mechanism by which KPNA2 promotes the nuclear translocation of the transcription factor c-Myc, thereby suppressing p53-dependent p21 expression and enhancing cancer cell proliferation and chemoresistance. These findings indicate that KPNA2 is a promising prognostic biomarker for advanced colorectal cancer and may represent a novel molecular target for future therapeutic strategies.

■Title
High KPNA2 expression predicts poor prognosis in pathological T4 colorectal cancer by importing c-Myc into the nucleus to suppress p53-dependent p21 expression

Gendensuren Dorjkhorloo1*, Bilguun Erkhem-Ochir2*, Takuya Shiraishi1*, Haruka Okami2, Arisa Yamaguchi1, Ikuma Shioi1, Nobuhiro Hosoi1, Chika Komine1, Nobuhiro Nakazawa1, Yuta Shibasaki1,
Takuhisa Okada1, Katsuya Osone1, Akihiko Sano1, Makoto Sakai1, Atsushi Shibata3, Takehiko Yokobori2†, Ken Shirabe1, and Hiroshi Saeki1
＊These authors contributed equally, †Corresponding author
1　Department of General Surgical Science, Graduate School of Medicine, Gunma University
2　Division of Gene Therapy Science, Gunma University Initiative for Advanced Research (GIAR)
3　Division of Molecular Oncological Pharmacy, Faculty of Pharmacy, Keio University

■Journal
British Journal of Cancer　(IF: 6.8)
DOI https://doi.org/10.1038/s41416-026-03552-5

■Link
Dr.YOKOBORI Laboratory

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