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PBK expression predicts favorable survival in colorectal cancer patients.
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- Author(s): Nagano-Matsuo, Aya; Inoue, Satoshi; Koshino, Akira; Ota, Akinobu; Nakao, Kenju; Komura, Masayuki; Kato, Hiroyuki; Naiki-Ito, Aya; Watanabe, Kawori; Nagayasu, Yuko; Hosokawa, Yoshitaka; Takiguchi, Shuji; Kasugai, Kunio; Kasai, Kenji; Inaguma, Shingo; Takahashi, Satoru
- Source:
Virchows Archiv: European Journal of Pathology; Aug2021, Vol. 479 Issue 2, p277-284, 8p - Source:
- Additional Information
- Abstract: Colorectal cancer (CRC) is one of the most common gastrointestinal cancers worldwide with high morbidity and mortality rates. The discovery of small molecule anticancer reagents has significantly affected cancer therapy. However, the anticancer effects of these therapies are not sufficient to completely cure CRC. PDZ-binding kinase (PBK) was initially identified as a mitotic kinase for mitogen-activated protein kinase and is involved in cytokinesis and spermatogenesis. Aberrant expression of PBK has been reported to be closely associated with malignant phenotypes of many cancers and/or patient survival. However, the expression of PBK and its association to patient survival in CRC have not been fully elucidated. In the present study, 269 primary CRCs were evaluated immunohistochemically for PBK expression to assess its ability as a prognostic factor. CRC tumor cells variably expressed PBK (range, 0-100%; median, 32%) in the nucleus and cytoplasm. Univariate analyses identified a significant inverse correlation between PBK expression and pT stage (P<0.0001). Furthermore, patients carrying CRC with higher PBK expression showed significantly favorable survival (P=0.0094). Multivariate Cox proportional hazards regression analysis revealed high PBK expression (HR, 0.52; P=0.015) as one of the potential favorable factors for CRC patients. PBK expression showed significant correlation to Ki-67 labeling indices (ρ=0.488, P<0.0001). In vitro, the PBK inhibitor OTS514 suppressed cellular proliferation of CRC cells with PBK expression through downregulation of P-ERK and induction of apoptosis. These results suggest that PBK-targeting therapeutics may be useful for the treatment of PBK-expressing CRC patients. [ABSTRACT FROM AUTHOR]
- Abstract: Copyright of Virchows Archiv: European Journal of Pathology is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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