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KLK10 Upregulation Drives Aggressiveness and Radioresistance and Has a Negative Prognostic Impact on Rectal Cancer
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DOI：10.1016/j.labinv.2026.106128.png)
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Abstract
En 中文
Rectal cancer is a heterogeneous disease with widely variable treatment responses. Beyond the tumor-node-metastasis (TNM) staging system, no reliable biomarkers currently exist to predict the efficacy of concurrent chemoradiotherapy (CCRT) in rectal cancer, limiting the personalization of curative-intent treatment. Proteolytic enzymes promote extracellular matrix degradation and tumor progression, with serine proteases playing a key role. Consequently, this study intended to investigate their potential to predict preoperative CCRT response and survival in rectal cancer. In our rectal cancer cohort (n = 343), high kallikrein-related peptidase 10 (KLK10) immunoreactivity was considerably linked to adverse clinicopathologic characteristics, comprising pre-CCRT nodal status (cN1–2; p = 0.032), post-CCRT tumor stage (ypT3–4; p = 0.001), post-CCRT nodal status (ypN1–2; p < 0.001), perineural invasion (p < 0.001), vascular invasion (p < 0.001), and poor tumor regression (p = 0.001). Multivariate survival analyses indicated that high KLK10 immunoreactivity was independently correlated with worse disease-specific survival [hazard ratio (HR), 3.647; 95% confidence interval (CI), 1.854–7.171; p < 0.001], locoregional recurrence-free survival (HR, 3.591; 95% CI, 1.523–8.463; p = 0.003), and metastasis-free survival (HR, 2.459; 95% CI, 1.346–4.492; p = 0.003). Additionally, cellular analyses revealed that KLK10 contributes to cancer progression by promoting aggressive phenotypes and radiation resistance. These findings suggest that KLK10 could be a predictive and prognostic biomarker as well as a promising therapeutic target in rectal cancer.
Keywords:
KLK10
rectal cancer
chemoradiotherapy
biomarker
prognosis
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