Ask about this productRelated genes to: KLK10 protein
- Gene:
- KLK10 NIH gene
- Name:
- kallikrein related peptidase 10
- Previous symbol:
- PRSSL1
- Synonyms:
- NES1
- Chromosome:
- 19q13.41
- Locus Type:
- gene with protein product
- Date approved:
- 1997-05-09
- Date modifiied:
- 2016-11-15
Related products to: KLK10 protein
Related articles to: KLK10 protein
- 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. - Source: PubMed
Publication date: 2026/04/20
Chou Chia-LinLin Cheng-WeiLi Wan-ShanLee Sung-WeiKuo Yu-HsuanShiue Yow-LingLi Chien-FengLai Hong-YueYang Ching-Chieh - Differential expression of Kallikreins (KLKs) was described for established metastatic pancreatic ductal adenocarcinoma (PDAC), but their potential as markers for early detection is not known. We have performed comprehensive in silico and in situ analyses of KLK expression in PDAC at different stages of tumor development. We found that upregulation of KLK7 and KLK10 RNA and protein occurs early in tumor development and marks carcinoma in-situ lesions (stage 0, PanIN3) and early-stage (stage 1) PDAC, while non-cancerous low grade lesions stain negative for these proteases. Moreover, both KLKs are co-expressed with desmoglein-3 (DSG3) in PDAC cell lines as well as PDAC samples from treatment naïve patients. DSG3 serves as a substrate for both KLK7 and KLK10 resulting in a 30 kDa extracellular fragment. Overall, our data suggest that analyses for expression of KLK7 and KLK10 as well as their substrates could have potential as diagnostic biomarkers to distinguish non-cancerous low-grade lesions from earliest cancerous lesions in the pancreas. - Source: PubMed
Publication date: 2026/04/13
Eisenhauer JillianArgo RyanMartinez Alicia K FlemingMaldosevic EmirBastea Ligia IWehrkamp Cody JDöppler Heike REdenfield Brandy HLewis Jason TWallace Michael BStorz Peter - Long non-coding RNAs (lncRNAs) have emerged as key regulatory molecules involved in driving cancer progression. However, the specific functional roles of numerous lncRNAs in ovarian cancer (OC) remain largely underexplored. The present study aimed to elucidate the role and underlying mechanisms of potassium voltage-gated channel subfamily Q member 1 opposite strand/antisense transcript 1 (KCNQ1OT1) in OC progression. Bioinformatics prediction using the TargetScan and starBase databases revealed that both KCNQ1OT1 and kallikrein-related peptidase 10 (KLK10) harbor complementary binding sites for microRNA (miR)-140-5p. The direct interaction between miR-140-5p and KCNQ1OT1 or KLK10 was experimentally validated using miRNA pull-down assays. Analysis of GEO datasets (GSE66957 and GSE47841), followed by RT-qPCR validation in SKOV3 and IOSE80 cells, revealed that KCNQ1OT1 and KLK10 were markedly upregulated, whereas miR-140-5p was downregulated in OC compared with that in normal ovarian controls. CCK-8 and wound-healing assays demonstrated that silencing KCNQ1OT1 markedly suppressed OC cell proliferation and migration, effects that were reversed by miR-140-5p inhibition. Conversely, inhibition of miR-140-5p enhanced OC cell proliferation and migration, which were abrogated by KLK10 knockdown. Collectively, these findings identified a previously unrecognized regulatory axis in OC, in which KCNQ1OT1 promotes tumor cell proliferation and migration by modulating the miR-140-5p/KLK10 pathway. The present study advances the mechanistic understanding of lncRNA-mediated oncogenesis and provides preliminary evidence supporting a potential role of KCNQ1OT1 in OC progression. - Source: PubMed
Publication date: 2026/03/11
Duan RenjieTao ZhenyuTao ShunYang AichenYang XuLi ChangzhengZhu XiaoxiangZhang KexinLi ZhuofuTao Shanjun - Cisplatin resistance severely limits the efficacy of chemotherapy for cervical cancer (CC), and its molecular mechanisms remain incompletely understood. While epigenetic alterations such as DNA methylation are recognized as important contributors, the upstream regulatory networks, particularly the role of long non-coding RNAs (lncRNAs), are still unclear. This study aimed to explore novel mechanisms influencing cisplatin resistance in cervical cancer. Cisplatin-resistant CC cells (HeLa and SiHa) were established. A comprehensive approach employing mRNA and lncRNA microarrays, RT-qPCR, methylation-specific PCR (MSP-PCR), chromatin immunoprecipitation, luciferase reporter assays, RNA pull-down, RNA immunoprecipitation, cellular functional assays, and a mouse subcutaneous xenograft tumor model was utilized. The study found that Kallikrein 10 (KLK10) expression was significantly downregulated in cisplatin-resistant CC cells due to promoter hypermethylation mediated by DNA methyltransferase 1 (DNMT1). LncRNA microarray analysis revealed that TMPO-AS1 was the most significantly upregulated lncRNA in resistant cells. Functional assays confirmed that TMPO-AS1 promoted cisplatin resistance, proliferation, migration, and invasion of CC cells. Mechanistically, TMPO-AS1 acted as a competitive endogenous RNA (ceRNA) by sponging miR-140-5p, thereby relieving its inhibitory effect on DNMT1 mRNA, upregulating DNMT1 expression, enhancing KLK10 promoter methylation, and leading to its silencing. In vivo experiments further demonstrated that silencing TMPO-AS1 inhibited tumor growth. This study unveils a novel TMPO-AS1/miR-140-5p/DNMT1/KLK10 regulatory axis that plays a critical role in cisplatin resistance in CC, providing a potential therapeutic target for overcoming chemoresistance. - Source: PubMed
Publication date: 2026/02/05
Yang JianShi ZhouhongSong TingShao YuruiHou ShunyuCheng ChenLiang BaoquanYang Xiaojun - Breast cancer remains the leading cause of cancer-related deaths among women, underscoring the need for more sensitive and specific biomarkers. Traditional markers such as CA15-3 lack sufficient diagnostic and prognostic accuracy. Quantification of plasma cell-free DNA (cfDNA) offers a minimally invasive liquid-biopsy approach for tumor detection and monitoring. This case-control study assessed a cfDNA panel comprising KLK10, SOX17, WNT5A, and MSH2 in 100 breast cancer patients and 100 matched controls. Plasma cfDNA levels, quantified by qPCR, and CA15-3 levels, measured by ELISA, were evaluated for diagnostic and prognostic value using ROC analyses and a 35-month follow-up for survival endpoints. All cfDNA genes were significantly elevated in patients (p<0.001) and exhibited superior diagnostic accuracy versus CA15-3, with MSH2 showing the highest AUC (95.3%), sensitivity (92%), and specificity (89%). Elevated cfDNA correlated strongly with metastasis and adverse pathological features, outperforming CA15-3 in predicting metastasis (AUC = 0.962-0.987). High cfDNA concentrations associated with poorer disease-free and overall survival (p<0.001). Detection of a cfDNA panel, rather than a single gene, demonstrates superior utility as a minimally invasive biomarker promising for early detection, risk assessment, and disease monitoring in breast cancer. - Source: PubMed
Publication date: 2025/12/24
El-Fatah Rofida M AbdBadawy Heba KPasha Heba FMesbah Noha MAbo-Elmatty Dina MAbdel-Hamed Asmaa R