KLK10 (Kallikrein Related Peptidase 10)

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.

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.

This study deciphers the multidimensional clinic-molecular network orchestrated by centrosome amplification in PDAC, revealing its dual-pathogenic mechanism in fueling tumor aggressiveness through coordinated induction of genomic instability and immunosuppressive microenvironment reprogramming. These findings establish a translational framework for developing centrosome dynamics-based prognostic stratification and molecularly targeted therapeutic strategies.

In breast cancer patients aged>50 years, the high methylation levels of KLK10_CpG_3 (OR=1.13, 95%CI: 1.03-1.25) and KLK10_CpG_4 (OR=1.60, 95%CI: 1.37-1.86) sites were positively correlated with invasive breast cancer (all P<0.05). Hypermethylation of the KLK10 gene in female breast tumor tissue is associated with the risk of invasive breast cancer.

We revealed the cellular heterogeneity of liver metastasis and provided a crucial research foundation for developing novel therapeutic strategies to specifically target metastatic cell subtypes, thereby enhancing patient prognosis.

These results suggest that FGFBP1 may promote the proliferation, migration and invasion of TNBC cells through the KLK10-AKT axis. Targeting FGFBP1 may serve as a new therapeutic strategy for TNBC.

We established a robust disulfidptosis prognostic model for CRC through comprehensive multi-omics analysis. Our findings provide valuable insights into the role of DRGs in CRC progression and disease management, presenting an important resource for further research.

KLK7 could be essential in the cancerous advancement of PTC by influencing the EMT via the MAPK/ERK signaling pathway, thereby impacting the growth, migration, and invasiveness of PTC cells. KLK7 appears to be a promising candidate for targeting in PTC therapy.

These research findings provide scientific insights for further development and application of the 1,2,3-triazole compound. The study highlights the potential of the compound as a multifunctional pharmaceutical agent, particularly in cancer therapies, and lays the foundation for its future clinical applications in targeting drug-protein interactions.

We observed a 14.28% occurrence of HCMV in the Indian cohort, similar to that observed from next-generation sequencing. A combinatorial approach of rank-based meta-analysis and ranking of groups based on an expectation-maximization algorithm identified that the upregulated LINC02864 and MAGEA10 correlated with poor survival of GC patients and downregulated tumor suppressor genes enriching for gastric acid secretion pathway to be associated with HCMV-positive GC patients, revealing the progressive role of HCMV infection in GC.

Interestingly, the luciferase activities of constructed vectors were significantly decreased in HepG2 cells pre-transfected with miR-141 overexpression vector, while increasing in cells pre-transfected with miR-141 specific inhibitor. In summary, these data suggest the crucial role of miR-141 in liver cancer development via targeting KLK10 and TNFSF-15 and provide miR-141 as an attractive candidate in liver cancer treatment and protection.

In conclusion, KLK10 derived from TECs accelerates colon cancer cell proliferation and hematogenous liver metastasis formation. KLK10 in TECs might offer a promising therapeutic target in CRLM.