MUC13 (Mucin 13)

RUNX1 knockdown suppressed HCC cell proliferation, migration, and invasion by attenuating Wnt/β-catenin/EMT signaling activity. These findings highlight RUNX1 as a potential prognostic biomarker and therapeutic target, offering mechanistic insight into HCC pathogenesis and avenues for improved precision oncology.

Using a novel data-driven approach, six potential imaging targets were successfully identified and validated. CEACAM5 and CEACAM6 emerged as strong targets that, regardless of neoadjuvant therapy, covered nearly the entire CRLM population-supporting their further probe development and clinical translation.

Additionally, elevated GALNT7 level enhances resistance to lenvatinib-based chemotherapy regimens. Thus, GALNT7 is a critical regulator of oncogenic processes in HCC. Targeting the GALNT7-MUC13-PI3K/AKT axis represents a novel therapeutic strategy for combating HCC.

In conclusion, aberrant mucin signatures reflect distinct molecular pathways in (pre)malignant GIT lesions and highlight their potential utility as biomarkers and therapeutic targets. Schematic representation of the main findings regarding altered mucin signalling in several precancerous lesions (adenomatous (i.e., conventional pathway 1) and serrated polyps (i.e. pathway 2)) and small intestinal (SIA) and colorectal (CRC) adenocarcinomas and its clinicopathological significance (outcome, anatomical location (proximal/distal), molecular subtypes (MSI, (non)-mucinous).

In vitro cell experiments showed that the knockdown of MAST1 in Hela cells reduced cell invasion ability and downregulated the p-AKT and p-P38 signaling pathways. This study contributes to a deeper understanding of the role of MAST1 in the invasion of CC, affecting the occurrence and development of malignant tumors in the cervix through the p-AKT and p-P38 classical signaling pathways, and can serve as a potential therapeutic target for patients with CC.

In conclusion, our findings suggest MUC3A/MUC4/MUC13/MUC16 as robust diagnostic and prognostic biomarkers and liquid biopsy as a noninvasive approach to be integrated into daily clinical practice. This analysis can also be extended to other malignancies.

Therapeutic strategies targeting anoikis and NETosis, including inhibitors of integrins, EGFR, and NET components (e.g., DNase I, CXCR2 antagonists), inhibitors of autophagy (e.g., CQ, HCQ, azithromycin) are discussed. This comprehensive analysis advances understanding of CRCLM pathogenesis and provides novel perspectives for targeted interventions.

The study successfully identified and validated a panel of biomarkers specific to pancreatic cancer, with potential applications in early diagnosis and treatment. The findings highlight the importance of multi-omics data integration in cancer research and the potential of personalized medicine in improving patient outcomes. The in-silico drug targeting analysis provides a foundation for the development of novel drugs for PanCa treatment. Hence TFF1, S100P, MUC13, and UGT1A1 showcased themselves as most promising biomarkers and novel drug targets.

Finally, the hub gene COL5A1 was obviously correlated with B cells memory, dendritic cells activated, macrophages M0, macrophages M2, plasma cells, T cells follicular helper in GC. This study reveals a novel tumor differentiation grade-related genes signature, and COL5A1 represents a promising biomarker in GC.

Finally, we leveraged the emerging spatial transcriptomic to validate the co-expressed pair in situ. A standalone R package (https://github.com/Bin-Chen-Lab/bsAbsFinder).

Mass spectrometry of the products revealed a ligand glycan, tri-sialylated T antigen. These results indicate that Siglec-7 interaction with its ligand generates bidirectional signals in NK and cancer cells, leading to the efficient escape of cancers from host immune surveillance.