COLEC10 (Collectin Subfamily Member 10)

Drug-gene interaction mining mapped 78 target proteins to clinically relevant compounds, including tolrestat, alcuronium, metyrosine, and 4-phenylbutyric acid...Physicochemical and pharmacokinetic profiling further prioritised tolrestat as a computationally favourable candidate (MW = 357.35, LogP = 3.64, TPSA = 81.86 Ų), exhibiting acceptable drug-likeness, high predicted gastrointestinal absorption, and low synthetic complexity (SA = 2.34), in contrast to alcuronium (MW = 666.89, SA = 7.86), which showed multiple rule violations. Collectively, this in silico study proposes a robust diagnostic gene signature for HCC and identifies tolrestat as a promising repurposing candidate that warrants experimental validation, demonstrating the utility of integrating machine learning, network biology, and molecular simulation in translational cancer research.

MARCO overexpression experiments in HCC cells revealed significant alterations in MAPK pathway-related genes, suggesting potential therapeutic implications through pathway modulation. This investigation provides the first comprehensive identification of clinically relevant eRNA biomarkers for HCC, establishing their dual roles in disease progression and therapeutic targeting.

Moreover, we found that the immune microenvironment was different between the high and low risk groups, and these four genes were associated with different immune cell infiltration. We identified four key genes: BMP2, COLEC10, MASP2, and GCGR, which play significant roles in the radiosensitivity, immune microenvironment, and prognosis of RC.

Correlation analysis revealed that a MAGI2-AS3/hsa-miR-450b-5p/COLEC10 axis might play a crucial role in the progression of HCC. The ceRNA network constructed could provide insight into HCC tumorigenesis and might lead to new molecular biomarkers for diagnosing and treating HCC.

COLEC10 is an independent prognostic factor of HCC. COLEC10 regulates EMT, Hedgehog, and PI3K-AKT pathways, providing new ideas for targeted therapy of HCC.

While LYC down regulated miR-224-5p level and inhibited the HCC malignant progression. In conclusion, LYC can down regulate the levels of miR-224-5p, upregulate the levels of COLEC10 and thus inhibit the malignant progression of HCC.

COLEC10 inhibits HCC stemness by downregulating the Wnt/β-catenin pathway, which is a promising target for liver CSC therapy.

COLEC10 overexpressing HCC cells generated a relatively high ROS level and switched to apoptotic cell death under sorafenib-treated conditions. Our study provides the first novel view that COLEC10 inhibits HCC progression by regulating GRP78-mediated ER stress signaling and may serve as a promising therapeutic and prognostic biomarker.

Thus, FYN may be central to the development of LIHC and maybe a novel biomarker for clinical diagnosis and treatment.