Recombinant Human Collagen Type III α1 / COL3A1

Xiao, Jian-hua, et al. "Unveiling ADAMTS12: A key driver of bladder cancer progression via COL3A1-Mediated activation of the FAK/PI3K/AKT signaling pathway." Journal of Biological Chemistry 301.2 (2025).

Collagen type III alpha 1 chain (COL3A1) has recently emerged as a pivotal molecular player in bladder cancer (BCa) biology. In a comprehensive study investigating the oncogenic role of ADAMTS12 in BCa, COL3A1 was identified as a direct downstream effector and functional mediator. Using bioinformatics analysis of the TCGA-BLCA dataset and STRING-based protein–protein interaction networks, researchers established a strong positive correlation between COL3A1 and ADAMTS12 expression.

Functional assays including qRT-PCR, Western blotting, and co-immunoprecipitation (Co-IP) confirmed that COL3A1 expression is positively regulated by ADAMTS12. Experimental suppression of COL3A1 in T24 BCa cells reversed the tumor-promoting effects of ADAMTS12 overexpression, significantly reducing cell proliferation and invasion while restoring apoptosis. These findings were validated in both in vitro and in vivo models, underscoring the importance of COL3A1 in the activation of the FAK/PI3K/AKT pathway.

Thus, COL3A1 serves not only as a biomarker of BCa progression but also as a functional target for disrupting ADAMTS12-driven oncogenic signaling. This highlights its utility in mechanistic cancer research and therapeutic target validation. COL3A1 is therefore indispensable in studies aiming to dissect tumor-stromal interactions and matrix remodeling in cancer microenvironments.

Chen, Wen-Kang, et al. International Immunopharmacology 127 (2024): 111416.

Collagen type III alpha 1 chain (COL3A1) is a key extracellular matrix component that has been identified as a critical hub gene in the pathogenesis of primary synovial chondromatosis (SC). In a recent study, COL3A1 was found to be significantly upregulated in SC-derived cartilage tissues compared to normal knee cartilage. Functional assays demonstrated that COL3A1 promotes chondrocyte migration and cell cycle progression, highlighting its pivotal role in SC tissue remodeling.

Silencing COL3A1 expression in SC-derived chondrocytes via siRNA markedly reduced both mRNA and protein levels. Transwell and scratch assays confirmed that COL3A1 knockdown significantly inhibited chondrocyte migration. Furthermore, flow cytometry revealed that COL3A1 silencing induced G2/M phase arrest, indicating its essential role in cell cycle regulation.

Histological analysis revealed that glycosaminoglycan (GAG) and collagen content in SC tissues were equal to or higher than in normal cartilage, supporting the notion of an active ECM remodeling environment. Clinically, COL3A1 exhibited diagnostic potential with an area under the curve (AUC) of 0.82 and correlated positively with the neutrophil-to-lymphocyte ratio (NLR), suggesting a role in inflammation-associated SC progression.

Taken together, COL3A1 is a functional driver of chondrocyte behavior in SC and a promising diagnostic biomarker. Its application in mechanistic studies of cartilage pathology offers valuable insights into the molecular basis of SC and supports its potential as a therapeutic target.

Zhu, Yu, et al. Molecular and Cellular Endocrinology 577 (2023): 112036.

Collagen type III alpha 1 chain (COL3A1) has been identified as a key functional component within extracellular vesicles derived from Sertoli cells (SEVs), particularly those from prepubertal mice. In a recent study, SEVs from 12–14-day-old mice significantly promoted proliferation of Sertoli cells, a cell type traditionally considered mitotically quiescent after puberty. Proteomic analysis revealed COL3A1 as a critical factor enriched in SEVs, suggesting its potential developmental role.

Functional validation through siRNA-mediated silencing of Col3a1 in primary Sertoli cells from 14-day-old mice demonstrated a marked decrease in Col3a1 mRNA and protein expression. This downregulation led to significantly reduced proliferation, as confirmed by CCK8 and EdU incorporation assays. Conversely, COL3A1 overexpression enhanced proliferative capacity, further supporting its regulatory function in Sertoli cell growth.

Transcriptomic profiling of Sertoli cells treated with DMSO or GW4869, an exosome inhibitor, showed altered expression patterns consistent with SEV-mediated COL3A1 signaling. These findings reveal that COL3A1 delivered via SEVs acts as a paracrine signal promoting Sertoli cell proliferation during early testicular development.

This study highlights a novel application of COL3A1 in reproductive biology and extracellular matrix signaling, providing valuable insights into testicular development and potential therapeutic avenues for disorders related to Sertoli cell dysfunction. COL3A1 thus emerges as a key molecular agent in promoting cell proliferation via extracellular vesicle-mediated pathways.