Abstract
How to cite this article: Potdar PD, Chaudhary S. Molecular characterization of cancer-associated fibroblasts isolated from human colorectal cancer as a major stromal cell component promoting metastasis. J Unexplored Med Data 2017;2:1-8. Aim: Colorectal cancer (CRC) remains a disease with poor prognosis and limited overall 5-year survival rate, which highlights a clear clinical need for novel treatment strategies. The stromal cancer-associated fibroblasts (CAFs) strongly dictate the metastatic potential of CRC and hence warrant investigation for clinical outcome. Methods: The authors established primary cultures of CAFs from metastatic CRC patients and performed cellular characterization using phase contrast microscopy and histological staining followed by light microscopy. The isolated CAFs were further explored for the molecular characterization of genes which promote the process of metastasis. Results: The stromal CAFs maintain their fibroblastic phenotype in vitro and manifested high proliferation potential. To explore the gene expression profile, total RNA was isolated from the primary culture of CAFs and qualitative RT-PCR was performed. The cultured CAFs exhibited gene signatures associated with cancer stemness, epithelial to mesenchymal transition induction and inflammatory cytokines/chemokines favoring metastasis. These genes play a pivotal role in chemotherapy resistance and are also associated with poor prognosis in CRC. Conclusion: This study further delineates the role of CAFs as a part of the " corrupted " stromal cells within the tumor microenvironment in establishing and orchestrating the metastatic fate of CRC. The gene expression profile clearly indicates that CAFs represent a potential target for improved therapy of CRC.
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CITATION STYLE
Potdar, P. D., & Chaudhary, S. (2017). Molecular characterization of cancer-associated fibroblasts isolated from human colorectal cancer as a major stromal cell component promoting metastasis. Journal of Unexplored Medical Data, 2(1). https://doi.org/10.20517/2572-8180.2016.10
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