Mechanosensitive changes in the expression of genes in colorectal cancer-associated fibroblasts

Most solid tumors become stiff with progression of cancer. Cancer Associated Fibroblasts (CAFs), most abundant stromal cells in the tumor microenvironment (TME), are known to mediate such stiffening. While the biochemical crosstalk between CAFs and cancer cells have been widely investigated, it is not clear if and how CAFs in stiffer TME promote metastatic progression. To gather insights into the process, we controlled the mechanical stiffness of the substrates and collected gene expression data with human colorectal CAFs. We cultured human primary CAFs on 2D polyacrylamide hydrogels with increasing elastic modulus (E) of 1, 10 and 40 kPa, and performed genome-wide transcriptome analyses in these cells to identify expression levels of similar to 16000 genes. The high-quality RNAseq results can be an excellent data-source for bioinformatic analysis for identifying novel pathways and biomarkers in cancer development and metastatic progression. With thorough analysis and accurate interpretation, this data may help researchers understand the role of mechanical stiffness of the TME in CAF-cancer cell crosstalk.

Automated summary

Most solid tumors become stiff with progression of cancer, which is mediated by Cancer Associated Fibroblasts (CAFs). However, how CAFs in stiffer tumor microenvironment (TME) promote metastatic progression is not clear. In this study, we controlled the mechanical stiffness of substrates and collected gene expression data with human colorectal CAFs to understand the role of TME stiffness in CAF-cancer cell crosstalk.