In cancer, collagen binding to DDR1 receptors triggers signals that help tumor cells spread and invade other tissues, which is a key step in cancer progression.
Scientific Claim
Collagen binding to DDR1 in cancer cells promotes epithelial-mesenchymal transition (EMT) and metastasis through activation of NF-κB and STAT3 pathways.
Original Statement
“DDR1 activates EMT via stimulating the protein expression of N-cadherin and vimentin and phosphorylation of Pyk2 and MKK7 in prostate cancer. In vitro 3D cell culture demonstrated that the DDR1 enhances chemo-resistance by the STAT3 and NF-kB signaling pathway in Jurkat cells and T47D breast cancer cells. The collagen-bound DDR1 upregulates MMP2,9,10, Hes1, Hey2, N-Cadherin, vimentin, XIAP, COX-2 and Bcl-xl, and downregulates E-cadherin expression through RAS/RAF/MEK/ERK1/2, PI3K/AKT/mTOR, Pyk2/MKK7, FAK/p130CAS/JNK1/c-JUN, NF-kb and STAT3 downstream signaling mediators.”
Evidence Quality Assessment
Claim Status
appropriately stated
Study Design Support
Design supports claim
Appropriate Language Strength
definitive
Can make definitive causal claims
Assessment Explanation
The causal relationship is supported by experimental data from multiple cancer models, justifying definitive language.
Evidence from Studies
Supporting (1)
The Molecular Interaction of Collagen with Cell Receptors for Biological Function