Collagen type X alpha 1 promotes proliferation, invasion and epithelial-mesenchymal transition of cervical cancer through activation of TGF-β/Smad signaling.

BACKGROUND

Collagen type X alpha 1 (COL10A1) belongs to the collagen family and constitutes the main component of the interstitial matrix. COL10A1 was found to be dysregulated in various cancers, and to participate in tumorigenesis. However, the role of COL10A1 in cervical cancer (CC) remains unclear.

METHODS

Expression of COL10A1 in CC cells and tissues was detected by western blot and qRT-PCR. CC cells were transfected with pcDNA-COL10A1 or si-COL10A1, and the effect of COL10A1 on cell proliferation of CC was assessed by MTT and colony formation assays. Cell metastasis was detected by wound healing and transwell assays. Western blot was applied to evaluate epithelial-mesenchymal transition.

RESULTS

COL10A1 was significantly elevated in CC tissues and cells (P < 0.001). Over-expression of COL10A1 increased cell viability of CC (P < 0.001), and enhanced the number of colonies (P < 0.001). However, knockdown of COL10A1 reduced the cell proliferation of CC (P < 0.001). Over-expression of COL10A1 also promoted cell migration (P < 0.001) and invasion (P < 0.001) of CC, whereas silencing of COL10A1 suppressed cell metastasis (P < 0.001). Protein level of E-cadherin in CC was reduced (P < 0.05), whereas N-cadherin and vimentin were enhanced by COL10A1 over-expression (P < 0.001). Silencing of COL10A1 reduced the protein level of TGF-β1 (P < 0.01), and down-regulated the phosphorylation of Smad2 and Smad3 in CC (P < 0.001).

CONCLUSION

Down-regulation of COL10A1 suppressed cell proliferation, metastasis, and epithelial-mesenchymal transition of CC through inactivation of TGF-β/Smad signaling.