Epithelial mesenchymal transition (EMT) is a cellular trans-differentiation phenomenon, where polarized epithelial cells convert to motile and invasive mesenchymal cell through remodeling of cytoskeletal protein, cell-cell and cell-matrix interaction. The EMT program is crucial in embryogenesis, wound healing, fibrosis and cancer metastasis. Molecular mechanism lead to EMT are well-studied whereas influence of matrix mechanical property has not been studied yet. In this study, HaCaT (epithelial normal) and AW13516 (epithelial cancer) cells were cultured on two different PDMS substrate viz, 10: 1 and 40: 1 having Young's Modulus 1.26±0.047 MPa and 795±15 kPa respectively with treatment of EMT inducing transforming growth factor beta-1 (TGFβ-1) upto 72 hours. HaCaT and AW13516 cells were observed very compact on 10: 1 and 40: 1 PDMS substrate at 0 hr, whereas after 72 hrs PDMS (10: 1) showed more elongated morphology and loose cell-cell interaction. The proliferation rate was decreased on both substrates validated by Ki67 expression. Additionally, expression of E-cadherin was analyzed where 40: 1 PDMS substrate induced membranous expression indicated strong cell-cell interaction in comparison to 10: 1. Interestingly, mesenchymal markers, vimentin and fibronectin were seen decreased on 40: 1 PDMS substrate with increased expression of mechanosensitive vinculin aid the formation of E-cadherin based junctional complex which elucidated the inhibition of EMT progression. This study thus indicated that by modulating the mechanical property of the substrate, the EMT process can be inhibited which itself is revolutionary in the field of cancer diagnosis and therapy.