9th Annual Symposium
Physics of Cancer
Leipzig, Germany
September 24-26, 2018
Contributed Talk
Mechanical cyclic stretching inhibits cancer cell growth but promotes normal cell growth
ajay tijore1, yu-hsiu wang1, chwee teck lim1, michael sheetz1,2
1Mechanobiology Institute, National University of Singapore, Singapore 117411
2Department of Biological Sciences, Columbia University, New York NY10027
Cancer cells generally ignore cues from the microenvironment and grow indefinitely. Here we report that mechanical cyclic stretching promotes cancer cell apoptosis and inhibits proliferation on both rigid and soft surfaces. In cancer cells, stretch-induced apoptosis is mediated by calcium-activated calpain activity. However, in normal cells, cyclic stretching protects them from apoptosis while, death associated protein kinase1 (DAPK1) triggers apoptosis on non stretched soft surface. Further, the decline in cancer cell proliferation correlates with the absence cytoskeletal protein, tropomyosin 2.1 (TPM2.1). When transformed cancer cells are restored to normal rigidity-dependent growth by restoration of depleted TPM2.1, mechanical stretch activates growth particularly on soft surface. Also, mechanical stretch causes elongation of cancer cells but not of the normal cells or normalized cancer cells. This cell elongation is dependent on both magnitude and frequency of mechanical stretch. Based upon these findings we suggest that the transformed cell state makes cells vulnerable to mechanical stretch and suppresses cancer growth.
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