Abstract
Rectal cancer treatment still fails with local and distant relapses of the disease. It is hypothesized that radiotherapy could stimulate cancer cell dissemination and metastasis. In this study, we evaluated the effect of X-radiation on collagen type I strap formation potential, i.e. matrix remodeling associated with mesenchymal cell migration, and behaviors of SW480, SW620, HCT116 p53+/+ and HCT116 p53−/− colon cancer cells. We determined a radiation-induced increase in collagen type I strap formation and migration potentials of SW480 and HCT116 p53+/+. Further studies with HCT116 p53+/+, indicated that after X-radiation strap forming cells have an increased motility. More, we detected a decrease in adhesion potential and mature integrin β1 expression, but no change in non-muscle myosin II expression for HCT116 p53+/+ after X-radiation. Integrin β1 neutralization resulted in a decreased cell adhesion and collagen type I strap formation in both sham and X-radiated conditions. Our study indicates collagen type I strap formation as a potential mechanism of colon cancer cells with increased migration potential after X-radiation, and suggests that other molecules than integrin β1 and non-muscle myosin II are responsible for the radiation-induced collagen type I strap formation potential of colon cancer cells. This work encourages further molecular investigation of radiation-induced migration to improve rectal cancer treatment outcome.
Highlights
Surgery is the mainstay of curative rectal cancer treatments, and radiotherapy in combination with chemotherapy significantly decreases local relapse and improves overall survival [1]
We evaluated the effect of X-radiation on collagen type I strap formation potential, i.e. matrix remodeling associated with mesenchymal cell migration, and behaviors of SW480, SW620, HCT116 p53+/+ and HCT116 p53−/− colon cancer cells
Our study indicated col-I strap formation (SF) as a mechanism upregulated by colon cancer cells with increased migration potential after X-radiation
Summary
Surgery is the mainstay of curative rectal cancer treatments, and radiotherapy in combination with chemotherapy significantly decreases local relapse and improves overall survival [1]. Radiation may as well stimulate cancer metastasis via various molecular mechanisms [4, 5]. Cancer cell migration is a key process of metastasis [6] and the mechanistic elucidation of radiation-induced (RI) migration is crucial to improve rectal cancer treatment outcome. Cancer cells migrate through a heterogeneous tumor microenvironment according a mesenchymal or amoeboid pattern. Mesenchymal migrating cancer cells actively remodel their surrounding matrix by deposition of new extracellular matrix (ECM), degradation of existing ECM components and ECM protein fiber alignment. Amoeboid migrating cells do not rely on matrix remodeling for propagation [7]
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