Kim, Mi Ra Chang, Hyo Won Nam, Hae Yun Han, Myung Woul Moon, So Young Kim, Hyo Jung Lee, Hee Jin Roh, Jong-Lyel Kim, Seong Who Kim, Sang Yoon 2024-01-20T15:31:22Z 2024-01-20T15:31:22Z 2021-09-05 2012-02-10 0006-291X https://pubs.kist.re.kr/handle/201004/129545 The issue of whether aberrant expression of beta 1-integrin is associated with cancer progression and development of resistance to cytotoxic therapy is of considerable interest. Studies to date have shown that the anchorage-independent survival of cancer is attributed, in part, to epithelial-to-mesenchymal transition (EMT). Here, we have reported a novel alternative mechanism of anchorage-independent survival of cancer cells. Cell lines derived from head and neck cancer patients (AMC-HN-3 and AMC-HN-9) and the well-known EMT cancer cell line, MDA-MB231, were examined. The EMT features of AMC-HN-9 cells were comparable to those of MDA-MB231, whereas AMC-HN-3 cells showed no EMT characteristics. Although the pattern and degree of beta 1-integrin expression were similar in all three cell lines, sensitivities of the cells to beta 1-integrin knockdown with small interfering RNA (siRNA) were different. Cancer cells with no EMT features underwent cell death to a more significant extent following beta 1-integrin silencing than those with EMT. Intriguingly, we observed reactive activation of the p53-p21 pathway after beta 1-integrin silencing in AMC-HN-9 cells lacking an apparent cell death response. Simultaneous knockdown of wild-type p53 and beta 1-integrin in this cell line promoted cell death. Our data collectively indicate that beta 1-integrin-related cell death is closely associated with EMT phenotypes and activation of the p53-p21 pathway is partly involved in the acquisition of resistance to apoptosis induced by beta 1-integrin silencing. Further clarification of the mechanisms underlying p53 integration with beta 1-integrin signaling may facilitate the development of novel anti-cancer strategies. (C) 2012 Elsevier Inc. All rights reserved. English ACADEMIC PRESS INC ELSEVIER SCIENCE DAMAGE-INDUCED APOPTOSIS TUMOR-SUPPRESSOR P53 DNA-DAMAGE ANOIKIS INTEGRINS SURVIVAL ADHESION ACCUMULATION MODULATION PROGNOSIS Activation of p53-p21 is closely associated with the acquisition of resistance to apoptosis caused by beta 1-integrin silencing in head and neck cancer cells Article 10.1016/j.bbrc.2012.01.007 1 BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.418, no.2, pp.260 - 266 BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 418 2 260 266 scie scopus 000300478900011 2-s2.0-84862823243 Biochemistry & Molecular Biology Biophysics Biochemistry & Molecular Biology Biophysics Article DAMAGE-INDUCED APOPTOSIS TUMOR-SUPPRESSOR P53 DNA-DAMAGE ANOIKIS INTEGRINS SURVIVAL ADHESION ACCUMULATION MODULATION PROGNOSIS beta-Integrin p53 EMT Head and neck cancer cell lines