Flightless-1 inhibits ER stress-induced apoptosis in colorectal cancer cells by regulating Ca2+ homeostasis
2020
Sun Sil Choi | Sang Kwon Lee | Joong Kwan Kim | Hye-Kyung Park | Eujin Lee | Jinho Jang | Yo Han Lee | Keon Woo Khim | Ji-Min Hyun | Hye-jin Eom | Semin Lee | Byuong Heon Kang | Young Chan Chae | Kyungjae Myung | Seung-Jae Myung | Chan Young Park | Jang Hyun Choi
Cancer: Protein enhances survival of tumor cells under stress A cytoskeletal protein that helps tumors avoid cell death offers a promising new drug target for fighting cancer. A team led by Jang Hyun Choi and Sun Sil Choi of the Ulsan National Institute of Science and Technology, South Korea, detailed how a protein called Flightless I (FliI) that normally regulates the remodeling of structural filaments in the cell can, in colorectal cancer cells, serve as a tumor promoter through its action on calcium levels. Typically, cells respond to chronic stress by altering calcium signaling to promote their own death. In tumors, however, FliI maintains normal calcium levels to enhance cell survival even in the face of chemotherapy and other stressful stimuli. Suppressing FliI activity could thus help sensitize cancer cells to other stress- and death-inducing drug regimens.
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