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논문 기본 정보

자료유형
학술저널
저자정보
Lee Ga-Eun (The Catholic University of Korea) Bang Geul (Korea Basic Science Institute) Byun Jiin (The Catholic University of Korea) Lee Cheol-Jung (The Catholic University of Korea) Chen Weidong (The Catholic University of Korea) Jeung Dohyun (The Catholic University of Korea) An Hyun-Jung (The Catholic University of Korea) Kang Han Chang (The Catholic University of Korea) Lee Joo Young (The Catholic University of Korea) Lee Hye Suk (The Catholic University of Korea) Hong Young-Soo (Korea Research Institute of Bioscience and Biotechnology) Kim Dae Joon (University of Texas Rio Grande Valley) Keniry Megan (University of Texas Rio Grande Valley) Kim Jin Young (Korea Basic Science Institute) Choi Jin-Sung (The Catholic University of Korea) Fanto Manolis (Maurice Wohl Clinical Neuroscience Institute) Cho Sung-Jun (University of Minnesota) Kim Kwang-Dong (Gyeongsang National University) Cho Yong-Yeon (The Catholic University of Korea)
저널정보
대한생화학·분자생물학회 Experimental and Molecular Medicine Experimental and Molecular Medicine Vol.56
발행연도
2024.3
수록면
1 - 14 (14page)
DOI
10.1038/s12276-024-01195-1

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Cancer cells often exhibit resistance to apoptotic cell death, but they may be vulnerable to other types of cell death. Elucidating additional mechanisms that govern cancer cell death is crucial for developing new therapies. Our research identified cyclic AMP-responsive element-binding protein 3 (CREB3) as a crucial regulator and initiator of a unique cell death mechanism known as karyoptosis. This process is characterized by nuclear shrinkage, deformation, and the loss of nuclear components following nuclear membrane rupture. We found that the N-terminal domain (aa 1-230) of full-length CREB3 (CREB3-FL), which is anchored to the nuclear inner membrane (INM), interacts with lamins and chromatin DNA. This interaction maintains a balance between the outward force exerted by tightly packed DNA and the inward constraining force, thereby preserving INM integrity. Under endoplasmic reticulum (ER) stress, aberrant cleavage of CREB3-FL at the INM leads to abnormal accumulation of the cleaved form of CREB3 (CREB3-CF). This accumulation disrupts the attachment of CREB3-FL to the INM, resulting in sudden rupture of the nuclear membrane and the onset of karyoptosis. Proteomic studies revealed that CREB3-CF overexpression induces a DNA damage response akin to that caused by UVB irradiation, which is associated with cellular senescence in cancer cells. These findings demonstrated that the dysregulation of CREB3-FL cleavage is a key factor in karyoptotic cell death. Consequently, these findings suggest new therapeutic strategies in cancer treatment that exploit the process of karyoptosis.

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