干旱区生态环境知识资源中心(Arid): CREB3L1 /OASIS: cell cycle regulator and tumor suppressor

Arid

DOI	10.1111/febs.17052
	CREB3L1 /OASIS: cell cycle regulator and tumor suppressor
	Saito, Atsushi; Omura, Issei; Imaizumi, Kazunori
通讯作者	Saito, A
来源期刊	FEBS JOURNAL
ISSN	1742-464X
EISSN	1742-4658
出版年	2024
英文摘要	Cell cycle checkpoints detect DNA errors, eventually arresting the cell cycle to promote DNA repair. Failure of such cell cycle arrest causes aberrant cell proliferation, promoting the pathogenesis of multiple diseases, including cancer. Endoplasmic reticulum (ER) stress transducers activate the unfolded protein response, which not only deals with unfolded proteins in ER lumen but also orchestrates diverse physiological phenomena such as cell differentiation and lipid metabolism. Among ER stress transducers, cyclic AMP-responsive element-binding protein 3-like protein 1 (CREB3L1) [also known as old astrocyte specifically induced substance (OASIS)] is an ER-resident transmembrane transcription factor. This molecule is cleaved by regulated intramembrane proteolysis, followed by activation as a transcription factor. OASIS is preferentially expressed in specific cells, including astrocytes and osteoblasts, to regulate their differentiation. In accordance with its name, OASIS was originally identified as being upregulated in long-term-cultured astrocytes undergoing cell cycle arrest because of replicative stress. In the context of cell cycle regulation, previously unknown physiological roles of OASIS have been discovered. OASIS is activated as a transcription factor in response to DNA damage to induce p21-mediated cell cycle arrest. Although p21 is directly induced by the master regulator of the cell cycle, p53, no crosstalk occurs between p21 induction by OASIS or p53. Here, we summarize previously unknown cell cycle regulation by ER-resident transcription factor OASIS, particularly focusing on commonalities and differences in cell cycle arrest between OASIS and p53. This review also mentions tumorigenesis caused by OASIS dysfunctions, and OASIS's potential as a tumor suppressor and therapeutic target.
英文关键词	astrocyte cell cycle arrest DNA damage glioblastoma methylation OASIS p21 p53 tumor suppressor tumorigenesis
类型	Review ; Early Access
语种	英语
开放获取类型	hybrid
收录类别	SCI-E
WOS记录号	WOS:001141830100001
WOS关键词	TRANSCRIPTION FACTOR CREB3L1 ; UNFOLDED PROTEIN RESPONSE ; STRESS TRANSDUCER OASIS ; D-DEPENDENT KINASES ; ENDOPLASMIC-RETICULUM ; CREB/ATF-FAMILY ; RETINOBLASTOMA PROTEIN ; CDK INHIBITORS ; GENE-EXPRESSION ; BREAST-CANCER
WOS类目	Biochemistry & Molecular Biology
WOS研究方向	Biochemistry & Molecular Biology
资源类型	期刊论文
条目标识符	http://119.78.100.177/qdio/handle/2XILL650/403716
推荐引用方式 GB/T 7714	Saito, Atsushi,Omura, Issei,Imaizumi, Kazunori. CREB3L1 /OASIS: cell cycle regulator and tumor suppressor[J],2024.
APA	Saito, Atsushi,Omura, Issei,&Imaizumi, Kazunori.(2024).CREB3L1 /OASIS: cell cycle regulator and tumor suppressor.FEBS JOURNAL.
MLA	Saito, Atsushi,et al."CREB3L1 /OASIS: cell cycle regulator and tumor suppressor".FEBS JOURNAL (2024).