生物
卵巢癌
表观遗传学
癌症研究
甲基化
癌变
DNA甲基化
甲基转移酶
癌细胞
癌症
遗传学
基因表达
DNA
基因
作者
Yanping Jin,JIANPING QIU,XIUFANG LU,YAN MA,GUOWEI LI
出处
期刊:Oncology Research
[Cognizant, LLC]
日期:2023-01-01
卷期号:31 (2): 169-179
被引量:7
标识
DOI:10.32604/or.2023.027815
摘要
Previous study revealed that ferritin heavy chain-1 (FTH1) could regulate ferritinophagy and affect intracellular Fe2+ content in various tumors, while its N6-methyladenosine (m6A) RNA methylation was closely related the prognosis of ovarian cancer patients. However, little is known about the role of FTH1 m6A methylation in ovarian cancer (OC) and its possible action mechanisms. In this study we constructed FTH1 m6A methylation regulatory pathway (LncRNA CACNA1G-AS1/IGF2BP1) according to related bioinformatics analysis and research, through clinical sample detections we found that these pathway regulatory factors were significantly up-regulated in ovarian cancer tissues, and their expression levels were closely related to the malignant phenotype of ovarian cancer. In vitro cell experiments showed that LncRNA CACNA1G-AS1 could up-regulate FTH1 expression through IGF2BP1 axis, thus inhibited ferroptosis by regulating ferritinophagy, and finally promoted proliferation and migration in ovarian cancer cells. Tumor-bearing mice studies showed that the knock-down of LncRNA CACNA1G-AS1 could inhibited the tumorigenesis of ovarian cancer cells in vivo condition. Our results demonstrated that LncRNA CACNA1G-AS1 could promote the malignant phenotypes of ovarian cancer cells through FTH1-IGF2BP1 regulated ferroptosis.
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