生物
下调和上调
三阴性乳腺癌
乳腺癌
基因敲除
癌症研究
癌症
分子生物学
遗传学
基因
细胞凋亡
生物化学
作者
Jianshun Li,Pei-Ting Li,Wei Wu,B. Ding,Yanguang Wen,Haikang Cai,S. Liu,Tao Hong,Jian-Fei Zhang,Jian-Da Zhou,Liyuan Qian,Du Juan
出处
期刊:Epigenomics
[Future Medicine]
日期:2024-02-01
卷期号:16 (4): 215-231
被引量:2
标识
DOI:10.2217/epi-2023-0100
摘要
Background: Triple-negative breast cancer (TNBC) is a subtype of BC with high rates of mortality. The mechanism of PTPRG-AS1 in ferroptosis of TNBC was investigated. Methods: Chromatin immunoprecipitation and dual-luciferase reporter assays were used to measure intermolecular relationships. MTT and colony formation assays detected cell viability and proliferation. Kits detected Fe2+ and reactive oxygen species levels. The role of PTPRG-AS1 in tumor growth was analyzed in vivo. Results: PTPRG-AS1 was increased in TNBC tissues and cells. PTPRG-AS1 silencing increased the reduction of glutathione and GPX4, increased Fe2+ and reactive oxygen species in erastin-treated cells and inhibited proliferation. POU2F2 transcriptionally upregulated PTPRG-AS1. PTPRG-AS1 targeted miR-376c-3p to upregulate SLC7A11. PTPRG-AS1 knockdown suppressed tumor growth in vivo. Conclusion: POU2F2 transcriptionally activates PTPRG-AS1 to modulate ferroptosis and proliferation by miR-376c-3p/SLC7A11, promoting TNBC.
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