POU2F2-mediated upregulation of lncRNA PTPRG-AS1 inhibits ferroptosis in breast cancer via miR-376c-3p/SLC7A11 axis.
Jun LiPei-Ting LiWei WuBo-Ni DingYan-Guang WenHai-Lin CaiShuang-Xi LiuTao HongJian-Fei ZhangJian-Da ZhouLi-Yuan QianJuan DuPublished in: Epigenomics (2024)
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 Fe 2+ 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 Fe 2+ 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.
Keyphrases
- reactive oxygen species
- cell proliferation
- long non coding rna
- signaling pathway
- cell death
- induced apoptosis
- long noncoding rna
- cell cycle arrest
- gene expression
- risk factors
- young adults
- dna methylation
- oxidative stress
- high resolution
- coronary artery disease
- pi k akt
- cancer therapy
- metal organic framework
- high throughput sequencing