AI Article Synopsis
- Long noncoding RNAs (lncRNAs) are increasingly recognized for their crucial role in regulated cell death (RCD), particularly in cancer therapy through a process called ferroptosis.
- LINC00551, a specific lncRNA found at low levels in lung adenocarcinoma (LUAD), can suppress cancer cell growth and promote both autophagy and ferroptosis when overexpressed.
- The study reveals that LINC00551 acts as a competing endogenous RNA (ceRNA) by binding to miR-4328, which leads to increased levels of DDIT4, inhibiting mTOR and thereby facilitating autophagy and ferroptosis in LUAD cells.
Article Abstract
According to mounting evidence, long noncoding RNAs (lncRNAs) play a vital role in regulated cell death (RCD). A potential strategy for cancer therapy involves triggering ferroptosis, a novel form of RCD. Although it is thought to be an autophagy-dependent process, it is still unclear how the two processes interact. This study characterized a long intergenic noncoding RNA, LINC00551, expressed at a low level in lung adenocarcinoma (LUAD) and some other cancers. Overexpression of LINC00551 suppresses cell viability while promoting autophagy and RSL-3-induced ferroptosis in LUAD cells. LINC00551 acts as a competing endogenous RNA (ceRNA) and binds with miR-4328 which up-regulates the target DNA damage-inducible transcript 4 (DDIT4). DDIT4 inhibits the activity of mTOR, promotes LUAD autophagy, and then promotes the ferroptosis of LUAD cells in an autophagy-dependent manner. This study provided an insight into the molecular mechanism regulating ferroptosis and highlighted LINC00551 as a potential therapeutic target for LUAD.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9772902 | PMC |
| http://dx.doi.org/10.7717/peerj.14180 | DOI Listing |
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