AI Article Synopsis
- Lidamycin (LDM) has a strong anti-cancer effect on pancreatic cancer by impacting mitochondrial function in these cells.
- Mitofusin-2 (Mfn2) is believed to help inhibit cancer and is linked to mitochondrial autophagy in pancreatic cancer.
- Research shows that LDM enhances Mfn2 expression, influences processes like epithelial-mesenchymal transition (EMT), and regulates key mitochondrial autophagy proteins, indicating Mfn2's role in promoting mitophagy in pancreatic cancer cells.
Article Abstract
Lidamycin (LDM) has been confirmed to have a strong anti-pancreatic cancer effect and can affect the mitochondrial function of pancreatic cancer cells. Mitofusin-2 (Mfn2) is located in the outer membrane of mitochondria, and Mfn2 is currently believed to play a role in cancer inhibition in pancreatic cancer. In order to explore whether the anti-pancreatic cancer effect of LDM is related to Mfn2-mediated mitophagy, Bioinformatics and in vitro cell experiments are used for experimental research. The experimental results demonstrated that Mfn2 is correlated with mitochondrial autophagy in pancreatic cancer. Lidamycin can increase the expression of Mfn2 in pancreatic cancer and affect the process of EMT, affect the level of reactive oxygen species and mitochondrial membrane potential, and increase the expression of mitochondrial autophagy marker proteins BNIP3L and Beclin1. These results demonstrate that Mfn2 affects mitophagy in pancreatic cancer cells by regulating the expression of Mfn2.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11377765 | PMC |
| http://dx.doi.org/10.1038/s41598-024-71377-4 | DOI Listing |
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