AI Article Synopsis
- The study identified high levels of MCF2L in hepatocellular carcinoma (HCC) tissues, suggesting it plays a role in resistance to sorafenib, a common cancer treatment.
- Various experiments confirmed that reducing MCF2L levels increased cell death when treated with sorafenib, and that this process is linked to ferroptosis, a specific type of cell death.
- The research also indicated that MCF2L influences the PI3K/AKT signaling pathway via a RhoA/Rac1-dependent mechanism, making it a potential target for overcoming treatment resistance in HCC.
Article Abstract
Methods And Results: The levels of MCF2L were detected by PCR and western blotting assay. The effect of MCF2L on ferroptosis was confirmed by MTT, colony formation assay, Brdu, in vivo animal experiment, and the content of Iron, GSH, ROS, and MDA. The underlying mechanisms were explored by PCR, western blotting, and affinity precipitation assay. Our findings demonstrated that MCF2L is remarkedly upregulated in HCC tissues, and sorafenib can induce the levels of MCF2L, suggesting that MCF2L might function in sorafenib resistance of HCC. Further analysis showed that downregulation of MCF2L enhances HCC cell death induced by sorafenib, and ferroptosis inhibitor can reverse this process. Subsequent experiments showed that downregulation of MCF2L elevates the content of Iron, ROS, and MDA, which are all indicators of ferroptosis. Finally, mechanism analysis showed that MCF2L regulates the PI3K/AKT pathway in a RhoA/Rac1 dependent manner.
Conclusions: Our study showed that targeting MCF2L may be a hopeful method to overcome sorafenib-resistance through inducing ferroptosis in HCC.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9626212 | PMC |
| http://dx.doi.org/10.1155/2022/6138941 | DOI Listing |
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Downregulation of MCF2L Promoted the Ferroptosis of Hepatocellular Carcinoma Cells through PI3K/mTOR Pathway in a RhoA/Rac1 Dependent Manner.
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Article Synopsis
- The study identified high levels of MCF2L in hepatocellular carcinoma (HCC) tissues, suggesting it plays a role in resistance to sorafenib, a common cancer treatment.
- Various experiments confirmed that reducing MCF2L levels increased cell death when treated with sorafenib, and that this process is linked to ferroptosis, a specific type of cell death.
- The research also indicated that MCF2L influences the PI3K/AKT signaling pathway via a RhoA/Rac1-dependent mechanism, making it a potential target for overcoming treatment resistance in HCC.
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