1. Study on the mechanism of mitochondrial dysfunction and CPT1A/ERK signal transduction pathway regulating malignant behavior in breast cancer
- Author
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JIANG Dan, SONG Guoqing, WANG Xiaodan
- Subjects
breast cancer ,mitochondria ,carnitine palmitoyl transferase 1a ,extracellular signal-regulated kinase ,malignant behavior ,Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,RC254-282 - Abstract
Background and purpose: The overexpression of carnitine palmitoyl transferase 1A (CPT1A) is related to the poor prognosis of breast cancer, and it can promote the utilization of fatty acids by mitochondria and maximize triphosphate (ATP) production. However, the role of CPT1A in breast cancer metastasis is still unclear. This study aimed to explore the mechanism that mitochondrial dysfunction and CPT1A/extracellular signal-regulated kinase (ERK) signaling pathway in breast cancer jointly regulate the malignant behavior of breast cancer. Methods: The lentivirus system and shRNA tools were used to overexpress or knock down CPT1A in human breast cancer cell lines MDA-MB-231 and MCF7, and the cells were divided into NC group, CPT1A group and shCPT1A group. The invasion ability of cells was detected by transwell assay, and the protein expressions of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), ERK1/2 and CPT1A were analyzed by Western blot. The mitochondrial morphology of MDA-MB-231 and MCF7 cell lines was analyzed using mitochondrial red staining, and mitochondrial respiratory capacity was analyzed by oxygen consumption rate. Results: Compared with cells expressing control vector, overexpression of CPT1A resulted in enhanced invasion abilities of MCF7 cells and MDA-MB-231 cells (P
- Published
- 2024
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