F-box and leucine-rich repeat protein 16 controls tamoxifen sensitivity via regulation of mitochondrial respiration in estrogen receptor-positive breast cancer cells

Chen, Feng; Wang, Lu; Feng, Yongzhong; Ma, Wei; Liu, J; Bi, Qiu; Song, Yong; Gao, Rong; Jia, Yanhan

doi:10.1007/s13577-023-00961-z

Cited by 1 publication

(1 citation statement)

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“…Tamoxifen, as a potent selective estrogen receptor modulator (SERM), has been reported to competitively bind to the estrogen receptor (ER) on tumor cells, thereby preventing the promotion of estrogen on tumor cell growth and proliferation [35]. However, Tamoxifen resistance remains a significant obstacle which lead to tumor relapse and metastasis in most of breast cancer patients, and there is no effective method to reverse Tamoxifen resistance in clinic[6]. Therefore, searching for novel non-toxic, broad-spectrum yet cost-effective alternative agents to overcoming Tamoxifen resistance is crucial against breast cancer.…”

Section: Introductionmentioning

confidence: 99%

Propofol overcome Tamoxifen resistance in breast cancer by modulating tumorogenesis, immune response and metabolism

Yin,

Gao,

Guo

et al. 2024

Preprint

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Although 70% of estrogen receptor (ER)-positive breast cancer patients benefit from Tamoxifen therapy, the developing resistance to Tamoxifen leads to high rates of metastasis and poor prognosis. Propofol, a commonly used anesthetic, has been shown to inhibit the occurrence and development of breast cancer. However, its role in anti-endocrine resistance in ER-positive breast cancer remains unclear. In this study, we found that Propofol significantly promotes cell cycle arrest, induces apoptosis, and inhibits proliferation in Tamoxifen-resistant breast cancer cells. Furthermore, transcriptome sequencing analysis revealed 1065 differentially expressed genes (DEGs) between Propofol-treated Tamoxifen-resistant MCF-7 (MCF7-TR) cells and none-treated MCF7-TR cells. Gene ontology annotation enrichment analysis (GO), Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis (KEGG), and gene set enrichment analysis (GSEA) showed that Propofol affects the expression of genes located in the plasma membrane and cell periphery, mainly regulating signals involved in cell cycle regulation, immune response modulation, and metabolism. Our results provide new insights into the mechanism by which Propofol controls resistance to Tamoxifen in breast cancer progression and offer a theoretical basis for clinical treatment.

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Section: Introductionmentioning

confidence: 99%