RGS10 deficiency facilitates distant metastasis by inducing epithelial-mesenchymal transition in breast cancer.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 39145770.
- Also identified by DOI 10.7554/eLife.97327 and PMC identifier 11326775.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
Distant metastasis is the major cause of death in patients with breast cancer. Epithelial-mesenchymal transition (EMT) contributes to breast cancer metastasis. Regulator of G protein-signaling (RGS) proteins modulates metastasis in various cancers. This study identified a novel role for RGS10 in EMT and metastasis in breast cancer. RGS10 protein levels were significantly lower in breast cancer tissues compared to normal breast tissues, and deficiency in RGS10 protein predicted a worse prognosis in patients with breast cancer. RGS10 protein levels were lower in the highly aggressive cell line MDA-MB-231 than in the poorly aggressive, less invasive cell lines MCF7 and SKBR3. Silencing <i>RGS10</i> in SKBR3 cells enhanced EMT and caused SKBR3 cell migration and invasion. The ability of RGS10 to suppress EMT and metastasis in breast cancer was dependent on lipocalin-2 and <i>MIR539-5p</i>. These findings identify RGS10 as a tumor suppressor, prognostic biomarker, and potential therapeutic target for breast cancer.
Medical subject headings
- RGS Proteins
- Epithelial-Mesenchymal Transition
- Breast Neoplasms
- Neoplasm Metastasis
- Cell Movement