GPR110 promotes progression and metastasis of triple-negative breast cancer.
Hye-Jung NamYeon-Ju KimJae-Hyeok KangSu-Jae LeePublished in: Cell death discovery (2022)
Breast cancer is the most common type of cancer in women, and approximately 70% of all breast cancer patients use endocrine therapy, such as estrogen receptor modulators and aromatase inhibitors. In particular, triple-negative breast cancer (TNBC) remains a major threat due to the lack of targeted treatment options and poor clinical outcomes. Here, we found that GPR110 was highly expressed in TNBC and GPR110 plays a key role in TNBC progression by engaging the RAS signaling pathway (via Gαs activation). High expression of GPR110 promoted EMT and CSC phenotypes in breast cancer. Consequently, our study highlights the critical role of GPR110 as a therapeutic target and inhibition of GPR110 could provide a therapeutic strategy for the treatment of TNBC patients.
Keyphrases
- fatty acid
- estrogen receptor
- signaling pathway
- end stage renal disease
- ejection fraction
- epithelial mesenchymal transition
- newly diagnosed
- small molecule
- prognostic factors
- type diabetes
- stem cells
- cancer therapy
- papillary thyroid
- peritoneal dialysis
- insulin resistance
- oxidative stress
- combination therapy
- bone marrow
- induced apoptosis
- replacement therapy
- pregnancy outcomes
- binding protein
- smoking cessation
- squamous cell