MiR-128 regulation of glucose metabolism and cell proliferation in triple-negative breast cancer
| Autor: | Shusheng Jia, Min Xiao, X Cai, Y Yang, Yuanxi Huang, C Lou, H Xiao, C Li |
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| Rok vydání: | 2017 |
| Předmět: |
Adult
Male 0301 basic medicine Oncology medicine.medical_specialty Blotting Western Triple Negative Breast Neoplasms Metastasis Mice 03 medical and health sciences Breast cancer Cell Line Tumor Internal medicine Biomarkers Tumor medicine Carcinoma Animals Humans Triple-negative breast cancer Survival analysis Aged Cell Proliferation Aged 80 and over Mice Inbred BALB C biology Reverse Transcriptase Polymerase Chain Reaction business.industry Carcinoma Ductal Breast Mammary Neoplasms Experimental Cancer Middle Aged Prognosis medicine.disease Survival Analysis IRS1 Gene Expression Regulation Neoplastic MicroRNAs Insulin receptor Glucose 030104 developmental biology Lymphatic Metastasis biology.protein Female Surgery Neoplasm Grading business |
| Zdroj: | British Journal of Surgery. 105:75-85 |
| ISSN: | 1365-2168 0007-1323 |
| Popis: | Background Triple-negative breast cancer (TNBC) is prone to metastasis and has a poor prognosis, with lower survival rates than other breast cancer subtypes. MicroRNAs have recently emerged as powerful regulators of cancer processes and become a promising target in cancer therapy. Methods Expression of miR-128 was examined in invasive ductal breast cancer, and its relationship with clinicopathological features analysed. A series of in vitro and in vivo experiments were performed to investigate the function and mechanism of miR-128 in the development of invasive ductal breast cancer. Results A cohort of 110 women with TNBC and 117 with non-TNBC were included in the study. In multivariable Cox regression analysis, overall and disease-free survival were significantly associated with lymph node metastasis, histological grade and molecular subtype. Subgroup analysis showed that low expression of miR-128 correlated with shorter overall and disease-free survival in TNBC (P < 0·001), and shorter overall but not disease-free survival in non-TNBC. In addition, miR-128 was able to inhibit glucose metabolism, mitochondrial respiration and proliferation of TNBC cells. These effects were consistent with miR-128 targeting inhibition of the insulin receptor and insulin receptor substrate 1. Conclusion MiR-128 might be a prognostic marker and possible molecular target for therapy in patients with TNBC. |
| Databáze: | OpenAIRE |
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