1. Molecular mediators of breast cancer metastasis
- Author
-
Amitava Das and Ragini Yeeravalli
- Subjects
Population ,Breast Neoplasms ,Malignancy ,Metastasis ,Breast cancer ,Cancer stem cell ,Recurrence ,medicine ,Humans ,Diseases of the blood and blood-forming organs ,Epithelial–mesenchymal transition ,Neoplasm Metastasis ,Relapse ,education ,RC254-282 ,education.field_of_study ,business.industry ,Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,Hematology ,General Medicine ,Molecular mediators ,medicine.disease ,Epithelial-mesenchymal transition ,Breast cancer stem cells ,Metastasis Suppressor Gene ,Lymphatic system ,Oncology ,Cancer research ,Female ,RC633-647.5 ,business - Abstract
Breast cancer has the highest incidence rate of malignancy in women worldwide. A major clinical challenge faced by patients with breast cancer treated by conventional therapies is frequent relapse. This relapse has been attributed to the cancer stem cell (CSC) population that resides within the tumor and possess stemness properties. Breast CSCs are generated when breast cancer cells undergo epithelial-mesenchymal transition resulting in aggressive, highly metastatic, and invasive phenotypes that exhibit resistance towards chemotherapeutics. Metastasis, a phenomenon that aids in the migration of breast CSCs, occurs through any of three different routes: hematogenous, lymphatic, and transcoelomic. Hematogenous dissemination of breast CSCs leads to metastasis towards distant unrelated organs like lungs, liver, bone, and brain causing secondary tumor generation. Activation of metastasis genes or silencing of metastasis suppressor genes often leads to the advancement of metastasis. This review focuses on various genes and molecular factors that have been implicated to regulate organ-specific breast cancer metastasis by defying the available therapeutic interventions.
- Published
- 2021