Abstract
Breast cancer is a widely distributed type of cancer in women worldwide, and tumor relapse is the major cause of breast cancer death. In breast cancers, the acquisition of metastatic ability, which is responsible for tumor relapse and poor clinical outcomes, has been linked to the acquisition of the epithelial-mesenchymal transition (EMT) program and self-renewal traits (CSCs) via various signaling pathways. These phenomena confer resistance during current therapies, thus creating a major hurdle in radiotherapy/chemotherapy. The role of very low doses of radiation (LDR) in the context of EMT has not yet to be thoroughly explored. Here, we report that a 0.1 Gy radiation dose reduces cancer progression by deactivating the JAK1/STAT3 pathway. Furthermore, LDR exposure also reduces sphere formation and inhibits the self-renewal ability of breast cancer cells, resulting in an attenuated CD44+/CD24− population. Additionally, in vivo findings support our data, providing evidence that LDR is a promising option for future treatment strategies to prevent cancer metastasis in breast cancer cases.
Highlights
Tumor relapse after high-dose radiotherapy is the major cause of the failure of current treatment approaches and follow-up with the above mentioned beneficial effect of low-dose radiation (LDR), recently researchers are becoming more interested in checking epithelial-mesenchymal transition (EMT) processes with the use of LDR
As cancer stem cells are highly responsible for tumor relapse after radiotherapy[15], we initially focused on investigating the response of LDR in breast cancer cells with regard to CSC maintenance
To check the response of LDR in breast cancer, we initially examined a CD44+/CD24− population, i.e., those survived within breast cancer and maintained stemness, in LDR-exposed MDA-MB231 breast cancer cell lines
Summary
Tumor relapse after high-dose radiotherapy is the major cause of the failure of current treatment approaches and follow-up with the above mentioned beneficial effect of LDR, recently researchers are becoming more interested in checking epithelial-mesenchymal transition (EMT) processes with the use of LDR. Earlier data showed that breast tumor relapse after therapy is a hallmark of EMT12. In breast cancer cases, the EMT state is linked to a cancer stem cell (CSC)-like population harboring the CD44+/CD24− profile, which shows resistance to therapies. We showed that LDR reduces the malignant phenotype in oncogene KRAS (Kirsten rat sarcoma viral oncogene homolog) transformed breast epithelial cells. This phenomenon is due to the LDR-induction of antioxidants counteracting KRAS-induced ROS levels in LDR-exposed cells[14]. As metastasis is associated with increased malignant tumor progression, we sought to examine the effects of LDR with regard to EMT in breast cancer cells. Using LDR along with an anticancer drug may be a more effective as well as the safest cancer treatment in future time
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