Metastatic Breast Cancer, Organotropism and Therapeutics: A Review.

The final stage of breast cancer involves spreading breast cancer cells to the vital organs like the brain, liver lungs and bones in the process called metastasis. Once the target organ is overtaken by the metastatic breast cancer cells, its usual function is compromised causing organ dysfunction and death. Despite the significant research on breast cancer metastasis, it's still the main culprit of breast cancer-related deaths. Exploring the complex molecular pathways associated with the initiation and progression of breast cancer metastasis could lead to the discovery of more effective ways of treating the devastating phenomenon. The present review article highlights the recent advances to understand the complexity associated with breast cancer metastases, organotropism and therapeutic advances.

Relaxin protects cardiomyocytes against hypoxia-induced damage in in-vitro conditions: Involvement of Nrf2/HO-1 signaling pathway.

Relaxin, a peptide hormone has emerged as a cardioprotective agent against the heart failure and has been found to protect cardiac muscle cells against hypoxia/reoxygenation injury under in vitro conditions. The present study was conducted to study its possible role in activating the Nrf2/HO-1 signaling pathway in cardiomyocytes, as a means to counter hypoxia associated oxidative damage and cell death. H9C2 cell line was induced with chemical hypoxia alone or together with relaxin. Hypoxia associated cellular damage and reactive oxygen species (ROS) production was accessed by Lactate dehydrogenase (LDH) release and DCFDA activity respectively. The anti-oxidative property of RLXH2 was measures by assessing the activities of different enzymes like Superoxide dismutase (SOD), Catalase (CAT) and Glutathione peroxidase (GSX). Expression levels of Nrf2 and HO-1 was studied by immunoblotting and quantitative real time PCR (qRT-PCR). Translocation of Nrf2 to nucleus was studied by immunoblotting. Our results found that hypoxia associated lactate dehydrogenase leakage and ROS production is countered by RLXH2 treatment. Similarly, RLXH2 was able to counter hypoxia induced oxidative damage as evident by increased activities of SOD, CAT and GSX. Furthermore, it was found that RLXH2 treatment induces translocation of Nrf2 from cytosol to nucleus and in turn enhances expression level of HO-1. Our results suggest that RLXH2 exerts cytoprotective action in cardiomyocytes against the hypoxia induced damage and activates Nrf2/HO-1 signaling pathway.