The self-destruction of cells infected with viruses undergoes the process of apoptosis generally to restrict infection and the spread of viral progeny. To avoid infection host has evolved interconnected complex defence network that comprises innate and acquired immune response. Mitochondria being considered as powerhouse of a cell is not limited to only energy production, but mitochondria perform various other functions in (disease, apoptosis and host innate immune system) which make them absolutely indispensable to the cell. This makes them a target of almost all the invading pathogens including viruses. Therefore being a multifunctional organelle, the viruses choose mitochondria as a favourite organelle as they can easily take control of the whole cell and make it to promote or block apoptosis as per their need.

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The mammalian STE 20-like protein kinase 4 (MST4) gene is highly expressed in several cancer types, but little is known about the role of MST4 in breast cancer, and the function of MST4 during epithelial-mesenchymal transition (EMT) has not been fully elucidated. Here we report that overexpression of MST4 in breast cancer results in enhanced cell growth, migration, and invasion, whereas inhibition of MST4 expression significantly attenuates these properties. Further study shows that MST4 promotes EMT by activating Akt and its downstream signaling molecules such as E-cadherin/N-cadherin, Snail, and Slug. MST4 also activates AKT and its downstream pro-survival pathway. Furthermore, by analyzing breast cancer patient tissue microarray and silicon datasets, we found that MST4 expression is much higher in breast tumor tissue compared to normal tissue, and significantly correlates with cancer stage, lymph node metastasis and a poor overall survival rate (p < 0.05). Taken together, our findings demonstrate the oncogenic potential of MST4 in breast cancer, highlighting its role in cancer cell proliferation, migration/invasion, survival, and EMT, suggesting a possibility that MST4 may serve as a novel therapeutic target for breast cancer.