Ashwagandha can help cure cancer, says study

Hyderabad: Researchers of the International Laboratory for Advanced Biomedicine, National Institute of Advanced Industrial Science and Technology, Tsukuba (Japan), Department of Bio-chemical Engineering and Biotechnology of Indian Institute of Technology (IIT), Delhi, have found Ashwagandha has potential to treat cancer.

In a paper submitted to the International Conference on Bio-technological Research and Innovation for Sustainable Development (Bio-SD 2018) which concluded at the Indian Institute of Chemical Technology (IICT) recently, the researchers concluded that Withaferin A (Wi-A), a major Withanolide constituent of Withania Somnifera, an herb commonly used in Indian traditional home medicine, has been shown to exert anti-tumor activity. The researchers said, “We used unique isogenic cells with or without telomerase and investigated anti-cancer potential of Wi-A. We found that Wi-A caused stronger cyto-toxity to ALT (Alternative Mechanism of lengthening of Telomeres) cells and was associated with inhibition of ALT -associated promyelocytic leukemia (PML) nuclear bodies.”

According to the paper, comparative analyses of telomerase positive and ALT cells revealed that Wi-A caused stronger telomere dysfunction and upregulation of DNA damage response in ALT cells. Bioinformatics, molecular docking and molecular analyses revealed that treatment with Wi-A led to activation of DNA damage signaling through transcriptional MRN and NFKB signaling. The results suggest that Wi-A may be a candidate drug for cancer treatment. It warrants further studies on the pharmacokinetics, molecular mechanisms and clinical trials. The researchers described cancer as a complex disorder, largely defined as abnormal growth of cells. In contrast to normal cells that divide limited number of times, cancer cells keep dividing automatically and can develop into unwanted mass of cells anywhere in the body or even acquire the capacity to invade to secondary distant tissues.

Maintenance of telomere length is a most consistent attribute of cancer cells. Tightly connected to their capacity to overcome replicative mortality, it is achieved either by activation of telomerase or switching-on of ALT. Interruption of either of these mechanisms has been shown to activate DNA damage signaling leading to senescene or apoptosis in cancer cells.