Israeli Researchers Say They Can Reprogram Cancer Cells Back To Their Pre-Cancer State
Cancer cells typically acquire a common set of properties, including unlimited proliferation potential, self-sufficiency in growth signals, resistance to cell death, and an ability to activate invasion and metastasis, as described in a seminal 2000 study by American biologists and cancer researchers Douglas Hanahan and Robert Weinberg. While cancers are diverse in type and etiology, the researchers also say they all share metabolism abnormalities, regardless of cellular or tissue origin. Tumor cell metabolism is now seen as cancer’s Achilles’ heel, providing a unique therapeutic opportunity to effectively eliminate tumor cells by targeting their energy metabolism.
Now, a group of researchers from Israel’s Ben-Gurion University of the Negev (BGU) have developed a new molecule that they claim inhibits the growth of cancer cells and reprograms them to act non-cancerous. The groundbreaking treatment is based on preventing the expression of the protein VDAC1, which is highly expressed in different types of tumors and found to alter cancer hallmarks, including the rewiring of pathways for growth and survival that underlie the malignant phenotype.
VDAC1 is a “gatekeeper” of the mitochondria, the powerhouse of the cell, and is the “key to opening and closing the door to mitochondrial metabolism,” says the head of the research team Professor Varda Shoshan-Barmatz of the Department of Life Sciences and the National Institute for Biotechnology in the Negev (NIBN), an independent research institute facilitating pre-clinical studies of biotech research located within BGU. VDAC1 is crucial for supplying the high energy demands that characterize malignant cells, the univeristy said in a statement.
Ben-Gurion University of the Negev. Photo by NoCamels Staff
“As VDAC1 controls cell energy and metabolic homeostasis, depletion of VDAC1 in cancer cell blocks the communication between the mitochondria and the rest of the cells,” Shoshan-Barmatz tells NoCamels.
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