Targeting Cancer cell metabolism via Target of Rapamycin

Cancer cells acquire many metabolic rearrangements to provide energy and macromolecules required for continuous growth and proliferation. Warburg suggested that cancerous cells rely only on glycolysis for energy and biosynthesis of macromolecules. It's still unexplainable that how this metabolic switch allows predominance of cancer cell in the hypoxic and metabolically highly active conditions around the cancerous cells. Understanding of signaling particularly, role of Ser/Thr PI3 kinase Target of Rapamycin TOR, “central regulator of growth” in cancer cell metabolism has ignited interest in comprehending the precise mechanism linking cancer cell environment to metabolic rearrangements ensuring cancer proliferation. The focus of present review is to summarize the role of TOR in metabolic rearrangements prevalent in glycolysis and TCA occurring in cancerous cell. The insights from mechanistic of mTOR signaling in cancer cell metabolism have led to identification of several downstream candidates to be explored in anticancer therapeutics. Thus usage of drug directly targeting macromolecular biosynthesis in combination with environment responder, mTOR inhibitor, is more promising in cancer therapeutics.