![]() ![]() Moreover, CSCs do not depend on metabolic pathways that are associated with conventional cancer cell populations additionally, they hold similar metabolic signatures to noncancerous cells. The dormant CSCs are distinct populations of cancer cells that have traits in common with stem or progenitor cells. Therefore, singly targeting the Warburg pathway may not be enough to supply therapeutic benefits.Īnother popular concept of drug resistance in cancer involves the reawakening of dormant cancer stem cells (CSCs). For instance, silencing glycolytic genes can restrict the Warburg pathway, but leads to the hyperactivation of the fatty acid oxidation (FAO) pathway and mitochondrial biogenesis in cancer cells. However, targeting this pathway eventually turns on dormant metabolic pathways that can replace the Warburg pathway. Most cancer cells upregulate glucose and/or glutamate uptake to supply carbon for biosynthesis and cope with energy requirements even in the presence of oxygen (Warburg effect). ![]() ![]() Metabolic reprogramming is a major obstacle to cancer therapy because metabolite deprivation therapy not only accelerates the growth of tumors but can cause immune cells to become dysfunctional in the tumor microenvironment. The ability of cancer cells to modify their metabolism to meet the increased energy demand caused by continuous growth, fast multiplication, and other traits distinctive to neoplastic cells is known as metabolic reprogramming. CSC: cancer stem cells, “↑” indicates upregulation and “?” indicates the probable pathway activation (This figure was drawn using the Bio Render app). The evolved drug-resistant tumors are more aggressive and do metastasize to distant sites in the human body and form secondary tumors. Moreover, the theory of CSC’s self-renewal is now a popular area of study, which might be a factor that controls tumor recurrence. The first line of cancer therapy with multiple pathway blockers can inhibit the oncogenic activations, but in turn, cancer cells reprogram themselves, and dependency upon the Warburg pathway shifts to other metabolic pathways. ![]() Primary tumors are metabolically dependent on the Warburg pathway for fast energy and carbon sources, and several oncogenic activations feed into it. ![]()
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