Nitric oxide (NO) plays a multifaceted role in CRC, acting as both a promoter and an inhibitor of cancer progression depending on its concentration, timing, and cellular context.
First-pass extracted concept
nitric oxide in colorectal cancer
Candidate: concept label1 source documents7 linked claims
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Aliases
CRC nitric oxide signaling, nitric oxide, NO
Evidence Snippets
Supporting Sources
Linked Claims
High concentrations of nitric oxide can exert anti-tumor effects in colorectal cancer, including induction of cell death.
Low concentrations of nitric oxide promote angiogenesis in colorectal cancer, enabling tumor growth and metastasis.
Nitric oxide has a biphasic role in ferroptosis in colorectal cancer: high exogenous nitric oxide can induce ferroptosis, whereas lower endogenous nitric oxide can protect against ferroptosis by terminating lipid peroxidation.
Nitric oxide has context-dependent opposing effects in colorectal cancer, promoting or inhibiting cancer progression depending on concentration, timing, and cellular context.
Nitric oxide influences colorectal cancer by modulating the tumor microenvironment, mechanostress responses during metastasis, and extracellular vesicle signaling that aids immune evasion.
Nitric oxide reprograms colorectal cancer cell metabolism by enhancing glucose utilization and mitochondrial activity to support growth in hypoxic conditions.
Targeting nitric-oxide-related processes including ferroptosis, metabolic adaptations, and immune modulation is presented as a promising therapeutic strategy to improve colorectal cancer treatment outcomes.