First-pass extracted concept

c-Myc signaling

Candidate: concept label2 source documents7 linked claims

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Aliases

c-Myc

Evidence Snippets

signaling pathways, such as AMPK, HIF-1, and c-Myc, play key roles in tumor metabolic regulation

Evidence 1Source 1DOI PubMedprovenance

We identified c-Myc signaling as a central determinant of macrophage antimycobacterial function.

Evidence 2Source 2DOI PubMedprovenance

Supporting Sources

Source 1primary paper2026MEDDOI PubMed

1 evidence snippet 3 linked claims Claim 1 Claim 2 Claim 3

Source 2primary paper2025MEDDOI PubMed

1 evidence snippet 4 linked claims Claim 1 Claim 2 Claim 3

Linked Claims

Claim 1mechanistic modelsupports2026Source 1DOI PubMed

Metabolic and signaling mechanisms interact synergistically to allow hepatocellular carcinoma cells to survive and proliferate despite targeted therapies, resulting in drug resistance.

Quoted textsource-backed

These mechanisms interact synergistically, allowing HCC cells to endure and proliferate despite targeted therapies, ultimately resulting in drug resistance.

Claim 2mechanistic rolesupports2026Source 1DOI PubMed

AMPK, HIF-1, and c-Myc signaling pathways play key roles in tumor metabolic regulation relevant to hepatocellular carcinoma drug resistance.

Quoted textsource-backed

Moreover, signaling pathways, such as AMPK, HIF-1, and c-Myc, play key roles in tumor metabolic regulation, influencing energy balance, gene expression under hypoxia, and metabolic pathway control.

Claim 3therapeutic rationalesupports2026Source 1DOI PubMed

Understanding metabolic and signaling regulation of aerobic glycolysis may reveal causes of drug resistance in hepatocellular carcinoma and provide new therapeutic targets and strategies.

Quoted textsource-backed

Therefore, a deeper understanding of these metabolic and signaling regulatory mechanisms will help reveal the fundamental causes of drug resistance in HCC and provide new targets and directions for future therapeutic strategies.

Claim 4associationsupports2025Source 2DOI PubMed

Higher c-Myc expression is strongly associated with MTB persistence and active tuberculosis in murine models and human granuloma histopathology.

Quoted textsource-backed

In vivo analyses, including murine models and human clinical histopathology, revealed strong associations between c-Myc expression, MTB persistence, and active tuberculosis.

Claim 5mechanistic rolesupports2025Source 2DOI PubMed

c-Myc signaling is a central determinant of macrophage antimycobacterial function.

Quoted textsource-backed

We identified c-Myc signaling as a central determinant of macrophage antimycobacterial function.

Claim 6perturbation effectsupports2025Source 2DOI PubMed

Inhibition of c-Myc via Omomyc enhances bacterial control partly through mTORC1-dependent metabolic reprogramming and nitric oxide production.

Quoted textsource-backed

Inhibition of c-Myc via Omomyc enhanced bacterial control partly through mTORC1-dependent metabolic reprogramming and nitric oxide production.

Claim 7therapeutic implicationsupports2025Source 2DOI PubMed

c-Myc represents a promising host-directed therapeutic target to enhance macrophage function in MTB infection.

Quoted textsource-backed

c-Myc mediates immune privilege in MTB infection and represents a promising target for host-directed therapies to enhance macrophage function.