Autophagy pathway in tumor cells

Autophagy is a conserved cellular degradation pathway where cytoplasmic components, including damaged organelles and proteins, are encapsulated within autophagosomes and degraded in lysosomes. In tumor cells, the autophagy pathway can both suppress tumor initiation by maintaining cellular homeostasis and quality control, and promote established tumor growth by enabling survival during metabolic stress and resistance to therapies[2][3][5]. Many core proteins, such as ULK1/2, Beclin-1, ATG5, ATG7, and LC3, orchestrate this pathway, which is dynamically regulated by signals including mTOR, AMPK, and p53[4][5]. Therapeutic targeting of autophagy in cancer is an area of active investigation, with molecules such as chloroquine and rapamycin modulating this pathway to alter tumor sensitivity to stress and cytotoxic agents. However, given autophagy's context-dependent role in cancer—sometimes promoting and sometimes inhibiting tumor growth—therapeutic modulation carries significant complexity and safety concerns[2][3][5][1]. **Additional context on "is_incorrect":** "Autophagy pathway in tumor cells" is not a specific molecular target (such as a protein or receptor) but rather a complex, multi-component signaling and catabolic pathway. While autophagy and its core proteins (e.g., Beclin-1, ATG5) are widely recognized as therapeutic targets, the pathway itself is a cellular process, not a single molecular entity. For structured target annotation, specify a major autophagy regulator (such as "Beclin-1" or "ULK1") for more precise mapping.

Other names

AutophagyAutophagic pathwayATG pathwayTumor cell autophagy

Inhibition of lysosomal degradation (by chloroquine/hydroxychloroquine) - mTOR inhibition (by rapamycin/temsirolimus), leading to autophagy induction - Modulation of upstream signaling (e.g., AMPK, RAS-MAPK pathways) - Sensitization or protection of tumor cells by altering autophagy status in response to chemotherapy