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We began analyzing https://link.springer.com/article/10.1007/s12032-025-02607-6, but it redirected us to https://link.springer.com/article/10.1007/s12032-025-02607-6. The analysis below is for the second page.

Title[redir]:
Autophagy induced by metabolic processes leads to solid tumor cell metastatic dormancy and recurrence | Medical Oncology
Description:
A crucial cellular mechanism that has a complex impact on the biology of cancer, particularly in solid tumors, is autophagy. This review explores how metabolic processes trigger autophagy, which helps metastatic tumor cells go dormant and recur. During metastasis, tumor cells frequently encounter severe stressors, such as low oxygen levels and nutritional deprivation, which causes them to activate autophagy as a survival tactic. This process allows cancer stem cells (CSCs) to withstand severe conditions while also preserving their features. After years of dormancy, dormant disseminated tumor cells (DTCs) may reappear as aggressive metastatic cancers. The capacity of autophagy to promote resistance to treatments and avoid immune detection is intimately related to this phenomenon. According to recent research, autophagy promotes processes, such as the epithelial-to-mesenchymal transition (EMT) and helps build a pre-metastatic niche, which makes treatment strategies more challenging. Autophagy may be a promising therapeutic target because of its dual function as a tumor suppressor in early-stage cancer and a survival promoter in advanced stages. To effectively treat metastatic diseases, it is crucial to comprehend how metabolic processes interact with autophagy and affect tumor behavior. In order to find novel therapeutic approaches that can interfere with these processes and improve patient outcomes, this study highlights the critical need for additional investigation into the mechanisms by which autophagy controls tumor dormancy and recurrence.

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Keywords {🔍}

pubmed, article, google, scholar, cas, cancer, autophagy, cell, central, cells, tumor, biol, wang, metastasis, zhang, dormancy, res, metastatic, metabolism, nat, mol, metabolic, breast, resistance, role, survival, chen, sci, human, rev, recurrence, mechanisms, commun, inhibition, zalpoor, stem, clin, regulation, biochem, kim, suppressor, med, front, yang, liu, activation, dormant, therapy, nature, pathway,

Topics {✒️}

month download article/chapter amp-activated protein kinase hif-1α-mediated metabolic adaption myeloid-derived suppressor cells increased v-atpase activity anoikis-resistant cancer cells rna-dependent protein kinase triple-negative breast cancer p16ink4a–rb pathway cooperate jnk-p38 map kinases p62-dependent keap1 degradation beclin1-binding protein uvrag vander griend dj parkin-mediated mitochondrial clearance egfr-mutant lung adenocarcinoma cell-intrinsic survival signals gα-interacting protein stimulates distinct cis-acting sequences hypoxia-inducible factor induction autophagy-dependent/independent ferroptosis single-cell analysis unveils pancreatic adenocarcinoma cells cetuximab-mediated cancer therapy mammalian autophagy-specific factor evidence-based functional foods full article pdf l-arginine induces autophagy disseminated tumor cells bioresearch open access enhancing cisplatin-induced autophagy breast carcinoma cells references torres-lópez vascular endothelium leads p38 kinases mkk4 hypoxia-inducible factor 1 early-stage cancer breast cancer cells seyedi asl fs cancer stem cells fahimeh maleki-sheikhabadi rinker-schaeffer cw lopez-gonzalez js privacy choices/manage cookies dormant carcinoma cells autophagy supports generation cell proteostasis network chambers af high cd44 expression metabolic switch required aguirre-ghiso ja

Questions {❓}

KISS1 metastasis suppressor in tumor dormancy: a potential therapeutic target for metastatic cancers?
The Warburg effect: how does it benefit cancer cells?
Tumor cell dormancy induced by p38SAPK and ER-stress signaling: an adaptive advantage for metastatic cells?

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