
DOI . ORG {
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Title[redir]:
Regulation and signaling pathways in cancer stem cells: implications for targeted therapy for cancer | Molecular Cancer | Full Text
Description:
Cancer stem cells (CSCs), initially identified in leukemia in 1994, constitute a distinct subset of tumor cells characterized by surface markers such as CD133, CD44, and ALDH. Their behavior is regulated through a complex interplay of networks, including transcriptional, post-transcriptional, epigenetic, tumor microenvironment (TME), and epithelial-mesenchymal transition (EMT) factors. Numerous signaling pathways were found to be involved in the regulatory network of CSCs. The maintenance of CSC characteristics plays a pivotal role in driving CSC-associated tumor metastasis and conferring resistance to therapy. Consequently, CSCs have emerged as promising targets in cancer treatment. To date, researchers have developed several anticancer agents tailored to specifically target CSCs, with some of these treatment strategies currently undergoing preclinical or clinical trials. In this review, we outline the origin and biological characteristics of CSCs, explore the regulatory networks governing CSCs, discuss the signaling pathways implicated in these networks, and investigate the influential factors contributing to therapy resistance in CSCs. Finally, we offer insights into preclinical and clinical agents designed to eliminate CSCs.
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Keywords {🔍}
cancer, pubmed, article, google, scholar, cscs, cas, cells, cell, stem, tumor, central, csc, signaling, stemness, resistance, cscassociated, expression, breast, targeting, metastasis, therapy, wang, control, zhang, pathway, selfrenewal, res, cancers, characteristics, leukemia, promotes, clinical, notch, regulation, emt, liu, proliferation, nat, mol, agents, sox, mrna, pathways, maintenance, role, rna, inhibitors, kim, epigenetic,
Topics {✒️}
amino]pyrimidin-4-yl]-1 h-indol-7-yl]-2 eif4f–stat1–pd-l1 axis wnt/β-catenin-dependent cd44 expression hyperactivated wnt/β-catenin signaling wnt/β-catenin signaling pathway hif-1α/pfkfb3/pfk1 pathway simultaneously activating wnt/β-catenin modulating wnt/β-catenin signaling serine/threonine kinase domains wnt/β-catenin signaling inhibitors blocking c-myc/max heterodimerization activating wnt/β-catenin signaling activated wnt/β-catenin signaling twist1-induced epithelial-mesenchymal transition stk11-/lkb1-deficient lung cancer wnt/β-catenin directs tgf-β-mediated dna demethylation hypoxia-inducible factor-1α expression ccl2 mediates cross-talk d347-2761 blocked c-myc wnt/β-catenin signaling tyrosine kinase-related receptors full-length gli activates il-6-jak1-stat3-oct-4 pathway cutaneous t-cell lymphoma cd123-targeted antibody-drug conjugate 3-methoxy-1-methyl-pyrazol-4-yl human colon-cancer-initiating cells snail-mediated e-cadherin repression cdk8-β-catenin signaling cxcl12/cxcr4-dependent manner hif-2α-dependent manner [242] promotes epithelial-mesenchymal transition shh-smo-gli axis prostate stem/progenitor cells oncogenic kras-induced leukemogeneis tgf-β signaling pathway cooperative stat3-smad3 signaling tgf-β/smad signaling p38-mediated mapk1 activation lin28-mediated post-transcriptional regulation kdm2a-mediated h3k36 demethylation jak/stat3 signaling pathway tgf-β induced emt upregulate m-csf secretion tgf-β induces mir-100 macrophage colony-stimulating factor lower-grade diffuse gliomas bigoni-ordóñez gd triple-negative breast cancer
Questions {❓}
- Downregulation of RNF128 activates Wnt/?
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headline:Regulation and signaling pathways in cancer stem cells: implications for targeted therapy for cancer
description:Cancer stem cells (CSCs), initially identified in leukemia in 1994, constitute a distinct subset of tumor cells characterized by surface markers such as CD133, CD44, and ALDH. Their behavior is regulated through a complex interplay of networks, including transcriptional, post-transcriptional, epigenetic, tumor microenvironment (TME), and epithelial-mesenchymal transition (EMT) factors. Numerous signaling pathways were found to be involved in the regulatory network of CSCs. The maintenance of CSC characteristics plays a pivotal role in driving CSC-associated tumor metastasis and conferring resistance to therapy. Consequently, CSCs have emerged as promising targets in cancer treatment. To date, researchers have developed several anticancer agents tailored to specifically target CSCs, with some of these treatment strategies currently undergoing preclinical or clinical trials. In this review, we outline the origin and biological characteristics of CSCs, explore the regulatory networks governing CSCs, discuss the signaling pathways implicated in these networks, and investigate the influential factors contributing to therapy resistance in CSCs. Finally, we offer insights into preclinical and clinical agents designed to eliminate CSCs.
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headline:Regulation and signaling pathways in cancer stem cells: implications for targeted therapy for cancer
description:Cancer stem cells (CSCs), initially identified in leukemia in 1994, constitute a distinct subset of tumor cells characterized by surface markers such as CD133, CD44, and ALDH. Their behavior is regulated through a complex interplay of networks, including transcriptional, post-transcriptional, epigenetic, tumor microenvironment (TME), and epithelial-mesenchymal transition (EMT) factors. Numerous signaling pathways were found to be involved in the regulatory network of CSCs. The maintenance of CSC characteristics plays a pivotal role in driving CSC-associated tumor metastasis and conferring resistance to therapy. Consequently, CSCs have emerged as promising targets in cancer treatment. To date, researchers have developed several anticancer agents tailored to specifically target CSCs, with some of these treatment strategies currently undergoing preclinical or clinical trials. In this review, we outline the origin and biological characteristics of CSCs, explore the regulatory networks governing CSCs, discuss the signaling pathways implicated in these networks, and investigate the influential factors contributing to therapy resistance in CSCs. Finally, we offer insights into preclinical and clinical agents designed to eliminate CSCs.
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