Tumor microenvironment enriches the stemness features: the architectural event of therapy resistance and metastasis.
Cancer stem cells
Fibroblasts
Metastatic stem cells
Therapy resistance
Tumor microenvironment
Journal
Molecular cancer
ISSN: 1476-4598
Titre abrégé: Mol Cancer
Pays: England
ID NLM: 101147698
Informations de publication
Date de publication:
22 12 2022
22 12 2022
Historique:
received:
22
05
2022
accepted:
16
11
2022
entrez:
22
12
2022
pubmed:
23
12
2022
medline:
27
12
2022
Statut:
epublish
Résumé
Cancer divergence has many facets other than being considered a genetic term. It is a tremendous challenge to understand the metastasis and therapy response in cancer biology; however, it postulates the opportunity to explore the possible mechanism in the surrounding tumor environment. Most deadly solid malignancies are distinctly characterized by their tumor microenvironment (TME). TME consists of stromal components such as immune, inflammatory, endothelial, adipocytes, and fibroblast cells. Cancer stem cells (CSCs) or cancer stem-like cells are a small sub-set of the population within cancer cells believed to be a responsible player in the self-renewal, metastasis, and therapy response of cancer cells. The correlation between TME and CSCs remains an enigma in understanding the events of metastasis and therapy resistance in cancer biology. Recent evidence suggests that TME dictates the CSCs maintenance to arbitrate cancer progression and metastasis. The immune, inflammatory, endothelial, adipocyte, and fibroblast cells in the TME release growth factors, cytokines, chemokines, microRNAs, and exosomes that provide cues for the gain and maintenance of CSC features. These intricate cross-talks are fueled to evolve into aggressive, invasive, migratory phenotypes for cancer development. In this review, we have abridged the recent developments in the role of the TME factors in CSC maintenance and how these events influence the transition of tumor progression to further translate into metastasis and therapy resistance in cancer.
Identifiants
pubmed: 36550571
doi: 10.1186/s12943-022-01682-x
pii: 10.1186/s12943-022-01682-x
pmc: PMC9773588
doi:
Substances chimiques
MicroRNAs
0
Cytokines
0
Types de publication
Journal Article
Review
Research Support, Non-U.S. Gov't
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
225Subventions
Organisme : NCI NIH HHS
ID : U01 CA200466
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA228524
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA263575
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA256973
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA273349
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA210637
Pays : United States
Organisme : NCI NIH HHS
ID : P01 CA217798
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA201444
Pays : United States
Organisme : NCI NIH HHS
ID : U01 CA210240
Pays : United States
Informations de copyright
© 2022. The Author(s).
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