CDR 2021
DOI: 10.20517/cdr.2021.32
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Cancer stem cells, epithelial-mesenchymal transition, ATP and their roles in drug resistance in cancer

Abstract: The cancer stem cell (CSC) state and epithelial-mesenchymal transition (EMT) activation are tightly interconnected. Cancer cells that acquire the EMT/CSC phenotype are equipped with adaptive metabolic changes to maintain low reactive oxygen species levels and stemness, enhanced drug transporters, anti-apoptotic machinery and DNA repair system. Factors present in the tumor microenvironment such as hypoxia and the communication with non-cancer stromal cells also promote cancer cells to enter the EMT/CSC state an… Show more

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Cited by 22 publications
(31 citation statements)
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References 217 publications
(526 reference statements)
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“…The stepwise increases in many miRNAs, including miR-185 -5p, being statistically significant in patients with local, locally advanced, and metastatic PC (p < 0.05), suggesting that this miRNA may be used as biomarkers in disease prognosis (Table 4). Increasing evidence suggests that cancer stem cells (CSCs) in PC tissue are responsible for treatment failure due to their key role in metastasis, epithelial-mesenchymal transition, and drug resistance [56,57]. Moreover, aberrant miRNA expression has been reported to play an important role in maintaining PCSC associated with drug resistance, metastasis, and therapeutic failures [58].…”
Section: Upregulated Mir-185mentioning
confidence: 99%
“…The stepwise increases in many miRNAs, including miR-185 -5p, being statistically significant in patients with local, locally advanced, and metastatic PC (p < 0.05), suggesting that this miRNA may be used as biomarkers in disease prognosis (Table 4). Increasing evidence suggests that cancer stem cells (CSCs) in PC tissue are responsible for treatment failure due to their key role in metastasis, epithelial-mesenchymal transition, and drug resistance [56,57]. Moreover, aberrant miRNA expression has been reported to play an important role in maintaining PCSC associated with drug resistance, metastasis, and therapeutic failures [58].…”
Section: Upregulated Mir-185mentioning
confidence: 99%
“…Yet, there is evidence in traced lineages indicative of stochastic growth patterns in tumor tissue [202]. This indicates a sensitivity to the microenvironment suggestive of a feedback control loop in CSC maintenance [63,65,202]-in fact, TME regulation of CSC plasticity has even been linked to regulated quiescence [203,204], which is central to immune escape [110,205] and metastatic initiation in CSC and other tumor-initiating phenotypes [204,206,207]. Quiescence-induced tumorigenesis during immune-compromised conditions as well as the endowed immunosuppressive properties also contribute towards CSC-mediated chemoresistance [203][204][205]208].…”
Section: Stem Cell Involvement In Tumor Microenvironment Regulationmentioning
confidence: 99%
“…CSCs may acquire resistance to chemotherapy via several mechanisms: overexpression of ATP-binding cassette (ABC) transporters and antiapoptotic molecules, abnormal activation of signaling pathways, acquisition of multidrug resistance due to enhanced DNA repair activity, and the presence of a tumor microenvironment (TME) that protects tumor cells from drugs. There is a wide range of possibilities, such as the formation of a niche to protect tumor cells from drugs via the tumor microenvironment (TME) or dormancy (inactivity) in the body, followed by activation (after several years or decades) [ 154 , 155 ]. In the tumor microenvironment surrounding cells, mesenchymal stem cells (MSCs) could affect cancer cells to enhance their stemness [ 156 , 157 , 158 ].…”
Section: Stem Cells and Changes In Drug Efflux (Drug Transporters)mentioning
confidence: 99%