2022
DOI: 10.1038/s41388-022-02239-4
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Abstract: Breast cancer (BC) is the second cause of cancer-related deceases in the worldwide female population. Despite the successful treatment advances, 25% of BC develops resistance to current therapeutic regimens, thereby remaining a major hurdle for patient management. Current therapies, targeting the molecular events underpinning the adaptive resistance, still require effort to improve BC treatment. Using BC sphere cells (BCSphCs) as a model, here we showed that BC stem-like cells express high levels of Myc, which… Show more

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Cited by 8 publications
(5 citation statements)
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“…Targeting specific downstream HR effectors has shown promise in chemosensitising CSCs. For example, increased RAD51 mRNA expression is frequently observed in multiple types of CSCs compared to differentiated cancer cells, and inhibition with resveratrol or siRNA knockdown reduces CSC viability [ 141 , 181 , 182 , 183 , 184 ]. Indeed, while BCSCs derived from BRCA1 -mutant TNBC cell lines (SUM149) were resistant to olaparib, knockdown of RAD51 enabled re-sensitisation [ 181 ].…”
Section: Dna Damage Repair In Cscs and Therapeutic Interventionmentioning
confidence: 99%
See 1 more Smart Citation
“…Targeting specific downstream HR effectors has shown promise in chemosensitising CSCs. For example, increased RAD51 mRNA expression is frequently observed in multiple types of CSCs compared to differentiated cancer cells, and inhibition with resveratrol or siRNA knockdown reduces CSC viability [ 141 , 181 , 182 , 183 , 184 ]. Indeed, while BCSCs derived from BRCA1 -mutant TNBC cell lines (SUM149) were resistant to olaparib, knockdown of RAD51 enabled re-sensitisation [ 181 ].…”
Section: Dna Damage Repair In Cscs and Therapeutic Interventionmentioning
confidence: 99%
“…This approach, however, is presumably restricted to BRCA2 wild-type cancer cells. Regarding CSCs, one study has shown that combining RAD51 inhibition and genetic suppression of the PARP1 coactivator SAM68 increased the susceptibility of the BCSC-rich mammosphere cultures to RS, thereby reducing their cell viability [ 184 ]. Overall, these studies exemplify the crucial role of RAD51 recombinase in mediating chemoresistance and maintaining HR activity in CSCs, even in circumstances of BRCA1/2 deficiency.…”
Section: Dna Damage Repair In Cscs and Therapeutic Interventionmentioning
confidence: 99%
“…Notably, Alice et al. ( 103 ) showed that all molecular subtypes of breast cancer contain a subset of anti-therapeutic cells, which express high levels of Myc, Sam68 and Rad51, effectively inhibit cell survival. Analysis of a group of breast cancer patients showed that Sam68 was an independent negative factor associated with disease progression.…”
Section: Sam68mentioning
confidence: 99%
“…Analysis of a group of breast cancer patients showed that Sam68 was an independent negative factor associated with disease progression. Rad51 targeting significantly reduced the activity of Sam68-silenced breast cancer sphere cells (BCSphCs), and SAM68 is necessary as a coactivator of PARP and a synthetic lethal partner of Rad51 ( 103 ). This Sam68-PARP axis can play an important role in controlling the resistance of ER+ cells to endocrine therapy ( Figure 7 ).…”
Section: Sam68mentioning
confidence: 99%
“…Manic and co-workers demonstrated that in colorectal CSCs the treatment with chemotherapeutic agents induces the activation of the DDR players, such as PARP1, RAD51, and/or MRE11, resulting in higher DNA damage repair machinery [ 26 ]. In breast cancer, both BRCA1 wt and BRCA1 mut CSCs were highly resistant to PARP inhibitors, due to the high expression of Rad51 and Sam68, and the inhibition of this critical signaling axis hampered CSC viability [ 27 , 28 ]. In addition, CD133 + glioma CSCs displayed resistance to radiotherapy treatment by the activation of DNA-damage repair mechanisms, where Check-1 and Check-2 are the main players.…”
Section: Cancer Stem Cells: the Main Players In Drug Resistancementioning
confidence: 99%