Mechanisms for Breast Cancer Cell Resistance to Doxorubicin and Solutions to Resistance and Side Effects

2000 ◽  
Author(s):  
Tad H. Koch
Keyword(s):  
Breast Cancer ◽  
Side Effects ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cell Resistance ◽  
Resistance To Doxorubicin

scholarly journals ZRANB2 and SYF2-mediated splicing programs converging on ECT2 are involved in breast cancer cell resistance to doxorubicin

2020 ◽  
Vol 48 (5) ◽  
pp. 2676-2693 ◽  
Author(s):  
Iris Tanaka ◽  
Alina Chakraborty ◽  
Olivier Saulnier ◽  
Clara Benoit-Pilven ◽  
Sophie Vacher ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Messenger Rna ◽  
Splicing Factors ◽  
Cell Resistance ◽  
Regulatory Pathways ◽  
Doxorubicin Resistance ◽  
Resistance To Doxorubicin ◽  
Resistant Cells

Abstract Besides analyses of specific alternative splicing (AS) variants, little is known about AS regulatory pathways and programs involved in anticancer drug resistance. Doxorubicin is widely used in breast cancer chemotherapy. Here, we identified 1723 AS events and 41 splicing factors regulated in a breast cancer cell model of acquired resistance to doxorubicin. An RNAi screen on splicing factors identified the little studied ZRANB2 and SYF2, whose depletion partially reversed doxorubicin resistance. By RNAi and RNA-seq in resistant cells, we found that the AS programs controlled by ZRANB2 and SYF2 were enriched in resistance-associated AS events, and converged on the ECT2 splice variant including exon 5 (ECT2-Ex5+). Both ZRANB2 and SYF2 were found associated with ECT2 pre-messenger RNA, and ECT2-Ex5+ isoform depletion reduced doxorubicin resistance. Following doxorubicin treatment, resistant cells accumulated in S phase, which partially depended on ZRANB2, SYF2 and the ECT2-Ex5+ isoform. Finally, doxorubicin combination with an oligonucleotide inhibiting ECT2-Ex5 inclusion reduced doxorubicin-resistant tumor growth in mouse xenografts, and high ECT2-Ex5 inclusion levels were associated with bad prognosis in breast cancer treated with chemotherapy. Altogether, our data identify AS programs controlled by ZRANB2 and SYF2 and converging on ECT2, that participate to breast cancer cell resistance to doxorubicin.

Cancer cell bioenergetics and pH regulation influence breast cancer cell resistance to paclitaxel and doxorubicin

2013 ◽  
Vol 45 (5) ◽  
pp. 467-475 ◽  
Author(s):  
Diana Tavares-Valente ◽  
Fátima Baltazar ◽  
Roxana Moreira ◽  
Odília Queirós
Keyword(s):  
Breast Cancer ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Ph Regulation ◽  
Cell Resistance

scholarly journals Quercetin Enhances the Suppressive Effects of Doxorubicin on the Migration of MDA-MB-231 Breast Cancer Cell Line

2021 ◽  
Vol 14 (11) ◽  
Author(s):  
Mohammadreza Roshanazadeh ◽  
Hossein Babaahmadi Rezaei ◽  
Mojtaba Rashidi
Keyword(s):  
Breast Cancer ◽  
Side Effects ◽  
Cancer Cells ◽  
Cell Line ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Cancer Cell Line ◽  
Cancer Cell Line ◽  
Anticancer Activities ◽  
And Migration

Background: Cancer cell metastasis is facilitated by matrix-metalloproteinases through degradation of extracellular matrix (ECM) proteins and is a major cause of mortality. One of the most common remedies for cancer is chemotherapy, which has many side effects. Therefore, it seems necessary to find a way to reduce the side effects of these drugs while maintaining their anticancer effects. Quercetin (que) is a natural substance that has been reported to have anticancer activities. Objectives: This study aims at evaluating the effect of que in combination with doxorubicin (dox) on the migration of the MDA-MB-231 breast cancer cell line. Methods: The effects of que and dox on cell viability in 24h and 48 h was assessed by MTT assay. Also, the effects of the same drugs on the cancer cells migration were evaluated, using the wound healing assay. Lastly, the effects of que and dox were assessed on the expression of MMP-2 and MMP-9 genes. Results: The combination of 50 µM of que with 32 nM of dox was selected by CI comparison. The viability and migration of cancer cells and the gelatinases genes expression were decreased after treatment with individual drugs. The migration and the expression of MMP-2 and MMP-9 genes after treatment with the combination of que and dox was significantly reduced compared to the treatment with que and dox alone. Conclusions: Que inhibits the viability and migration of MDA-MB-231 cancer cells and synergistically enhances the effects of dox on the survival and migration of these cells. Hence, we propose this drug combination as a path for further research on breast cancer therapy.

scholarly journals Coupling to a cancer-selective heparan-sulfate-targeted branched peptide can by-pass breast cancer cell resistance to methotrexate

Oncotarget ◽  
2017 ◽  
Vol 8 (44) ◽  
pp. 76141-76152 ◽  
Author(s):  
Lorenzo Depau ◽  
Jlenia Brunetti ◽  
Chiara Falciani ◽  
Silvia Scali ◽  
Giulia Riolo ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Heparan Sulfate ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cell Resistance
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