ArticleCancer cell international2014
Differential drug resistance acquisition to doxorubicin and paclitaxel in breast cancer cells.
Article in Cancer cell international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 86 citations in OpenAlex.
- TheInternational journal of molecular sciences · 2021Trial
- Does the Sequence of Anthracycline and Taxane Matter? The NeoSAMBA Trial.The oncologist · 2020Trial
- TGF-β2 promotes autophagy-mediated resistance to doxorubicin in metastatic colon cancer cells via HMGB1.Medical oncology (Northwood, London, England) · 2026Article
- Generating drug resistance models in human and murine cancer cell lines and assessing cross-resistance to chemotherapeutics and KRAS inhibitors.STAR protocols · 2026Article
- Enhancing ferroptosis and inhibiting ABCB1 make the novel aldose reductase inhibitor 5F-E a promising sensitizer in liver cancer.Pharmaceutical science advances · 2025Article
- Pitavastatin is a novel Mcl-1 inhibitor that overcomes paclitaxel resistance in triple-negative breast cancer.Experimental hematology & oncology · 2025Article
- Genes Associated with Apoptosis in an Experimental Breast Cancer Model.International journal of molecular sciences · 2025Article
- Biofabrication of Tunable 3D Hydrogel for Investigating the Matrix Stiffness Impact on Breast Cancer Chemotherapy Resistance.ACS biomaterials science & engineering · 2025Article
- Review
- MiRNA-449 family is epigenetically repressed and sensitizes to doxorubicin through ACSL4 downregulation in triple-negative breast cancer.Cell death discovery · 2024Article
- Doxorubicin-induced chemoresistance in Duke's type B colon adenocarcinoma cell line is aggravated in the presence of TGF-β2 through non-apoptotic cell death.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024Article
- The Potential of Epigallocatechin Gallate in Targeting Cancer Stem Cells: A Comprehensive Review.Current medicinal chemistry · 2024Review
- Pyrazoline B-Paclitaxel or Doxorubicin Combination Drugs Show Synergistic Activity Against Cancer Cells: In silico Study.Advances and applications in bioinformatics and chemistry : AABC · 2024Article
- Cancer stem cells: an insight into the development of metastatic tumors and therapy resistance.Stem cell reviews and reports · 2023Review
- Development of Polymersomes Co-Delivering Doxorubicin and Melittin to Overcome Multidrug Resistance.Molecules (Basel, Switzerland) · 2023Article
- The Prognostic and Therapeutic Implications of the Chemoresistance Gene BIRC5 in Triple-Negative Breast Cancer.Cancers · 2022Article
- GASP1 enhances malignant phenotypes of breast cancer cells and decreases their response to paclitaxel by forming a vicious cycle with IGF1/IGF1R signaling pathway.Cell death & disease · 2022Article
- Article
- Doxorubicin-NO Releaser Molecular Hybrid Activatable by Green Light to Overcome Resistance in Breast Cancer Cells.ACS omega · 2022Article
- Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSeveral signal transduction pathways have been reported being involved in the acquisition of P-glycoprotein (P-gp) mediated multi-drug resistance (MDR) upon exposure to anti-cancer drugs, whereas there is evidence indicating that the expression and activity of P-gp were not equally or even reversely modulated by different drugs.
methodsTo further illustrate this drug-specific effect, possible mechanisms that enable breast cancer cells MCF-7 to acquire MDR to either paclitaxel (PTX) or doxorubicin (DOX) were investigated in a time-dependent manner.
resultsThe results suggested that at least two pathways participated in this process. One was the short and transient activation of NF-κB, the second one was the relatively prolonged induction of PXR. Both PXR and NF-κB pathways took part in the PTX drug resistance acquisition, whereas DOX did not exert a significant effect on the PXR-mediated induction of P-gp. Furthermore, the property of NF-κB activation shared by DOX and PTX was not identical. An attempt made in the present study demonstrated that the acquired resistance to DOX was via or partially via NF-κB activation but not its upstream receptor TLR4, while PTX can induce the drug resistance via TLR4-NF-κB pathway.
conclusionsTo our knowledge, this report is among the first to directly compare the time dependence of NF-κB and PXR pathways. The current study provides useful insight into the distinct ability of DOX and PTX to induce P-gp mediated MDR in breast cancer. Different strategies may be required to circumvent MDR in the presence of different anti-cancer drugs.
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