Impact, mechanisms, and novel chemotherapy strategies for overcoming resistance to anthracyclines and taxanes in metastatic breast cancer

Perez, Edith A.

doi:10.1007/s10549-008-0005-6

Cited by 93 publications

(62 citation statements)

References 56 publications

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“…Chemotherapy is a standard treatment option for patients with cancers. However, resistance to chemotherapy is a major problem in the management of breast cancer (Perez 2009). Therefore, the development of novel effective agents that can suppress breast cancer growth is urgent and necessary to improve clinical outcome of patients.…”

Section: Introductionmentioning

confidence: 99%

Gambogenic Acid Induction of Apoptosis in a Breast Cancer Cell Line

Zhou¹,

Luo²,

Wang³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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Background: Gambogenic acid is a major active compound of gamboge which exudes from the Garcinia hanburyi tree. Gambogenic acid anti-cancer activity in vitro has been reported in several studies, including an A549 nude mouse model. However, the mechanisms of action remain unclear. Methods: We used nude mouse models to detect the effect of gambogenic acid on breast tumors, analyzing expression of apoptosis-related proteins in vivo by Western blotting. Effects on cell proliferation, apoptosis and apoptosis-related proteins in MDA-MB-231 cells were detected by MTT, flow cytometry and Western blotting. Inhibitors of caspase-3,-8,-9 were also used to detect effects on caspase family members. Results: We found that gambogenic acid suppressed breast tumor growth in vivo, in association with increased expression of Fas and cleaved caspase-3,-8,-9 and bax, as well as decrease in the anti-apoptotic protein bcl-2. Gambogenic acid inhibited cell proliferation and induced cell apoptosis in a concentration-dependent manner. Conclusion: Our observations suggested that Gambogenic acid suppressed breast cancer MDA-MB-231 cell growth by mediating apoptosis through death receptor and mitochondrial pathways in vivo and in vitro.

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Section: Introductionmentioning

confidence: 99%

Gambogenic Acid Induction of Apoptosis in a Breast Cancer Cell Line

Zhou¹,

Luo²,

Wang³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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“…More importantly, MDR can occur after repeated exposure to chemotherapeutic agents. In the drug-resistant cells, ATPbinding cassette proteins can actively translocate a variety of structurally different substrates outside the cell membrane utilizing the energy from ATP hydrolysis, 6 leading to accelerated drug efflux and decreased net drug accumulation in tumor. 32 It is, generally, believed that upregulation of the drug transporter proteins in the cell membrane is responsible for the increased efflux.…”

Section: Discussionmentioning

confidence: 99%

“…MDR has become a major obstacle in the treatment of breast cancer, where prolonged exposure to one type of chemotherapeutic agent can lead to the resistance to not only that drug but also many other anticancer compounds of different structure and mechanism of action. 6 Furthermore, most anticancer compounds have severe side effects to healthy tissues if delivered systemically.…”

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confidence: 99%

Targeted multidrug delivery system to overcome chemoresistance in breast cancer

Tang

Soroush

Tong

et al. 2017

IJN

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Chemotherapy has been widely used in breast cancer patients to reduce tumor size. However, most anticancer agents cannot differentiate between cancerous and normal cells, resulting in severe systemic toxicity. In addition, acquired drug resistance during the chemotherapy treatment further decreases treatment efficacy. With the proper treatment strategy, nanodrug carriers, such as liposomes/immunoliposomes, may be able to reduce undesired side effects of chemotherapy, to overcome the acquired multidrug resistance, and to further improve the treatment efficacy. In this study, a novel combinational targeted drug delivery system was developed by encapsulating antiangiogenesis drug bevacizumab into liposomes and encapsulating chemotherapy drug doxorubicin (DOX) into immunoliposomes where the human epidermal growth factor receptor 2 (HER2) antibody was used as a targeting ligand. This novel combinational system was tested in vitro using a HER2 positive and multidrug resistant breast cancer cell line (BT-474/MDR), and in vivo using a xenograft mouse tumor model. In vitro cell culture experiments show that immunoliposome delivery led to a high cell nucleus accumulation of DOX, whereas free DOX was observed mostly near the cell membrane and in cytoplasm due to the action of P-gp. Combining liposomal bevacizumab with immunoliposomal DOX achieved the best tumor growth inhibition and the lowest toxicity. Tumor size decreased steadily within a 60-day observation period indicating a potential synergistic effect between DOX and bevacizumab through the targeted delivery. Our findings clearly indicate that tumor growth was significantly delayed in the combinational liposomal drug delivery group. This novel combinational therapy has great potential for the treatment of patients with HER2/MDR double positive breast cancer.

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“…1 Many patients with advanced disease become refractory to conventional chemotherapeutic agents, resulting in recurrence and resistance to the treatment. [2][3][4] Cisplatin and its analogues are chemotherapeutic drugs used widely in cancer treatment. Cisplatin can form interstrand crosslinks (ICL), which stall the progression of replication forks during DNA replication.…”

Section: Introductionmentioning

confidence: 99%

Feedback regulation of methyl methanesulfonate and ultraviolet-sensitive gene clone 81 via ATM/Chk2 pathway contributes to the resistance of MCF-7 breast cancer cells to cisplatin

Qian

et al. 2017

Tumour Biol.

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The methyl methanesulfonate and ultraviolet-sensitive gene clone 81 protein is a structure-specific nuclease that plays important roles in DNA replication and repair. Knockdown of methyl methanesulfonate and ultraviolet-sensitive gene clone 81 has been found to sensitize cancer cells to chemotherapy. However, the underlying molecular mechanism is not well understood. We found that methyl methanesulfonate and ultraviolet-sensitive gene clone 81 was upregulated and the ATM/Chk2 pathway was activated at the same time when MCF-7 cells were treated with cisplatin. By using lentivirus targeting methyl methanesulfonate and ultraviolet-sensitive gene clone 81 gene, we showed that knockdown of methyl methanesulfonate and ultraviolet-sensitive gene clone 81 enhanced cell apoptosis and inhibited cell proliferation in MCF-7 cells under cisplatin treatment. Abrogation of ATM/Chk2 pathway inhibited cell viability in MCF-7 cells in response to cisplatin. Importantly, we revealed that ATM/Chk2 was required for the upregulation of methyl methanesulfonate and ultraviolet-sensitive gene clone 81, and knockdown of methyl methanesulfonate and ultraviolet-sensitive gene clone 81 resulted in inactivation of ATM/Chk2 pathway in response to cisplatin. Meanwhile, knockdown of methyl methanesulfonate and ultraviolet-sensitive gene clone 81 activated the p53/Bcl-2 pathway in response to cisplatin. These data suggest that the ATM/Chk2 may promote the repair of DNA damage caused by cisplatin by sustaining methyl methanesulfonate and ultraviolet-sensitive gene clone 81, and the double-strand breaks generated by methyl methanesulfonate and ultravioletsensitive gene clone 81 may activate the ATM/Chk2 pathway in turn, which provide a novel mechanism of how methyl methanesulfonate and ultraviolet-sensitive gene clone 81 modulates DNA damage response and repair.

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Impact, mechanisms, and novel chemotherapy strategies for overcoming resistance to anthracyclines and taxanes in metastatic breast cancer

Cited by 93 publications

References 56 publications

Gambogenic Acid Induction of Apoptosis in a Breast Cancer Cell Line

Gambogenic Acid Induction of Apoptosis in a Breast Cancer Cell Line

Targeted multidrug delivery system to overcome chemoresistance in breast cancer

Feedback regulation of methyl methanesulfonate and ultraviolet-sensitive gene clone 81 via ATM/Chk2 pathway contributes to the resistance of MCF-7 breast cancer cells to cisplatin

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