Metastatic ER+ Breast Cancer: Mechanisms of Resistance and Future Therapeutic Approaches

Raheem, Farah; Karikalan, Suganya Arunachalam; Batalini, Felipe; El Masry, Aya; Mina, Lida

doi:10.3390/ijms242216198

Cited by 18 publications

(8 citation statements)

References 101 publications

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“…Indeed, the choice of hormonal treatment is based on histological type [46]. The administration of VitC at high concentrations could be the cause of an unexpected lack of response to classic hormone therapy [42]. The slowing down of tumor mass growth could be misleading and there could be a late but rapid deterioration due to resistance to hormonal treatment.…”

Section: Discussionmentioning

confidence: 99%

“…Overall, these experiments showed that treatment of MCF7 with a high dose of VitC results in a reduction of tumor cell growth. Moreover, VitC reduces the expression of ER and therefore it is possible that the cells do not respond to antiestrogen therapy as selective estrogen receptor degraders and modulators (tamoxifen) and aromatase inhibitors (anastrazole, letrozole, exemestane) [42].…”

Section: Effect Of Vitamin C On Mcf7 and Mb-231 Cell Phenotypesmentioning

confidence: 99%

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Sphingomyelin Metabolism Modifies Luminal A Breast Cancer Cell Line under a High Dose of Vitamin C

Codini,

Fiorani,

Mandarano

et al. 2023

IJMS

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The role of sphingomyelin metabolism and vitamin C in cancer has been widely described with conflicting results ranging from a total absence of effect to possible preventive and/or protective effects. The aim of this study was to establish the possible involvement of sphingomyelin metabolism in the changes induced by vitamin C in breast cancer cells. The MCF7 cell line reproducing luminal A breast cancer and the MDA-MB-231 cell line reproducing triple-negative breast cancer were used. Cell phenotype was tested by estrogen receptor, progesterone receptor, human epidermal growth factor receptor 2 expression, and proliferation index percentage. Sphingomyelin was localized by an EGFP-NT-Lys fluorescent probe. Sphingomyelin metabolism was analyzed by RT-PCR, Western blotting and UFLC-MS/MS. The results showed that a high dose of vitamin C produced reduced cell viability, modulated cell cycle related genes, and changed the cell phenotype with estrogen receptor downregulation in MCF7 cell. In these cells, the catabolism of sphingomyelin was promoted with a large increase in ceramide content. No changes in viability and molecular expression were observed in MB231 cells. In conclusion, a high dose of vitamin C induces changes in the luminal A cell line involving sphingomyelin metabolism.

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Section: Discussionmentioning

confidence: 99%

Section: Effect Of Vitamin C On Mcf7 and Mb-231 Cell Phenotypesmentioning

confidence: 99%

Sphingomyelin Metabolism Modifies Luminal A Breast Cancer Cell Line under a High Dose of Vitamin C

Codini,

Fiorani,

Mandarano

et al. 2023

IJMS

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“…Breast cancer resistance protein (BCRP or ABCG2) is involved in cancer multidrug resistance and transports anticancer drugs out of cells [ 20 ]. Alterations in the estrogen receptor pathway (e. g., ESR1 mutations) or upstream growth factor signaling pathways (e. g., PI3K/Akt/mTOR pathway) can cause drug resistance in breast cancer patients [ 21 ]. Activation of EMT can also induce breast cancer cells to acquire resistance to chemotherapy [ 22 ].…”

Section: Mechanisms Of Drug Resistance In Breast Cancermentioning

confidence: 99%

Drug resistance in breast cancer is based on the mechanism of exocrine non-coding RNA

Ye,

Chen,

Yang

et al. 2024

Discov Onc

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Breast cancer (BC) ranks first among female malignant tumors and involves hormonal changes and genetic as well as environmental risk factors. In recent years, with the improvement of medical treatment, a variety of therapeutic approaches for breast cancer have emerged and have strengthened to accommodate molecular diversity. However, the primary way to improve the effective treatment of breast cancer patients is to overcome treatment resistance. Recent studies have provided insights into the mechanisms of resistance to exosome effects in BC. Exosomes are membrane-bound vesicles secreted by both healthy and malignant cells that facilitate intercellular communication. Specifically, exosomes released by tumor cells transport their contents to recipient cells, altering their properties and promoting oncogenic components, ultimately resulting in drug resistance. As important coordinators, non-coding RNAs (ncRNAs) are involved in this process and are aberrantly expressed in various human cancers. Exosome-derived ncRNAs, including microRNAs (miRNAs), long-noncoding RNAs (lncRNAs), and circular RNAs (circRNAs), have emerged as crucial components in understanding drug resistance in breast cancer. This review provides insights into the mechanism of exosome-derived ncRNAs in breast cancer drug resistance, thereby suggesting new strategies for the treatment of BC.

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“…Aberrations in components of the MAPK pathway, including NF1, KRAS/NRAS/HRAS, BRAF, and MAP2K1, are often reported in metastatic breast cancer [29,37]. Alterations in these genes may lead to increased or uncontrolled cell proliferation, leading to resistance to endocrine therapy in breast cancer [38].…”

Section: Growth Factor Receptor Pathwaysmentioning

confidence: 99%

Novel Endocrine Therapeutic Opportunities for Estrogen Receptor-Positive Ovarian Cancer—What Can We Learn from Breast Cancer?

Ottenbourgs,

Van Nieuwenhuysen

2024

Cancers

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Low-grade serous ovarian cancer (LGSOC) is a rare ovarian malignancy primarily affecting younger women and is characterized by an indolent growth pattern. It exhibits indolent growth and high estrogen/progesterone receptor expression, suggesting potential responsiveness to endocrine therapy. However, treatment efficacy remains limited due to the development of endocrine resistance. The mechanisms of resistance, whether primary or acquired, are still largely unknown and present a significant hurdle in achieving favorable treatment outcomes with endocrine therapy in these patients. In estrogen receptor-positive breast cancer, mechanisms of endocrine resistance have been largely explored and novel treatment strategies to overcome resistance have emerged. Considering the shared estrogen receptor positivity in LGSOC and breast cancer, we wanted to explore whether there are any parallel mechanisms of resistance and whether we can extend endocrine breast cancer treatments to LGSOC. This review aims to highlight the underlying molecular mechanisms possibly driving endocrine resistance in ovarian cancer, while also exploring the available therapeutic opportunities to overcome this resistance. By unraveling the potential pathways involved and examining emerging strategies, this review explores valuable insights for advancing treatment options and improving patient outcomes in LGSOC, which has limited therapeutic options available.

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Metastatic ER+ Breast Cancer: Mechanisms of Resistance and Future Therapeutic Approaches

Cited by 18 publications

References 101 publications

Sphingomyelin Metabolism Modifies Luminal A Breast Cancer Cell Line under a High Dose of Vitamin C

Sphingomyelin Metabolism Modifies Luminal A Breast Cancer Cell Line under a High Dose of Vitamin C

Drug resistance in breast cancer is based on the mechanism of exocrine non-coding RNA

Novel Endocrine Therapeutic Opportunities for Estrogen Receptor-Positive Ovarian Cancer—What Can We Learn from Breast Cancer?

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