Metabolic Modulation by CDK4/6 Inhibitor Promotes Chemokine-Mediated Recruitment of T Cells Into Mammary Tumors

Investigators showed that cyclin-dependent kinases 4 and 6 (CDK4/6i) could enhance efficacy of T cell-based therapies, such as adoptive T cell transfer or T cell-activating antibodies anti-OX40/anti-4-1BB, in murine breast cancer models.
[Cell Reports]
Uzhachenko, R. V., Bharti, V., Ouyang, Z., Blevins, A., Mont, S., Saleh, N., Lawrence, H. A., Shen, C., Chen, S.-C., Ayers, G. D., DeNardo, D. G., Arteaga, C., Richmond, A., & Vilgelm, A. E. (2021). Metabolic modulation by CDK4/6 inhibitor promotes chemokine-mediated recruitment of T cells into mammary tumors. Cell Reports, 35(1). https://doi.org/10.1016/j.celrep.2021.108944 Cite
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KDM3B-ETF1 Fusion Gene Downregulates LMO2 via the WNT/β-Catenin Signaling Pathway, Promoting Metastasis of Invasive Ductal Carcinoma

Scientists investigated the possible effects KDM3B-ETF1 fusion gene had on breast cancer cell metastasis, invasion and its downstream signaling mediators as revealed from RNA sequence data analysis.
[Cancer Gene Therapy]
Hu, A., Hong, F., Li, D., Xie, Q., Chen, K., Zhu, L., & He, H. (2021). KDM3B-ETF1 fusion gene downregulates LMO2 via the WNT/β-catenin signaling pathway, promoting metastasis of invasive ductal carcinoma. Cancer Gene Therapy, 1–10. https://doi.org/10.1038/s41417-021-00301-z Cite
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Proton Pump Inhibitors Suppress DNA Damage Repair and Sensitize Treatment Resistance in Breast Cancer by Targeting Fatty Acid Synthase

Researchers showed that the FDA-approved proton pump inhibitors effectively inhibited fatty acid synthase and suppressed breast cancer cell survival.
[Cancer Letters]
Wang, C. J., Li, D., Danielson, J. A., Zhang, E. H., Dong, Z., Miller, K. D., Li, L., Zhang, J.-T., & Liu, J.-Y. (2021). Proton pump inhibitors suppress DNA damage repair and sensitize treatment resistance in breast cancer by targeting fatty acid synthase. Cancer Letters. https://doi.org/10.1016/j.canlet.2021.03.026 Cite
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Antibody–Drug Nanoparticle Induces Synergistic Treatment Efficacies in HER2 Positive Breast Cancer Cells

Antibody–drug nanoparticles were engineered by synthesizing pure anti-cancer drug nanorods in the core of nanoparticles with a therapeutic monoclonal antibody, Trastuzumab on the surface of NRs for specific targeting and synergistic treatments of human epidermal growth factor receptor 2 positive breast cancer cells.
[Scientific Reports]
Abedin, M. R., Powers, K., Aiardo, R., Barua, D., & Barua, S. (2021). Antibody–drug nanoparticle induces synergistic treatment efficacies in HER2 positive breast cancer cells. Scientific Reports, 11(1), 7347. https://doi.org/10.1038/s41598-021-86762-6 Cite
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Breast Cancer Dependence on MCL-1 Is Due to Its Canonical Anti-apoptotic Function

Scientists investigated the role of MCL-1 in clinically relevant breast cancer models and address whether the canonical role of MCL-1 in apoptosis, which can be targeted using BH3-mimetic drugs, is the major function for MCL-1 in breast cancer.
[Cell Death & Differentiation]
Campbell, K. J., Mason, S. M., Winder, M. L., Willemsen, R. B. E., Cloix, C., Lawson, H., Rooney, N., Dhayade, S., Sims, A. H., Blyth, K., & Tait, S. W. G. (2021). Breast cancer dependence on MCL-1 is due to its canonical anti-apoptotic function. Cell Death & Differentiation, 1–12. https://doi.org/10.1038/s41418-021-00773-4 Cite
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MiR-142-3p Targets HMGA2 and Suppresses Breast Cancer Malignanc

The authors demonstrated that the miRNA miR-142-3p directly targeted the 3′ untranslated region of HMGA2, which encoded an onco-embryonic protein that was overexpressed in most cancers, including breast cancer.
[Life Sciences]
Mansoori, B., Duijf, P. H. G., Mohammadi, A., Safarzadeh, E., Ditzel, H. J., Gjerstorff, M. F., Cho, W. C.-S., & Baradaran, B. (2021). MiR-142-3p targets HMGA2 and suppresses breast cancer malignancy. Life Sciences, 119431. https://doi.org/10.1016/j.lfs.2021.119431 Cite
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RANK Signaling Increases after Anti-HER2 Therapy Contributing to the Emergence of Resistance in HER2-Positive Breast Cancer

Scientists showed that RANK bound to HER2 in breast cancer cells and that enhanced RANK pathway activation altered HER2 phosphorylation status.
[Breast Cancer Research]
Sanz-Moreno, A., Palomeras, S., Pedersen, K., Morancho, B., Pascual, T., Galván, P., Benítez, S., Gomez-Miragaya, J., Ciscar, M., Jimenez, M., Pernas, S., Petit, A., Soler-Monsó, M. T., Viñas, G., Alsaleem, M., Rakha, E. A., Green, A. R., Santamaria, P. G., Mulder, C., … Gonzalez-Suarez, E. (2021). RANK signaling increases after anti-HER2 therapy contributing to the emergence of resistance in HER2-positive breast cancer. Breast Cancer Research, 23(1), 42. https://doi.org/10.1186/s13058-021-01390-2 Cite
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Anti-Estrogenic and Anti-Aromatase Activities of Citrus Peels Major Compounds in Breast Cancer

The authors investigated the antitumor potential of the most potent compounds in citrus peels on breast cancer by exploring their anti-estrogenic and anti-aromatase activities.
[Scientific Reports]
El-Kersh, D. M., Ezzat, S. M., Salama, M. M., Mahrous, E. A., Attia, Y. M., Ahmed, M. S., & Elmazar, M. M. (2021). Anti-estrogenic and anti-aromatase activities of citrus peels major compounds in breast cancer. Scientific Reports, 11(1), 7121. https://doi.org/10.1038/s41598-021-86599-z Cite
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The Deubiquitinating Enzyme USP15 Stabilizes ERα and Promotes Breast Cancer Progression

By exploring the regulatory mechanisms of estrogen receptor α (ERα) at levels of post-translational modifications, investigators identified the deubiquitinase USP15 as a novel protector for preventing ERα degradation and a critical driver for breast cancer progression.
[Cell Death & Disease]
Xia, X., Huang, C., Liao, Y., Liu, Y., He, J., Shao, Z., Hu, T., Yu, C., Jiang, L., Liu, J., & Huang, H. (2021). The deubiquitinating enzyme USP15 stabilizes ERα and promotes breast cancer progression. Cell Death & Disease, 12(4), 1–15. https://doi.org/10.1038/s41419-021-03607-w Cite
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Oleandrin, a Cardiac Glycoside, Induces Immunogenic Cell Death via the PERK/elF2α/ATF4/CHOP Pathway in Breast Cancer

Researchers showed that oleandrin treatment triggered breast cancer cell immunogenic cell death by inducing calreticulin exposure on cell surface and the release of high-mobility group protein B1, heat shock protein 70/90, and adenosine triphosphate.
[Cell Death & Disease]
Li, X., Zheng, J., Chen, S., Meng, F., Ning, J., & Sun, S. (2021). Oleandrin, a cardiac glycoside, induces immunogenic cell death via the PERK/elF2α/ATF4/CHOP pathway in breast cancer. Cell Death & Disease, 12(4), 1–15. https://doi.org/10.1038/s41419-021-03605-y Cite
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Acetylation of ELF5 Suppresses Breast Cancer Progression by Promoting Its Degradation and Targeting CCND1

Investigators identified a list of p300-interacting proteins in human breast cancer cells. Among these, E74-like ETS transcription factor 5 (ELF5) was found to interact with p300 via acetylation, and the potential acetylation sites were identified.
[npj Precision Oncology]
Li, X., Li, S., Li, B., Li, Y., Aman, S., Xia, K., Yang, Y., Ahmad, B., & Wu, H. (2021). Acetylation of ELF5 suppresses breast cancer progression by promoting its degradation and targeting CCND1. Npj Precision Oncology, 5(1), 1–15. https://doi.org/10.1038/s41698-021-00158-3 Cite
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