CCL8 Mediates Crosstalk between Endothelial Colony Forming Cells and Triple-Negative Breast Cancer Cells through IL-8, Aggravating Invasion and Tumorigenicity

Using an indirect co-culture system, scientists showed that co-culture increased the invasive and migratory phenotypes of both MDA-MB-231 TNBC cells and endothelial colony-forming cells.
[Oncogene]
CCL8 mediates crosstalk between endothelial colony forming cells and triple-negative breast cancer cells through IL-8, aggravating invasion and tumorigenicity | Oncogene. (n.d.). Retrieved April 8, 2021, from https://www.nature.com/articles/s41388-021-01758-w Cite
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FDA Approves Trodelvy® the First Treatment for Metastatic Triple-Negative Breast Cancer Shown to Improve Progression-Free Survival and Overall Survival

Gilead Sciences, Inc. announced that the FDA has granted full approval to Trodelvy® for adult patients with unresectable locally advanced or metastatic TNBC who have received two or more prior systemic therapies, at least one of them for metastatic disease.
[Gilead Sciences, Inc.]
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MCPIP1-Mediated NFIC Alternative Splicing Inhibits Proliferation of Triple-Negative Breast Cancer via Cyclin D1-RB-E2F1 Axis

Investigators showed that monocyte chemotactic protein induced protein 1 (MCPIP1) was downregulated in 80 TNBC tissues and five TNBC cell lines compared to adjacent paracancerous tissues and one human immortalized breast epithelial cell line, while its high expression levels were associated with increased overall survival in TNBC patients.
[Cell Death & Disease]
Chen, F., Wang, Q., Yu, X., Yang, N., Wang, Y., Zeng, Y., Zheng, Z., Zhou, F., & Zhou, Y. (2021). MCPIP1-mediated NFIC alternative splicing inhibits proliferation of triple-negative breast cancer via cyclin D1-Rb-E2F1 axis. Cell Death & Disease, 12(4), 1–16. https://doi.org/10.1038/s41419-021-03661-4 Cite
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Targeting Nucleotide Metabolism Enhances the Efficacy of Anthracyclines and Anti-Metabolites in Triple-Negative Breast Cancer

Deoxyuridine 5′-triphosphate nucleotidohydrolase inhibition significantly sensitized TNBC cell lines to fluoropyrimidines and anthracyclines through imbalanced nucleotide pools and increased DNA damage leading to decreased proliferation and increased cell death.
[npj Breast Cancer]
Davison, C., Morelli, R., Knowlson, C., McKechnie, M., Carson, R., Stachtea, X., McLaughlin, K. A., Prise, V. E., Savage, K., Wilson, R. H., Mulligan, K. A., Wilson, P. M., Ladner, R. D., & LaBonte, M. J. (2021). Targeting nucleotide metabolism enhances the efficacy of anthracyclines and anti-metabolites in triple-negative breast cancer. Npj Breast Cancer, 7(1), 1–13. https://doi.org/10.1038/s41523-021-00245-5 Cite
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Nectin-4 and p95-ErbB2 Cooperatively Regulate Hippo Signaling-Dependent SOX2 Gene Expression, Enhancing Anchorage-Independent T47D Cell Proliferation

The authors found that nectin-4 and p95-ErbB2, but not nectin-4 and either ErbB2 or ErbB2∆Ex16, cooperatively enhanced SOX2 gene expression and cell proliferation in a suspension culture.
[Scientific Reports]
Kedashiro, S., Kameyama, T., Mizutani, K., & Takai, Y. (2021). Nectin-4 and p95-ErbB2 cooperatively regulate Hippo signaling-dependent SOX2 gene expression, enhancing anchorage-independent T47D cell proliferation. Scientific Reports, 11(1), 7344. https://doi.org/10.1038/s41598-021-86437-2 Cite
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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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The Modulation of PD-L1 Induced by the Oncogenic HBXIP for Breast Cancer Growth

The mechanisms of controlling programmed death ligand-1 (PD-L1) at the transcription and protein acetylation levels in promoting breast cancer growth are presented. Overexpressed PD-L1 accelerated breast cancer growth in vitro and in vivo.
[Acta Pharmacologica Sinica]
Xu, F., Sun, H., Fang, R., Zhang, L., Shi, H., Wang, X., Fu, X., Li, X., Shi, X., Wu, Y., Ye, K., Zhang, W., & Ye, L. (2021). The modulation of PD-L1 induced by the oncogenic HBXIP for breast cancer growth. Acta Pharmacologica Sinica, 1–17. https://doi.org/10.1038/s41401-021-00631-6 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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Epigenetic Remodeling Hydrogel Patches for Multidrug‐Resistant Triple‐Negative Breast Cancer

A tumor‐microenvironment‐responsive hydrogel patch was designed to modulate the plasticity of tumor‐initiating cells in triple‐negative breast cancer, which is insensitive to hormone‐ and HER2‐targeting.
[Advanced Materials]
Ji, X., Guo, D., Ma, J., Yin, M., Yu, Y., Liu, C., Zhou, Y., Sun, J., Li, Q., Chen, N., Fan, C., & Song, H. (n.d.). Epigenetic Remodeling Hydrogel Patches for Multidrug-Resistant Triple-Negative Breast Cancer. Advanced Materials, n/a(n/a), 2100949. https://doi.org/https://doi.org/10.1002/adma.202100949 Cite
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Breast Cancer as an Example of Tumor Heterogeneity and Tumor Cell Plasticity during Malignant Progression

Investigators used breast cancer as an example of the origins of tumor heterogeneity and of tumor cell plasticity, as well as considering interclonal cooperativity and cell plasticity as sources of cancer cell heterogeneity.
[British Journal of Cancer]
Lüönd, F., Tiede, S., & Christofori, G. (2021). Breast cancer as an example of tumour heterogeneity and tumour cell plasticity during malignant progression. British Journal of Cancer, 1–12. https://doi.org/10.1038/s41416-021-01328-7 Cite
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