Autophagy Blockade Limits HER2+ Breast Cancer Tumorigenesis by Perturbing HER2 Trafficking and Promoting Release via Small Extracellular Vesicles

By deleting an essential autophagy gene or disrupting its autophagy function, investigators determined a mechanism of HER2+ breast cancer tumorigenesis by directly regulating the oncogenic driver.
[Developmental Cell]
Hao, M., Yeo, S. K., Turner, K., Harold, A., Yang, Y., Zhang, X., & Guan, J.-L. (2021). Autophagy blockade limits HER2+ breast cancer tumorigenesis by perturbing HER2 trafficking and promoting release via small extracellular vesicles. Developmental Cell, 0(0). https://doi.org/10.1016/j.devcel.2020.12.016 Cite
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A Novel Hypoxic Long Noncoding RNA KB-1980E6.3 Maintains Breast Cancer Stem Cell Stemness via Interacting With IGF2BP1 to Facilitate C-Myc mRNA Stability

The enhanced long noncoding RNA KB-1980E6.3 facilitated breast cancer stem cells self-renewal and tumorigenesis under hypoxic microenvironment both in vitro and in vivo.
[Oncogene]
Zhu, P., He, F., Hou, Y., Tu, G., Li, Q., Jin, T., Zeng, H., Qin, Y., Wan, X., Qiao, Y., Qiu, Y., Teng, Y., & Liu, M. (2021). A novel hypoxic long noncoding RNA KB-1980E6.3 maintains breast cancer stem cell stemness via interacting with IGF2BP1 to facilitate c-Myc mRNA stability. Oncogene, 1–19. https://doi.org/10.1038/s41388-020-01638-9 Cite
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The Androgen Receptor Is a Tumor Suppressor in Estrogen Receptor–Positive Breast Cancer

Using a diverse, clinically relevant panel of cell-line and patient-derived models, the authors demonstrated that androgen receptor activation, not suppression, exerted potent antitumor activity in multiple disease contexts, including resistance to standard-of-care estrogen receptor and CDK4/6 inhibitors.
[Nature Medicine]
Hickey, T. E., Selth, L. A., Chia, K. M., Laven-Law, G., Milioli, H. H., Roden, D., Jindal, S., Hui, M., Finlay-Schultz, J., Ebrahimie, E., Birrell, S. N., Stelloo, S., Iggo, R., Alexandrou, S., Caldon, C. E., Abdel-Fatah, T. M., Ellis, I. O., Zwart, W., Palmieri, C., … Tilley, W. D. (2021). The androgen receptor is a tumor suppressor in estrogen receptor–positive breast cancer. Nature Medicine, 1–11. https://doi.org/10.1038/s41591-020-01168-7 Cite
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MEDAG Enhances Breast Cancer Progression and Reduces Epirubicin Sensitivity through the AKT/AMPK/mTOR Pathway

The authors found that the mesenteric estrogen-dependent adipogenesis gene (MEDAG) was highly expressed in breast cancer (BC) samples and that a high MEDAG expression was correlated with clinicopathological characteristics and poor survival in BC patients.
[Cell Death & Disease]
Li, Z., Li, C., Wu, Q., Tu, Y., Wang, C., Yu, X., Li, B., Wang, Z., Sun, S., & Sun, S. (2021). MEDAG enhances breast cancer progression and reduces epirubicin sensitivity through the AKT/AMPK/mTOR pathway. Cell Death & Disease, 12(1), 1–15. https://doi.org/10.1038/s41419-020-03340-w Cite
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Overexpression of β-Arrestins Inhibits Proliferation and Motility in Triple Negative Breast Cancer Cells

Investigators examined the direct influence of β-arrestins on cellular function and gene expression profiles by changing their expression levels in breast cancer cells, MDA-MB-231 and MDA-MB-468.
[Scientific Reports]
Bostanabad, S. Y., Noyan, S., Dedeoglu, B. G., & Gurdal, H. (2021). Overexpression of β-Arrestins inhibits proliferation and motility in triple negative breast cancer cells. Scientific Reports, 11(1), 1539. https://doi.org/10.1038/s41598-021-80974-6 Cite
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Decorin-Mediated Suppression of Tumorigenesis, Invasion, and Metastasis in Inflammatory Breast Cancer

Overexpression of decorin in inflammatory breast cancer (IBC) cells markedly decreased migration, invasion, and cancer stem cells in vitro and inhibited tumor growth and metastasis in IBC xenograft mouse models.
[Communications Biology]
Hu, X., Villodre, E. S., Larson, R., Rahal, O. M., Wang, X., Gong, Y., Song, J., Krishnamurthy, S., Ueno, N. T., Tripathy, D., Woodward, W. A., & Debeb, B. G. (2021). Decorin-mediated suppression of tumorigenesis, invasion, and metastasis in inflammatory breast cancer. Communications Biology, 4(1), 1–14. https://doi.org/10.1038/s42003-020-01590-0 Cite
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Cathepsin C Promotes Breast Cancer Lung Metastasis by Modulating Neutrophil Infiltration and Neutrophil Extracellular Trap Formation

Scientists showed that tumor-secreted protease cathepsin C promotes breast-to-lung metastasis by regulating recruitment of neutrophils and formation of neutrophil extracellular traps.
[Cancer Cell]
Xiao, Y., Cong, M., Li, J., He, D., Wu, Q., Tian, P., Wang, Y., Yang, S., Liang, C., Liang, Y., Wen, J., Liu, Y., Luo, W., Lv, X., He, Y., Cheng, D., Zhou, T., Zhao, W., Zhang, P., … Hu, G. (2021). Cathepsin C promotes breast cancer lung metastasis by modulating neutrophil infiltration and neutrophil extracellular trap formation. Cancer Cell, 0(0). https://doi.org/10.1016/j.ccell.2020.12.012 Cite
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Multiple Screening Approaches Reveal HDAC6 as a Novel Regulator of Glycolytic Metabolism in Triple-Negative Breast Cancer

Investigators set up a phenotypic small-molecule screen to reveal vulnerabilities in TNBC cells that were independent of mitochondrial apoptosis. Using a functional genetic approach, they identified that a “hit” compound, BAS-2, had a potentially similar mechanism of action to histone deacetylase inhibitors.
[Science Advances]
Dowling, C. M., Hollinshead, K. E. R., Grande, A. D., Pritchard, J., Zhang, H., Dillon, E. T., Haley, K., Papadopoulos, E., Mehta, A. K., Bleach, R., Lindner, A. U., Mooney, B., Düssmann, H., O’Connor, D., Prehn, J. H. M., Wynne, K., Hemann, M., Bradner, J. E., Kimmelman, A. C., … Chonghaile, T. N. (2021). Multiple screening approaches reveal HDAC6 as a novel regulator of glycolytic metabolism in triple-negative breast cancer. Science Advances, 7(3), eabc4897. https://doi.org/10.1126/sciadv.abc4897 Cite
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Prolactin Receptor-Driven Combined Luminal and Epithelial Differentiation in Breast Cancer Restricts Plasticity, Stemness, Tumorigenesis and Metastasis

The authors found that interfering with expression of the receptor for the lactogenic hormone prolactin in breast cancer cells representative of the luminal and epithelial breast cancer subtypes resulted in loss of their differentiation state, enriched for stem-like cell subpopulations, and increased their tumorigenic capacity in a subtype-specific manner.
[Oncogenesis]
Shams, A., Binothman, N., Boudreault, J., Wang, N., Shams, F., Hamam, D., Tian, J., Moamer, A., Dai, M., Lebrun, J.-J., & Ali, S. (2021). Prolactin receptor-driven combined luminal and epithelial differentiation in breast cancer restricts plasticity, stemness, tumorigenesis and metastasis. Oncogenesis, 10(1), 1–16. https://doi.org/10.1038/s41389-020-00297-5 Cite
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S100A8/A9 Mediate the Reprograming of Normal Mammary Epithelial Cells Induced by Dynamic Cell–Cell Interactions With Adjacent Breast Cancer Cells

To understand the potential effects of cancer cells on surrounding normal mammary epithelial cells, researchers performed direct co-culture of non-tumorigenic mammary epithelial MCF10A cells and various breast cancer cells.
[Scientific Reports]
Jo, S. H., Heo, W. H., Son, H.-Y., Quan, M., Hong, B. S., Kim, J. H., Lee, H.-B., Han, W., Park, Y., Lee, D.-S., Kwon, N. H., Park, M. C., Chae, J., Kim, J.-I., Noh, D.-Y., & Moon, H.-G. (2021). S100A8/A9 mediate the reprograming of normal mammary epithelial cells induced by dynamic cell–cell interactions with adjacent breast cancer cells. Scientific Reports, 11(1), 1337. https://doi.org/10.1038/s41598-020-80625-2 Cite
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LncRNA TINCR Favors Tumorigenesis via STAT3–TINCR–EGFR-Feedback Loop by Recruiting DNMT1 and Acting as a Competing Endogenous RNA in Human Breast Cancer

The oncogenic role of TINCR was examined in vitro and in vivo in breast cancer. The interaction between TINCR, DNMT1, and miR-503-5p methylation was explored.
[Cell Death & Disease]
Wang, Q., Liu, J., You, Z., Yin, Y., Liu, L., Kang, Y., Li, S., Ning, S., Li, H., Gong, Y., Xu, S., & Pang, D. (2021). LncRNA TINCR favors tumorigenesis via STAT3–TINCR–EGFR-feedback loop by recruiting DNMT1 and acting as a competing endogenous RNA in human breast cancer. Cell Death & Disease, 12(1), 1–16. https://doi.org/10.1038/s41419-020-03188-0 Cite
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