Tag Archives: EMT

Fibroblast Growth Factor Receptor Facilitates Recurrence of Minimal Residual Disease Following Trastuzumab Emtansine Therapy

Flow cytometric analyses indicated that induction of epithelial-mesenchymal transition decreased trastuzumab binding, prior to overt loss of HER2 expression in trastuzumab-emtansine-resistant (TDM1R) cells. Kinome analyses of TDM1R cells indicated increased phosphorylation of ErbB1, ErbB4, and FGFR1.
[npj Breast Cancer]
Akhand, S. S., Chen, H., Purdy, S. C., Liu, Z., Anderson, J. C., Willey, C. D., & Wendt, M. K. (2021). Fibroblast growth factor receptor facilitates recurrence of minimal residual disease following trastuzumab emtansine therapy. Npj Breast Cancer, 7(1), 1–11. https://doi.org/10.1038/s41523-020-00213-5 Cite
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Downregulation of E-cadherin in Pluripotent Stem Cells Triggers Partial EMT

Using a CRISPR interference system in human ESCs, scientists describe a molecular characterization of the effects of downregulation of E-cadherin, one of the main initiation events of EMT, as a unique start signal.
[Scientific Reports]
Aban, C. E., Lombardi, A., Neiman, G., Biani, M. C., La Greca, A., Waisman, A., Moro, L. N., Sevlever, G., Miriuka, S., & Luzzani, C. (2021). Downregulation of E-cadherin in pluripotent stem cells triggers partial EMT. Scientific Reports, 11(1), 2048. https://doi.org/10.1038/s41598-021-81735-1 Cite
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EEF1A2 Interacts with HSP90AB1 to Promote Lung Adenocarcinoma Metastasis via Enhancing TGF-β/SMAD Signaling

Scientists report that eukaryotic protein translation elongation factor 1α2 (EEF1A2) mediates the epithelial–mesenchymal transformation, to promote the metastasis of lung adenocarcinoma cells in vitro and in vivo.
[British Journal of Cancer]
Jia, L., Ge, X., Du, C., Chen, L., Zhou, Y., Xiong, W., Xiang, J., Li, G., Xiao, G., Fang, L., & Li, Z. (2021). EEF1A2 interacts with HSP90AB1 to promote lung adenocarcinoma metastasis via enhancing TGF-β/SMAD signalling. British Journal of Cancer, 1–11. https://doi.org/10.1038/s41416-020-01250-4 Cite
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Thrombospondin 4/Integrin α2/HSF1 Axis Promotes Proliferation and Cancer Stem-Like Traits of Gallbladder Cancer by Enhancing Reciprocal Crosstalk between Cancer-Associated Fibroblasts and Tumor Cells

Peritumoral fibroblasts and cancer-associated fibroblasts were extracted from gallbladder cancer (GBC) tissues. Thrombospondin expression in GBC was screened by RT-qPCR.
[Journal of Experimental & Clinical Cancer Research]
Shi, Y., Sun, L., Zhang, R., Hu, Y., Wu, Y., Dong, X., Dong, D., Chen, C., Geng, Z., Li, E., & Fan, Y. (2021). Thrombospondin 4/integrin α2/HSF1 axis promotes proliferation and cancer stem-like traits of gallbladder cancer by enhancing reciprocal crosstalk between cancer-associated fibroblasts and tumor cells. Journal of Experimental & Clinical Cancer Research, 40(1), 14. https://doi.org/10.1186/s13046-020-01812-7 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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Regulation of Carcinogenesis and Mediation through Wnt/β-Catenin Signaling by 3,3′-Diindolylmethane in an Enzalutamide-Resistant Prostate Cancer Cell Line

To investigate whether combined treatment with Enzalutamide (ENZ) and 3,3′-diindolylmethane (DIM) could overcome ENZ resistance by regulating Wnt signaling to inhibit androgen receptor signaling and EMT in ENZ-resistant prostate cancer cells, 22Rv1 cells were cultured in normal medium and treated with ENZ, DIM, and DIM with ENZ.
[Scientific Reports]
Tsao, C.-W., Li, J.-S., Lin, Y.-W., Wu, S.-T., Cha, T.-L., & Liu, C.-Y. (2021). Regulation of carcinogenesis and mediation through Wnt/β-catenin signaling by 3,3′-diindolylmethane in an enzalutamide-resistant prostate cancer cell line. Scientific Reports, 11(1), 1239. https://doi.org/10.1038/s41598-020-80519-3 Cite
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Interplay between Desmoglein2 and Hypoxia Controls Metastasis in Breast Cancer

Investigators found that high expression of desmoglein2, a component of desmosome-mediated intercellular adhesion complexes, promoted tumor growth, increased the prevalence of circulating tumor cell clusters, and facilitated distant organ colonization.
[Proceedings of the National Academy of Sciences of the United States of America]
Chang, P.-H., Chen, M.-C., Tsai, Y.-P., Tan, G. Y. T., Hsu, P.-H., Jeng, Y.-M., Tsai, Y.-F., Yang, M.-H., & Hwang-Verslues, W. W. (2021). Interplay between desmoglein2 and hypoxia controls metastasis in breast cancer. Proceedings of the National Academy of Sciences, 118(3). https://doi.org/10.1073/pnas.2014408118 Cite
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Human Umbilical Cord Mesenchymal Stem Cell-Derived Exosomal miR-27b Attenuates Subretinal Fibrosis via Suppressing Epithelial–Mesenchymal Transition by Targeting HOXC6

Human umbilical cord-derived mesenchymal stem cells were successfully cultured and identified, and exosomes were isolated from the supernatant by ultracentrifugation.
[Stem Cell Research & Therapy]
Li, D., Zhang, J., Liu, Z., Gong, Y., & Zheng, Z. (2021). Human umbilical cord mesenchymal stem cell-derived exosomal miR-27b attenuates subretinal fibrosis via suppressing epithelial–mesenchymal transition by targeting HOXC6. Stem Cell Research & Therapy, 12(1), 24. https://doi.org/10.1186/s13287-020-02064-0 Cite
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Zinc Dependent Regulation of ZEB1 and YAP1 Co-Activation Promotes EMT Plasticity and Metastasis in Pancreatic Cancer

Scientists demonstrated that ZIP4 activated ZEB1 and YAP1 through distinct mechanisms. The ZIP4-miR-373-LATS2-ZEB1/YAP1-ITGA3 signaling axis has a significant impact on pancreatic cancer metastasis and EMT plasticity.
[Gastroenterology]
Liu, M., Zhang, Y., Yang, J., Zhan, H., Zhou, Z., Jiang, Y., Shi, X., Fan, X., Zhang, J., Luo, W., Fung, K.-M. A., Xu, C., Bronze, M. S., Houchen, C. W., & Li, M. (2021). Zinc Dependent Regulation of ZEB1 and YAP1 Co-activation Promotes EMT Plasticity and Metastasis in Pancreatic Cancer. Gastroenterology, 0(0). https://doi.org/10.1053/j.gastro.2020.12.077 Cite
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PDLIM2 Prevents the Malignant Phenotype of Hepatocellular Carcinoma Cells by Negatively Regulating β-Catenin

Investigators explored the potential role of PDLIM2 in the development and epithelial-mesenchymal transition of hepatocellular carcinoma via a possible modulation of β-catenin.
[Cancer Gene Therapy]
Jiang, X., Chu, Z., Cao, Y., Tang, Y., Shi, Y., & Shi, X. (2021). PDLIM2 prevents the malignant phenotype of hepatocellular carcinoma cells by negatively regulating β-catenin. Cancer Gene Therapy, 1–12. https://doi.org/10.1038/s41417-020-00257-6 Cite
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Hypoxia-Induced Suppression of Alternative Splicing of MBD2 Promotes Breast Cancer Metastasis via Activation of FZD1

Researchers report that under hypoxic conditions, alternative splicing of MBD2 was suppressed, favoring the production of MBD2a which facilitated breast cancer metastasis.
[Cancer Research]
Liu, Z., Sun, L., Cai, Y., Shen, S., Zhang, T., Wang, N., Wu, G., Ma, W., Li, S.-T., Suo, C., Hao, Y., Jia, W.-D., Semenza, G. L., Gao, P., & Zhang, H. (2021). Hypoxia-induced suppression of alternative splicing of MBD2 promotes breast cancer metastasis via activation of FZD1. Cancer Research. https://doi.org/10.1158/0008-5472.CAN-20-2876 Cite
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