Alpha-Enolase (ENO1), Identified as an Antigen to Monoclonal Antibody 12C7, Promotes the Self-Renewal and Malignant Phenotype of Lung Cancer Stem Cells by AMPK/mTOR Pathway

Immunofluorescence was used for antigen localization. After targeted antigen purification by electrophoresis and immunoblot, the antigen was identified by LC-MALDI-TOF/TOF mass spectrometry, immunofluorescence, and immunoprecipitation.
[Stem Cell Research & Therapy]
Shu, X., Cao, K.-Y., Liu, H.-Q., Yu, L., Sun, L.-X., Yang, Z.-H., Wu, C.-A., & Ran, Y.-L. (2021). Alpha-enolase (ENO1), identified as an antigen to monoclonal antibody 12C7, promotes the self-renewal and malignant phenotype of lung cancer stem cells by AMPK/mTOR pathway. Stem Cell Research & Therapy, 12(1), 119. https://doi.org/10.1186/s13287-021-02160-9 Cite
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Regulatory T Cells Promote Glioma Cell Stemness through TGF-β–NF-κB–IL6–STAT3 Signaling

Mechanistic investigations indicated that TGF-β acted on cancer cells to induce the core cancer stem cell-related genes CD133, SOX2, NESTIN, MUSASHI1 and ALDH1A expression and spheres formation via NF-κB–IL6–STAT3 signaling pathway, resulting in the increased cancer stemness and tumorigenic potential.
[Cancer Immunology Immunotherapy]
Regulatory T cells promote glioma cell stemness through TGF-β–NF-κB–IL6–STAT3 signaling | SpringerLink. (n.d.). Retrieved February 17, 2021, from https://link.springer.com/article/10.1007%2Fs00262-021-02872-0 Cite
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Phosphorylation of the Proline-Rich Domain of WAVE3 Drives Its Oncogenic Activity in Breast Cancer

Researchers showed that phosphorylation of WAVE3 proline rich domain was essential for migration and invasion of breast cancer cells in vitro, as well as tumor growth and metastasis in vivo.
[Scientific Reports]
Kansakar, U., Wang, W., Markovic, V., & Sossey-Alaoui, K. (2021). Phosphorylation of the proline-rich domain of WAVE3 drives its oncogenic activity in breast cancer. Scientific Reports, 11(1), 3868. https://doi.org/10.1038/s41598-021-83479-4 Cite
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Targeting Cancer Stem Cells for Reversing Therapy Resistance: Mechanism, Signaling, and Prospective Agents

Researchers review the identification of CSCs, the intrinsic and extrinsic mechanisms of therapy resistance in CSCs, the signaling pathways of CSCs that mediate treatment failure, and potential CSC-targeting agents in various tumors from the clinical perspective.
[Signal Transduction and Targeted Therapy]
Zhou, H.-M., Zhang, J.-G., Zhang, X., & Li, Q. (2021). Targeting cancer stem cells for reversing therapy resistance: mechanism, signaling, and prospective agents. Signal Transduction and Targeted Therapy, 6(1), 1–17. https://doi.org/10.1038/s41392-020-00430-1 Cite
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PRMT5 Inhibition Disrupts Splicing and Stemness in Glioblastoma

Using two orthogonal-acting inhibitors of PRMT5, researchers showed that pharmacological inhibition of PRMT5 suppressed the growth of a cohort of 46 patient-derived glioblastoma stem cell cultures, with the proneural subtype showing greater sensitivity.
[Nature Communications]
Sachamitr, P., Ho, J. C., Ciamponi, F. E., Ba-Alawi, W., Coutinho, F. J., Guilhamon, P., Kushida, M. M., Cavalli, F. M. G., Lee, L., Rastegar, N., Vu, V., Sánchez-Osuna, M., Coulombe-Huntington, J., Kanshin, E., Whetstone, H., Durand, M., Thibault, P., Hart, K., Mangos, M., … Dirks, P. B. (2021). PRMT5 inhibition disrupts splicing and stemness in glioblastoma. Nature Communications, 12(1), 979. https://doi.org/10.1038/s41467-021-21204-5 Cite
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YAP and β-Catenin Cooperate to Drive Oncogenesis in Basal Breast Cancer

Scientists showed that the receptor tyrosine kinase Met promoted YAP activity in basal-like breast cancer and found enhanced YAP activity within the cancer stem cell population.
[Cancer Research]
Quinn, H. M., Vogel, R., Popp, O., Mertins, P., Lan, L., Messerschmidt, C., Landshammer, A., Lisek, K., Chateau-Joubert, S., Marangoni, E., Koren, E., Fuchs, Y., & Birchmeier, W. (2021). YAP and β-catenin cooperate to drive oncogenesis in basal breast cancer. Cancer Research. https://doi.org/10.1158/0008-5472.CAN-20-2801 Cite
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Gel-Free 3D Tumoroids with Stem Cell Properties Modeling Drug Resistance to Cisplatin and Imatinib in Metastatic Colorectal Cancer

Researchers investigatef whether Cisplatin, Imatinib, and 5-Fluorouracil alter the tumoroid growth of metastatic colorectal cancer.
[Cells]
Sogawa, C., Eguchi, T., Namba, Y., Okusha, Y., Aoyama, E., Ohyama, K., & Okamoto, K. (2021). Gel-Free 3D Tumoroids with Stem Cell Properties Modeling Drug Resistance to Cisplatin and Imatinib in Metastatic Colorectal Cancer. Cells, 10(2), 344. https://doi.org/10.3390/cells10020344 Cite
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Focal Adhesion Kinase Fine Tunes Multifaced Signals toward Breast Cancer Progression

Investigators recapitulate the multifaceted action exerted by focal adhesion kinase and its prognostic significance in breast cancer.
[Cancers]
Rigiracciolo, D. C., Cirillo, F., Talia, M., Muglia, L., Gutkind, J. S., Maggiolini, M., & Lappano, R. (2021). Focal Adhesion Kinase Fine Tunes Multifaced Signals toward Breast Cancer Progression. Cancers, 13(4), 645. https://doi.org/10.3390/cancers13040645 Cite
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Portrait of Cancer Stem Cells on Colorectal Cancer: Molecular Biomarkers, Signaling Pathways and miRNAome

Investigators summarize the epigenetic findings linked to miRNAome in the maintenance and regulation of colorectal cancer stem cells (CCSCs), including their relationships with different signaling pathways, which should help to identify specific diagnostic, prognostic, and predictive biomarkers for CRC, but also develop innovative CCSCs-targeted therapies.
[International Journal of Molecular Sciences]
Angius, A., Scanu, A. M., Arru, C., Muroni, M. R., Rallo, V., Deiana, G., Ninniri, M. C., Carru, C., Porcu, A., Pira, G., Uva, P., Cossu-Rocca, P., & De Miglio, M. R. (2021). Portrait of Cancer Stem Cells on Colorectal Cancer: Molecular Biomarkers, Signaling Pathways and miRNAome. International Journal of Molecular Sciences, 22(4), 1603. https://doi.org/10.3390/ijms22041603 Cite
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Control of Replication Stress and Mitosis in Colorectal Cancer Stem Cells through the Interplay of PARP1, MRE11 and RAD51

Researchers showed that the replication stress response was efficient in primary CSCs from colorectal cancer, and described unique roles for PARP1 and MRE11/RAD51.
[Cell Death & Differentiation]
Manic, G., Musella, M., Corradi, F., Sistigu, A., Vitale, S., Soliman Abdel Rehim, S., Mattiello, L., Malacaria, E., Galassi, C., Signore, M., Pallocca, M., Scalera, S., Goeman, F., De Nicola, F., Guarracino, A., Pennisi, R., Antonangeli, F., Sperati, F., Baiocchi, M., … Vitale, I. (2021). Control of replication stress and mitosis in colorectal cancer stem cells through the interplay of PARP1, MRE11 and RAD51. Cell Death & Differentiation, 1–23. https://doi.org/10.1038/s41418-020-00733-4 Cite
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IL-6 and IL-8, Secreted by Myofibroblasts in the Tumor Microenvironment, Activate HES1 to Expand the Cancer Stem Cell Population in Early Colorectal Tumor

Scientists investigated the cancer stem cell‐promoting effect of factors released from myofibroblasts into the microenvironment of early colorectal cancer tumors and its molecular mechanism.
[Molecular Carcinogenesis]
Kim, B., Seo, Y., Kwon, J.-H., Shin, Y., Kim, S., Park, S. J., Park, J. J., Cheon, J. H., Kim, W. H., & Kim, T. I. (n.d.). IL-6 and IL-8, secreted by myofibroblasts in the tumor microenvironment, activate HES1 to expand the cancer stem cell population in early colorectal tumor. Molecular Carcinogenesis, n/a(n/a). https://doi.org/https://doi.org/10.1002/mc.23283 Cite
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