Therapeutic Potential for Regulation of the Nuclear Factor Kappa-B Transcription Factor p65 to Prevent Cellular Senescence and Activation of Pro-Inflammatory in Mesenchymal Stem Cells

The authors found that p65 was activated during cellular senescence and inflammatory activation in human umbilical cord-derived MSCs.
[International Journal of Molecular Sciences]
Mato-Basalo, R., Morente-López, M., Arntz, O. J., van de Loo, F. A. J., Fafián-Labora, J., & Arufe, M. C. (2021). Therapeutic Potential for Regulation of the Nuclear Factor Kappa-B Transcription Factor p65 to Prevent Cellular Senescence and Activation of Pro-Inflammatory in Mesenchymal Stem Cells. International Journal of Molecular Sciences, 22(7), 3367. https://doi.org/10.3390/ijms22073367 Cite
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MicroRNA-499 Serves as a Sensitizer for Lung Cancer Cells to Radiotherapy by Inhibition of CK2α-Mediated Phosphorylation of p65

Researchers performed loss and gain of function experiments for the expression of miR-499 in lung cancer cells exposed to irradiation to determine the effect of miR-499 expression on cell viability and apoptosis as well as tumor growth.
[Molecular Therapy-Oncolytics]
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Inhibitory Effect of Immunologically Activated Mesenchymal Stem Cells on Lung Cancer Cell Growth and Metastasis

Human umbilical cord (HUC)-MSCs were separated from the umbilical cord using the adherence method. Surface markers of HUC-MSCs were detected by flow cytometry for MSC identification.
[Cancer Biotherapy and Radiopharmaceuticals]
Ye, H., Pan, J., Gong, E., Cai, X., Xu, C., Li, Y., Zheng, H., & Cao, Z. (2021). Inhibitory Effect of Immunologically Activated Mesenchymal Stem Cells on Lung Cancer Cell Growth and Metastasis. Cancer Biotherapy and Radiopharmaceuticals. https://doi.org/10.1089/cbr.2020.3855 Cite
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The CREB/KMT5A Complex Regulates PTP1B to Modulate High Glucose-Induced Endothelial Inflammatory Factor Levels in Diabetic Nephropathy

The authors hypothesized that cAMP response element-binding protein (CREB) associated with KMT5A to modulate PTP1B expression, thus contributing to high glucose-mediated glomerular endothelial inflammation.
[Cell Death & Disease]
Huang, T., Li, X., Wang, F., Lu, L., Hou, W., Zhu, M., & Miao, C. (2021). The CREB/KMT5A complex regulates PTP1B to modulate high glucose-induced endothelial inflammatory factor levels in diabetic nephropathy. Cell Death & Disease, 12(4), 1–14. https://doi.org/10.1038/s41419-021-03629-4 Cite
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Matrix Metalloproteinase-1 Decorated Polymersomes, a Surface-Active Extracellular Matrix Therapeutic, Potentiates Collagen Degradation and Attenuates Early Liver Fibrosis

The therapeutic effects of MMP-1 decorated polymersomes (MMPsomes), compared to matrix metalloproteinase-1 (MMP-1), were evaluated in vivo in carbon-tetrachloride-induced early liver fibrosis mouse model. MMPsomes exhibited favorable physicochemical properties, MMP-1 surface localization and improved therapeutic efficacy in TGFβ-activated human hepatic stellate cells in vitro.
[Journal of Controlled Release]
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Islet Neogenesis Associated Protein (INGAP) Protects Pancreatic β Cells from IL-1β and IFNγ-Induced Apoptosis

Researchers determined whether recombinant Islet NeoGenesis Associated Protein (rINGAP) and its active core, a pentadecapeptide INGAP104–118, protected β cells against cytokine-induced death.
[Cell Death Discovery]
Nano, E., Petropavlovskaia, M., & Rosenberg, L. (2021). Islet neogenesis associated protein (INGAP) protects pancreatic β cells from IL-1β and IFNγ-induced apoptosis. Cell Death Discovery, 7(1), 1–15. https://doi.org/10.1038/s41420-021-00441-z Cite
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The Role of PKM2 Nuclear Translocation in the Constant Activation of the NF-κB Signaling Pathway in Cancer-Associated Fibroblasts

The authors showed that mesenchymal stem cells differentiated into cancer-associated fibroblasts, induced by the exosomes derived from gastric cancer cells.
[Cell Death & Disease]
Gu, J., Li, X., Zhao, L., Yang, Y., Xue, C., Gao, Y., Li, J., Han, Q., Sun, Z., Bai, C., & Zhao, R. C. (2021). The role of PKM2 nuclear translocation in the constant activation of the NF-κB signaling pathway in cancer-associated fibroblasts. Cell Death & Disease, 12(4), 1–13. https://doi.org/10.1038/s41419-021-03579-x Cite
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Interfering MicroRNA-410 Attenuates Atherosclerosis via the HDAC1/KLF5/IKBα/NF-κB Axis

miR-410 expression was determined using qRT-PCR in both mouse models of atherosclerosis and HUVECs treated with ox-LDL.
[Molecular Therapy-Nucleic Acids]
Nan, S., Wang, Y., Xu, C., & Wang, H. (2021). Interfering microRNA-410 Attenuates Atherosclerosis Via the HDAC1/KLF5/IKBα/NF-κB Axis. Molecular Therapy - Nucleic Acids, 0(0). https://doi.org/10.1016/j.omtn.2021.03.009 Cite
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CTGF Regulates Cell Proliferation, Migration, and Glucose Metabolism through Activation of FAK Signaling in Triple-Negative Breast Cancer

Investigators demonstrated a mechanistic link between connective tissue growth factor (CTGF) and enhanced aerobic glycolysis in TNBC.
[Oncogene]
Kim, H., Son, S., Ko, Y., & Shin, I. (2021). CTGF regulates cell proliferation, migration, and glucose metabolism through activation of FAK signaling in triple-negative breast cancer. Oncogene, 1–15. https://doi.org/10.1038/s41388-021-01731-7 Cite
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Opposing Functions of β-Arrestin 1 and 2 in Parkinson’s Disease via Microglia Inflammation and Nprl3

β-arrestin 1 (ARRB1) ablation ameliorated whereas ARRB2 knockout aggravated, the pathological features of Parkinson’s disease, including dopaminergic neuron loss, neuroinflammation and microglia activation in vivo, and microglia-mediated neuron damage in vitro.
[Cell Death & Differentiation]
Fang, Y., Jiang, Q., Li, S., Zhu, H., Xu, R., Song, N., Ding, X., Liu, J., Chen, M., Song, M., Ding, J., Lu, M., Wu, G., & Hu, G. (2021). Opposing functions of β-arrestin 1 and 2 in Parkinson’s disease via microglia inflammation and Nprl3. Cell Death & Differentiation, 1–15. https://doi.org/10.1038/s41418-020-00704-9 Cite
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Pentraxin 3 Acts as a Functional Effector of Akt/NF-κB Signaling to Modulate the Progression and Cisplatin-Resistance in Non-Small Cell Lung Cancer

The biological roles of Pentraxin 3 in NSCLC progression and NSCLC cell resistance to cisplatin were evaluated using enzyme-linked immunosorbent assay, cell count kit-8, colony formation assay, flow cytometry, as well as xenograft tumor assay.
[Archives of Biochemistry and Biophysics]
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