Scientists found that there were some subtle connections between mesenchymal stem cells and liver lipid metabolism in the post-hepatectomy liver failure model.
[Cell Death & Disease]
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Scientists confirmed that nitrogen mustard (NM) dose-dependently caused cell death and induced autophagy in keratinocytes. Suppression of autophagy by 3-methyladenine, chloroquine, and bafilomycin A1 or ATG5 siRNA attenuated NM-induced keratinocyte cell death.
[Signal Transduction and Targeted Therapy]
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Chen, M., Dong, X., Deng, H., Ye, F., Zhao, Y., Cheng, J., Dan, G., Zhao, J., Sai, Y., Bian, X., & Zou, Z. (2021). Targeting TRPV1-mediated autophagy attenuates nitrogen mustard-induced dermal toxicity. Signal Transduction and Targeted Therapy, 6(1), 1–13. https://doi.org/10.1038/s41392-020-00389-z Cite
The tested the hypothesis that mucoepidermoid carcinoma (MEC) CSC are sensitive to therapeutic inhibition of mTOR. They report a correlation between the long-term clinical outcomes of 17 MEC patients and the intratumoral expression of p-mTOR and p-S6K1.
[Cell Death & Disease]
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Andrade, N. P., Warner, K. A., Zhang, Z., Pearson, A. T., Mantesso, A., Guimaraēs, D. M., Altemani, A., Mariano, F. V., Nunes, F. D., & Nör, J. E. (2021). Survival of salivary gland cancer stem cells requires mTOR signaling. Cell Death & Disease, 12(1), 1–16. https://doi.org/10.1038/s41419-021-03391-7 Cite
Investigators summarize the critical roles of miRNAs in regulating multiple signaling pathways such as Wnt/β-catenin, Notch, PI3K/AKT/mTOR, BMI-1 and STAT3 that are important for the breast cancer stem cell maintenance.
[Cancer Cell International]
Researchers developed two methods to inactivate mTOR, Raptor, or Rictor in early stage natural killer (NK) cells or in late-stage NK cells. They found that when mTOR was deleted by CD122-Cre during and after NK cell commitment, NK cell development was severely impaired.
[Cell Death & Differentiation]
To directly define the roles of insulin and IGF-1 receptors in the maintenance of pluripotency and differentiation of stem cells, scientists knocked out both the receptors in induced pluripotent stem cells.
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Okawa, E. R., Gupta, M. K., Kahraman, S., Goli, P., Sakaguchi, M., Hu, J., Duan, K., Slipp, B., Lennerz, J. K., & Kulkarni, R. N. (2021). Essential roles of insulin and IGF-1 receptors during embryonic lineage development. Molecular Metabolism, 101164. https://doi.org/10.1016/j.molmet.2021.101164 Cite
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]
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The authors investigated whether docosahexaenoic acid itself or select metabolites can account for its antitumor action.
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Chen, K.-M., Thompson, H., Vanden-Heuvel, J. P., Sun, Y.-W., Trushin, N., Aliaga, C., Gowda, K., Amin, S., Stanley, B., Manni, A., & El-Bayoumy, K. (2021). Lipoxygenase catalyzed metabolites derived from docosahexaenoic acid are promising antitumor agents against breast cancer. Scientific Reports, 11(1), 410. https://doi.org/10.1038/s41598-020-79716-x Cite
Investigators explored the efficacy of neratinib in combination with inhibitors of downstream signaling in HER2+ cancers in vitro and in vivo.
[Clinical Cancer Research]
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Zhao, M., Scott, S., Evans, K. W., Yuca, E., Saridogan, T., Zheng, X., Wang, H., Korkut, A., Pico, C. X. C., Demirhan, M. E., Kirby, B., Kopetz, S., Diala, I., Lalani, A. S., Piha-Paul, S., & Meric-Bernstam, F. (2021). Combining neratinib with CDK4/6, mTOR and MEK inhibitors in models of HER2-positive cancer. Clinical Cancer Research. https://doi.org/10.1158/1078-0432.CCR-20-3017 Cite
Researchers showed the protective effect of human recombinant CypA on hydrogen peroxide-induced oxidative damage in A549 cells, which play crucial roles in lung cancer.
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The authors reveal that even under physiological conditions, MSCs produce and release a low level of tumor necrosis factor alpha (TNFα), unexpectedly required for preserving the self-renewal and differentiation of MSCs via autocrine/paracrine signaling.