Researchers used asthma model bronchial smooth muscle cells to measure the biological behaviors of Histone deacetylase 4 (HDAC4)-mediated Kruppel-like factor 5 (KLF5)/Slug/CXC chemokine ligand-12 (CXCL12) axis on the development of asthma in regulation of airway inflammation and remodeling.
[Journal of Translational Medicine]
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Investigators studied effects of recombinant D-dopachrome tautomerase (DDT) on cell proliferation and survival by clonogenic assay and annexin V-PI staining respectively. DDT-induced signaling was investigated by Western blot.
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Song, S., Liu, B., Habibie, H., Bor, J. van den, Smit, M. J., Gosens, R., Wu, X., Brandsma, C.-A., Cool, R. H., Haisma, H. J., Poelarends, G. J., & Melgert, B. N. (2021). D-dopachrome tautomerase contributes to lung epithelial repair via atypical chemokine receptor 3-dependent Akt signaling. EBioMedicine, 68. https://doi.org/10.1016/j.ebiom.2021.103412 Cite
miR-1298-5p and suppressor of cytokine signaling 6 (SOCS6) were silenced or overexpressed in human bronchial epithelial cells. PKH-67 Dye was used to trace exosome endocytosis.
[Molecular and Cellular Biochemistry]
The tumor suppressing effects of MPDZ were determined in vitro and in vivo. The target molecules and signaling pathway that mediated the function of MPDZ were also identified.
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Reserachers investigated the effects of hyperbaric oxygen treatment (HBOT) on solid tumors, such as lung cancer. Non-small cell human lung carcinoma A549-cell-transferred severe combined immunodeficiency mice were selected as an in vivo model to detect the potential mechanism of HBOT in lung tumors.
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Chen, S.-Y., Tsuneyama, K., Yen, M.-H., Lee, J.-T., Chen, J.-L., & Huang, S.-M. (2021). Hyperbaric oxygen suppressed tumor progression through the improvement of tumor hypoxia and induction of tumor apoptosis in A549-cell-transferred lung cancer. Scientific Reports, 11(1), 12033. https://doi.org/10.1038/s41598-021-91454-2 Cite
The authors identified growth hormone receptor is mainly expressed in mesenchymal cells, and its expression is substantially decreased in idiopathic pulmonary fibrosis lungs.
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Comparison of the transcriptomes of the bronchoalveolar microenvironment and peripheral blood indicates alveolar macrophages, alveolar epithelial cells, and monocytes in lungs as the potential main sources of elevated cytokines mediating systemic immune responses and organ damages.
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Tan, Y., Zhang, W., Zhu, Z., Qiao, N., Ling, Y., Guo, M., Yin, T., Fang, H., Xu, X., Lu, G., Zhang, P., Yang, S., Fu, Z., Liang, D., Xie, Y., Zhang, R., Jiang, L., Yu, S., Lu, J., … Chen, S. (2021). Integrating longitudinal clinical laboratory tests with targeted proteomic and transcriptomic analyses reveal the landscape of host responses in COVID-19. Cell Discovery, 7(1), 1–19. https://doi.org/10.1038/s41421-021-00274-1 Cite
When combined with dabrafenib and/or trametinib, Melaleuca alternifolia synergistically reduced the viability of melanoma cells by activating apoptosis.
[Cell Death Discovery]
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Di Martile, M., Garzoli, S., Sabatino, M., Valentini, E., D’Aguanno, S., Ragno, R., & Del Bufalo, D. (2021). Antitumor effect of Melaleuca alternifolia essential oil and its main component terpinen-4-ol in combination with target therapy in melanoma models. Cell Death Discovery, 7(1), 1–13. https://doi.org/10.1038/s41420-021-00510-3 Cite
Scientists evaluated the effect of neutrophil elastase on lipopolysaccharide – induced interleukin 8 production and determined the molecular mechanism in human bronchial epithelial cells.
[Experimental and Molecular Medicine]
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ALKBH5 gain- or loss-of function could effectively reverse LKB1 regulated cell proliferation, colony formation, and migration of KRAS-mutated lung cancer cells.
[Cell Death & Disease]
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Zhang, D., Ning, J., Okon, I., Zheng, X., Satyanarayana, G., Song, P., Xu, S., & Zou, M.-H. (2021). Suppression of m6A mRNA modification by DNA hypermethylated ALKBH5 aggravates the oncological behavior of KRAS mutation/LKB1 loss lung cancer. Cell Death & Disease, 12(6), 1–14. https://doi.org/10.1038/s41419-021-03793-7 Cite
Investigators showed that KEAP1 deficiency promotes glucose dependency in lung cancer cells, and KEAP1-mutant/deficient lung cancer cells were more vulnerable to glucose deprivation than their WT counterparts.
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Koppula, P., Olszewski, K., Zhang, Y., Kondiparthi, L., Liu, X., Lei, G., Das, M., Fang, B., Poyurovsky, M. V., & Gan, B. (2021). KEAP1 deficiency drives glucose dependency and sensitizes lung cancer cells and tumors to GLUT inhibition. IScience, 0(0). https://doi.org/10.1016/j.isci.2021.102649 Cite