| Vol. 10.09 – 11 March, 2021 |
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| Genetic and pharmacological antagonism of PLK1 in combination with FGFR inhibitor therapy synergized to enhance anti-proliferative effects and drove cancer cell death in vitro and in vivo through activation of the γH2AX-CHK-E2F1 axis. [Cancer Research] |
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| PUBLICATIONSRanked by the impact factor of the journal |
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| Scientists investigated how lasR mutants modulate airway epithelial membrane bound mICAM-1, a surface adhesion molecule, and determined its impact on neutrophilic inflammation in vitro and in vivo. [PLoS Pathogens] |
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| The epithelial-to-mesenchymal transition and fibrotic effect of transforming growth factor-beta 1 (TGF-β1) was dependent on acetylated CCAAT/enhancer binding protein β (C/EBPβ)-mediated regulation of alpha-smooth muscle actin (α-SMA) gene activity. C/EBPβ acetylation might play a central role in pulmonary fibrosis. [Molecular Medicine] |
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| Investigators revealed that METTL3 positively regulated FBXW7 expression and confirmed the tumor-suppressive role of m6A-modified FBXW7, providing insight into its epigenetic regulatory mechanisms in lung adenocarcinoma initiation and development. [Journal of Experimental & Clinical Cancer Research] |
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| Researchers found that erastin synergized with celastrol to induce cell death at non‐toxic concentrations. The combined treatment with celastrol and erastin significantly increased reactive oxygen species generation, disrupted mitochondrial membrane potential, and promoted mitochondrial fission [Molecular Oncology] |
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| Downregulation of family with sequence similarity 201‐member A (FAM201A) suppressed the cell proliferation, migration and invasion and promoted the cell apoptosis in lung adenocarcinoma (LUAD) cells. FAM201A overexpression showed tumorigenesis effect on LUAD cells. researchers also demonstrated that FAM201A affected LUAD progression via targeting miR‐7515 to promote GLO1 expression. [Journal of Cellular Physiology] |
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| The combination of MS023, a type I protein arginine methyltransferases (PRMT) inhibitor, and the PARP inhibitor BMN-673 demonstrated strong synergistic interaction at low nanomolar concentrations in methylthioadenosine phosphorylase-negative NSCLC cell lines A549, SK-LU-1 and HCC4006. [Clinical Epigenetics] |
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| Curcumin inhibited NSCLC growth through downregulating circ-PRKCA, which regulated ITGB1 expression by adsorbing miR-384. [Biomedicine & Pharmacotherapy] |
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| RNA_0074027 (Circ_0074027) interacted with microRNA-2467-3p (miR-2467-3p), and ras homolog family member A (RHOA) was a target of miR-2467-3p in NSCLC cells. RHOA silencing blocked the malignant potential of NSCLC cells. Circ_0074027 silencing restrained the malignant phenotypes of NSCLC cells largely through up-regulating miR-2467-3p. [Journal of Bioenergetics and Biomembranes] |
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| The authors discuss the experimental models of lung cancer and metastasis, mechanisms in SCLC transfer and the challenges about clinical management of lung cancer. [Biomedicine & Pharmacotherapy] |
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| Spectrum Pharmaceuticals,Inc. announced that the FDA has granted Fast Track designation for poziotinib for the treatment of NSCLC in previously treated patients with HER2 exon 20 mutations. Spectrum plans to submit a new drug application for poziotinib later this year. [Spectrum Pharmaceuticals, Inc.] |
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| October 27 – 29, 2021 Tokyo, Japan |
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| Thomas Jefferson University – Philadelphia, Pennsylvania, United States |
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| UT Health Science Center at Tyler – Tyler, Texas, United States |
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| The Francis Crick Institute – London, England, United Kingdom |
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| University Hospital of Muenster – Münster, Germany |
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| H. Lee Moffitt Cancer Center & Research Institute – Tampa, Florida, United States |
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