Receptor-Driven ERK Pulses Reconfigure MAPK Signaling and Enable Persistence of Drug-Adapted BRAF-Mutant Melanoma Cells

In BRAFV600E melanomas, RAF and MEK inhibitors efficiently block oncogenic signaling, but persister cells emerge. Scientists showed that persister cells escaped drug-induced cell-cycle arrest via brief, sporadic ERK pulses generated by transmembrane receptors and growth factors operating in an autocrine/paracrine manner.
[Cell Systems]
Gerosa, L., Chidley, C., Fröhlich, F., Sanchez, G., Lim, S. K., Muhlich, J., Chen, J.-Y., Vallabhaneni, S., Baker, G. J., Schapiro, D., Atanasova, M. I., Chylek, L. A., Shi, T., Yi, L., Nicora, C. D., Claas, A., Ng, T. S. C., Kohler, R. H., Lauffenburger, D. A., … Sorger, P. K. (2020). Receptor-Driven ERK Pulses Reconfigure MAPK Signaling and Enable Persistence of Drug-Adapted BRAF-Mutant Melanoma Cells. Cell Systems, 0(0). https://doi.org/10.1016/j.cels.2020.10.002 Cite
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Fatty Acid Metabolism Underlies Venetoclax Resistance in Acute Myeloid Leukemia Stem Cells

Scientists demonstrated that resistance to venetoclax with azacitidine occurs via upregulation of fatty acid oxidation, which occurs either due to RAS pathway mutations or as a compensatory adaptation in relapsed disease.
[Nature Cancer]
Stevens, B. M., Jones, C. L., Pollyea, D. A., Culp-Hill, R., D’Alessandro, A., Winters, A., Krug, A., Abbott, D., Goosman, M., Pei, S., Ye, H., Gillen, A. E., Becker, M. W., Savona, M. R., Smith, C., & Jordan, C. T. (2020). Fatty acid metabolism underlies venetoclax resistance in acute myeloid leukemia stem cells. Nature Cancer, 1–12. https://doi.org/10.1038/s43018-020-00126-z Cite
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Identification of Drivers of Breast Cancer Invasion by Secretome Analysis: Insight Into CTGF Signaling

Scientists combined data from secretome and proteome analysis using mass spectrometry with microarray data from mesenchymal transformed breast cancer cells to elucidate the drivers of epithelial-mesenchymal transition and cell invasion.
[Scientific Reports]
Identification of drivers of breast cancer invasion by secretome analysis: insight into CTGF signaling | Scientific Reports. (n.d.). Retrieved October 21, 2020, from https://www.nature.com/articles/s41598-020-74838-8 Cite
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Post-Translational Modification of KRAS: Potential Targets for Cancer Therapy

The authors summarize the regulatory mode of post-translational modifications on KRAS. They also highlight the recent studies targeting these modifications having exhibited potent anti-tumor activities, including in prostate cancer.
[Acta Pharmacologica Sinica]
Wang, W., Yuan, T., Qian, M., Yan, F., Yang, L., He, Q., Yang, B., Lu, J., & Zhu, H. (2020). Post-translational modification of KRAS: potential targets for cancer therapy. Acta Pharmacologica Sinica, 1–11. https://doi.org/10.1038/s41401-020-00542-y Cite
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Roles of Src Family Kinase, Ras, and mTOR Signaling in Intestinal Epithelial Homeostasis and Tumorigenesis

Dysregulation of intestinal epithelial cells(IEC) homeostasis likely contributes to the development of intestinal inflammation and intestinal cancer. The roles of receptor protein tyrosine kinases and their downstream signaling molecules such as Src family kinases, Ras, and mammalian target of rapamycin in homeostatic regulation of IEC turnover have recently been evaluated.
[Cancer Science]
Matozaki, T., Kotani, T., Murata, Y., & Saito, Y. (n.d.). Roles of Src family kinase, Ras, and mTOR signaling in intestinal epithelial homeostasis and tumorigenesis. Cancer Science, n/a(n/a). https://doi.org/10.1111/cas.14702 Cite
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Siah2 Integrates Mitogenic and Extracellular Matrix Signals Linking Neuronal Progenitor Ciliogenesis with Germinal Zone Occupancy

Researchers determined that the Siah2 E3 ubiquitin ligase functions in a coincidence detection circuit linking responses to the Shh mitogen and the ECM to control cerebellar granule neurons germinal zone occupancy.
[Nature Communications]
Ong, T., Trivedi, N., Wakefield, R., Frase, S., & Solecki, D. J. (2020). Siah2 integrates mitogenic and extracellular matrix signals linking neuronal progenitor ciliogenesis with germinal zone occupancy. Nature Communications, 11(1), 5312. https://doi.org/10.1038/s41467-020-19063-7 Cite
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Evaluation of the RAS Signaling Network in Response to MEK Inhibition Using Organoids Derived from a Familial Adenomatous Polyposis Patient

Scientists used patient-derived organoids derived from a familial adenomatous polyposis patient to analyze the response to chemotherapeutic agents targeting EGFR, BRAF and MEK.
[Scientific Reports]
Osumi, H., Muroi, A., Sakahara, M., Kawachi, H., Okamoto, T., Natsume, Y., Yamanaka, H., Takano, H., Kusama, D., Shinozaki, E., Ooki, A., Yamaguchi, K., Ueno, M., Takeuchi, K., Noda, T., Nagayama, S., Koshikawa, N., & Yao, R. (2020). Evaluation of the RAS signaling network in response to MEK inhibition using organoids derived from a familial adenomatous polyposis patient. Scientific Reports, 10(1), 17455. https://doi.org/10.1038/s41598-020-74530-x Cite
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RASSF1A Inhibits PDGFB-Driven Malignant Phenotypes of Nasopharyngeal Carcinoma Cells in a YAP1-Dependent Manner

The authors observed that ras-association domain family protein1 isoform A (RASSF1A) expression inhibited the malignant phenotypes of nasopharyngeal carcinoma (NPC) cells. Stable silencing of RASSF1A in NPC cell lines induced self-renewal properties and tumorigenicity in vivo/in vitro and the acquisition of an invasive phenotype in vitro.
[Cell Death & Disease]
Liang, Y.-Y., Deng, X.-B., Lin, X.-T., Jiang, L.-L., Huang, X.-T., Mo, Z.-W., Yuan, Y.-W., & Teh, M.-T. (2020). RASSF1A inhibits PDGFB-driven malignant phenotypes of nasopharyngeal carcinoma cells in a YAP1-dependent manner. Cell Death & Disease, 11(10), 1–12. https://doi.org/10.1038/s41419-020-03054-z Cite
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Tim-3 Promotes Tube Formation and Decreases Tight Junction Formation in Vascular Endothelial Cells

Tim-3 was overexpressed in vascular endothelial HMVECs and HUVECs and in vitro assays were used to determine that Tim-3 promoted cell proliferation, migration, invasion and tube formation through activating cyclin D1, Ras homolog gene family member A and vascular endothelial growth factor receptor 2.
[Bioscience Reports]
Cong, Y., Wang, X., Wang, S., Qiao, G., Li, Y., Cao, J., Jiang, W. G., & Cui, Y. (n.d.). Tim-3 promotes tube formation and decreases tight junction formation in vascular endothelial cells. Bioscience Reports. https://doi.org/10.1042/BSR20202130 Cite
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LncRNA LL22NC03-N14H11.1 Promoted Hepatocellular Carcinoma Progression through Activating MAPK Pathway to Induce Mitochondrial Fission

Dysregulated lncRNAs in hepatocellular carcinoma (HCC) were identified through circlncRNAnet and GEPIA bioinformatics tools. Biological function of LL22NC03-N14H11.1 in HCC was detected by CCK-8 assay, flow cytometry analysis, transwell invasion, and wound healing assays.
[Cell Death & Disease]
Yi, T., Luo, H., Qin, F., Jiang, Q., He, S., Wang, T., Su, J., Song, S., Qin, X., Qin, Y., Zhou, X., & Huang, Z. (2020). LncRNA LL22NC03-N14H11.1 promoted hepatocellular carcinoma progression through activating MAPK pathway to induce mitochondrial fission. Cell Death & Disease, 11(10), 1–17. https://doi.org/10.1038/s41419-020-2584-z Cite
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Small GTPase RAB6 Deficiency Promotes Alveolar Progenitor Cell Renewal and Attenuates PM2.5-Induced Lung Injury and Fibrosis

Investigators demonstrated that knockout of RAB6 inhibited pulmonary fibrosis, oxidative stress, and type 2 alveolar epithelial cells (AEC2) cell death in fine particulate matter (PM2.5)-injured mice. In addition, knockout of RAB6 decreased Dickkopf 1 autocrine and activated proliferation, self-renewal, and wnt/β-catenin signaling of PM2.5-injured AEC2 cells.
[Cell Death & Disease]
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