Dissection of Two Routes to Naïve Pluripotency Using Different Kinase Inhibitors

Researchers use mass spectrometry to describe the molecular events triggered by inhibition of Mek1/2 and Gsk3 and inhibition of Cdk8/19 on ESCs.
[Nature Communications]
Martinez-Val, A., Lynch, C. J., Calvo, I., Ximénez-Embún, P., Garcia, F., Zarzuela, E., Serrano, M., & Munoz, J. (2021). Dissection of two routes to naïve pluripotency using different kinase inhibitors. Nature Communications, 12(1), 1863. https://doi.org/10.1038/s41467-021-22181-5 Cite
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FGFR2 Fusion Proteins Drive Oncogenic Transformation of Mouse Liver Organoids towards Cholangiocarcinoma

Tumor organoids and 2D cell lines derived from CCA lesions were addicted to FF signaling via Ras-Erk, regardless of FF identity or V565F mutation.
[Journal of Hepatology]
Cristinziano, G., Porru, M., Lamberti, D., Buglioni, S., Rollo, F., Amoreo, C. A., Manni, I., Giannarelli, D., Cristofoletti, C., Russo, G., Borad, M. J., Grazi, G. L., Diodoro, M. G., Giordano, S., Sacconi, A., Forcato, M., Anastasi, S., Leonetti, C., & Segatto, O. (2021). FGFR2 fusion proteins drive oncogenic transformation of mouse liver organoids towards cholangiocarcinoma. Journal of Hepatology. https://doi.org/10.1016/j.jhep.2021.02.032 Cite
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Generation of Macrophages with Altered Viral Sensitivity from Genome-Edited Rhesus Macaque iPSCs to Model Human Disease

Researchers established iPSCs from the peripheral blood of rhesus macaques (Rh-iPSCs) by combining the Yamanaka reprograming factors and two inhibitors and differentiated the cells into functional macrophages through hematopoietic progenitor cells.
[Molecular Therapy-Methods & Clinical Development]
Generation of macrophages with altered viral sensitivity from genome-edited rhesus macaque iPSCs to model human disease: Molecular Therapy - Methods & Clinical Development. (n.d.). Retrieved March 17, 2021, from https://www.cell.com/molecular-therapy-family/methods/fulltext/S2329-0501(21)00048-6 Cite
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SOX9 in Prostate Cancer Is Upregulated by Cancer-Associated Fibroblasts to Promote Tumor Progression through HGF/C-Met-FRA1 Signaling

An in vitro model of paracrine interaction between primary cancer-associated fibroblasts and prostate cancer (Pca) cells was applied to investigate the molecular mechanism of SOX9 upregulation during Pca progression.
[FEBS Journal]
Qin, H., Yang, Y., Jiang, B., Pan, C., Chen, W., Diao, W., Ding, M., Cao, W., Zhang, Z., Chen, M., Gao, J., Zhao, X., Qiu, X., & Guo, H. (n.d.). SOX9 in prostate cancer is upregulated by cancer-associated fibroblasts to promote tumor progression through HGF/c-Met-FRA1 signaling. The FEBS Journal, n/a(n/a). https://doi.org/https://doi.org/10.1111/febs.15816 Cite
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BH3 Mimetics Potentiate Pro-Apoptotic Activity of Encorafenib in BRAFV600E Melanoma Cells

Researchers investigated five BRAFV600E melanoma cell lines derived from drug-naïve tumor specimens to assess cell death response to encorafenib, a recently FDA-approved BRAFV600E inhibitor.
[Cancer Letters]
Hartman, M. L., Gajos-Michniewicz, A., Talaj, J. A., Mielczarek-Lewandowska, A., & Czyz, M. (2020). BH3 mimetics potentiate pro-apoptotic activity of encorafenib in BRAFV600E melanoma cells. Cancer Letters. https://doi.org/10.1016/j.canlet.2020.11.036 Cite
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MEK Inhibition Reprograms CD8+ T Lymphocytes Into Memory Stem Cells with Potent Antitumor Effects

Scientists found that MEK1/2 inhibition induced stem cell–like memory T cells that have naive phenotype with self-renewability, enhanced multipotency and proliferative capacity.
[Nature Immunology]
MEK inhibition reprograms CD8 + T lymphocytes into memory stem cells with potent antitumor effects | Nature Immunology. (n.d.). Retrieved November 23, 2020, from https://www.nature.com/articles/s41590-020-00818-9 Cite
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An On-Chip Wound Healing Assay Fabricated by Xurography for Evaluation of Dermal Fibroblast Cell Migration and Wound Closure

Lab-on-a-chip technology was used to investigate the effects of basic fibroblast growth factor, mitomycin C, MEK1/2 inhibitor and fetal calf serum on human dermal fibroblast cell migration.
[Scientific Reports]
Shabestani Monfared, G., Ertl, P., & Rothbauer, M. (2020). An on-chip wound healing assay fabricated by xurography for evaluation of dermal fibroblast cell migration and wound closure. Scientific Reports, 10(1), 16192. https://doi.org/10.1038/s41598-020-73055-7 Cite
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E3 Ubiquitin Ligase PARK2, an Inhibitor of Melanoma Cell Growth, Is Repressed by the Oncogenic ERK1/2-ELK1 Transcriptional Axis

Investigators showed that pharmacological inhibition of BRAF-V600E or ERK1/2 in melanoma cells increased PARK2 expression.
[Journal of Biological Chemistry]
Montagnani, V., Maresca, L., Apollo, A., Pepe, S., Carr, R. M., Fernandez-Zapico, M. E., & Stecca, B. (2020). E3 ubiquitin ligase PARK2, an inhibitor of melanoma cell growth, is repressed by the oncogenic ERK1/2-ELK1 transcriptional axis. Journal of Biological Chemistry, jbc.RA120.014615. https://doi.org/10.1074/jbc.RA120.014615 Cite
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IGF-1R Inhibition Induces MEK Phosphorylation to Promote Survival in Colon Carcinomas

Scientists discovered that prolonged treatment of colon cancer cells with insulin-like growth factor 1 receptor (IGF-1R) inhibitors stimulated p70 KDa ribosomal protein S6 kinase 1 (p70S6K1) activation, a well-known kinase signaling for cell survival. They also found that p70S6K1 activation by IGF-1R inhibition was independent of K-Ras and PIK3CA mutations that frequently occur in colon cancer.
[Signal Transduction and Targeted Therapy]
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Inhibition of MEK1/2 Forestalls the Onset of Acquired Resistance to Entrectinib in Multiple Models of NTRK1-Driven Cancer

Scientists showed that expression of the TPR-NTRK1 fusion kinase in immortalized mouse pancreatic ductal epithelial or mouse lung epithelial cells was sufficient to promote rapidly growing tumors in mice.
[Cell Reports]
Vaishnavi, A., Scherzer, M. T., Kinsey, C. G., Parkman, G. L., Truong, A., Ghazi, P., Schuman, S., Battistone, B., Garrido-Laguna, I., & McMahon, M. (2020). Inhibition of MEK1/2 Forestalls the Onset of Acquired Resistance to Entrectinib in Multiple Models of NTRK1-Driven Cancer. Cell Reports, 32(5). https://doi.org/10.1016/j.celrep.2020.107994 Cite
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