Researchers identified a profound dysregulation in the expression of relevant spliceosome components and splicing factors (at mRNA and protein levels) in well characterized cohorts of human high-grade astrocytomas, mostly glioblastomas, compared to healthy brain control samples, being SRSF3, RBM22, PTBP1 and RBM3 able to perfectly discriminate between tumours and control samples, and between proneural-like or mesenchymal-like tumours versus control samples from different mouse models with gliomas.
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Fuentes-Fayos, A. C., Vázquez-Borrego, M. C., Jiménez-Vacas, J. M., Bejarano, L., Pedraza-Arévalo, S., L-López, F., Blanco-Acevedo, C., Sánchez-Sánchez, R., Reyes, O., Ventura, S., Solivera, J., Breunig, J. J., Blasco, M. A., Gahete, M. D., Castaño, J. P., & Luque, R. M. (n.d.). Splicing machinery dysregulation drives glioblastoma development/aggressiveness: oncogenic role of SRSF3. Brain. https://doi.org/10.1093/brain/awaa273 Cite
Scientists interrogated transcriptome data from primary breast tumors and found that among genes in 17q23, PRR11 was a key gene associated with a poor response to therapeutic estrogen suppression.
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Lee, K., Guerrero-Zotano, A. L., Servetto, A., Sudhan, D. R., Lin, C.-C., Formisano, L., Jansen, V. M., González-Ericsson, P., Sanders, M. E., Stricker, T. P., Raj, G., Dean, K. M., Fiolka, R., Cantley, L. C., Hanker, A. B., & Arteaga, C. L. (2020). Proline rich 11 ( PRR11 ) overexpression amplifies PI3K signaling and promotes antiestrogen resistance in breast cancer. Nature Communications, 11(1), 5488. https://doi.org/10.1038/s41467-020-19291-x Cite
Gene set enrichment analysis and additional assays confirmed that ETV5 could promote angiogenesis by inducing the secretion of another tumor angiogenesis factor (CCL2) in CRC cells to facilitate Bevacizumab resistance.
[Cell Death & Disease]
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Investigators present a review of autophagy focusing on its interplay with targeted drugs used for breast cancer treatment.
[International Journal of Molecular Sciences]
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MTT assays, flow cytometric analysis, Western blotting and immunohistochemistry identified that ZJQ-24 effectively suppressed hepatocellular carcinoma cell proliferation via G2/M phase arrest and caspase-dependent apoptosis but had no cytotoxic on normal cells.
[Cell Death & Disease]
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Liu, J., Liu, Y., Zhang, J., Liu, D., Bao, Y., Chen, T., Tang, T., Lin, J., Luo, Y., Jin, Y., & Zhang, J. (2020). Indole hydrazide compound ZJQ-24 inhibits angiogenesis and induces apoptosis cell death through abrogation of AKT/mTOR pathway in hepatocellular carcinoma. Cell Death & Disease, 11(10), 1–13. https://doi.org/10.1038/s41419-020-03108-2 Cite
The aberrant glucose metabolism in cancer cells aerobic glycolysis is associated with resistance to chemotherapeutic agents. Drug-resistance cells and tumors were exposed to sorafenib to establish sorafenib-resistance cell lines and tumors.
[Cell Death & Disease]
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Scientists report that inhibiting neddylation activates the hypoxia-inducible factor 1α (HIF-1α) through the PI3K-Akt pathway, which eventually regulates the epithelial to mesenchymal transition-activator zinc finger E-box binding homeobox 1 (ZEB1) in various cancer cell lines.
Using a recently developed specific inhibitor, the authors found that vacuolar protein sorting 34 inhibition induces apoptosis in acute myeloid leukemia cells but not in normal CD34+ hematopoietic cells.
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On the basis of the above molecular mechanisms, details are given of potential treatment options for mitigating endothelial cell dysfunction and activation in neuroprogressive disorders.
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Researchers showed that SPARC enhanced the promoting effect of Muscarinic receptor agonist oxotremorine-M on insulin secretion in cultured mouse islets. Overexpression of SPARC down-regulated RGS4, a negative regulator of β-cell M3 muscarinic receptors.
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By performing a mouse-human cross species analysis between the TAp63 metastatic mammary adenocarcinoma mouse model and models of human breast cancer progression, researchers identified two TAp63-regulated oncogenic lncRNAs, TROLL-2 and TROLL-3.
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Napoli, M., Li, X., Ackerman, H. D., Deshpande, A. A., Barannikov, I., Pisegna, M. A., Bedrosian, I., Mitsch, J., Quinlan, P., Thompson, A., Rajapakshe, K., Coarfa, C., Gunaratne, P. H., Marchion, D. C., Magliocco, A. M., Tsai, K. Y., & Flores, E. R. (2020). Pan-cancer analysis reveals TAp63-regulated oncogenic lncRNAs that promote cancer progression through AKT activation. Nature Communications, 11(1), 5156. https://doi.org/10.1038/s41467-020-18973-w Cite