Splicing Machinery Dysregulation Drives Glioblastoma Development/Aggressiveness: Oncogenic Role of SRSF3

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.
[Brain]
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
Full Article
Bookmark

No account yet? Register

0
Share

Proline Rich 11 (PRR11) Overexpression Amplifies PI3K Signaling and Promotes Antiestrogen Resistance in Breast Cancer

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.
[Nature Communications]
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
Full Article
Bookmark

No account yet? Register

0
Share

Targeting Tumor Cell-Derived CCL2 as a Strategy to Overcome Bevacizumab Resistance in ETV5+ Colorectal Cancer

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]
Feng, H., Liu, K., Shen, X., Liang, J., Wang, C., Qiu, W., Cheng, X., & Zhao, R. (2020). Targeting tumor cell-derived CCL2 as a strategy to overcome Bevacizumab resistance in ETV5 + colorectal cancer. Cell Death & Disease, 11(10), 1–14. https://doi.org/10.1038/s41419-020-03111-7 Cite
Full Article
Bookmark

No account yet? Register

0
Share

Targeting Autophagy in Breast Cancer

Investigators present a review of autophagy focusing on its interplay with targeted drugs used for breast cancer treatment.
[International Journal of Molecular Sciences]
Cocco, S., Leone, A., Piezzo, M., Caputo, R., Di Lauro, V., Di Rella, F., Fusco, G., Capozzi, M., Gioia, G. di, Budillon, A., & De Laurentiis, M. (2020). Targeting Autophagy in Breast Cancer. International Journal of Molecular Sciences, 21(21), 7836. https://doi.org/10.3390/ijms21217836 Cite
Full Article
Bookmark

No account yet? Register

0
Share

Indole Hydrazide Compound ZJQ-24 Inhibits Angiogenesis and Induces Apoptosis Cell Death through Abrogation of AKT/mTOR Pathway in Hepatocellular Carcinoma

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]
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
Full Article
Bookmark

No account yet? Register

0
Share

The miR-30a-5p/CLCF1 Axis Regulates Sorafenib Resistance and Aerobic Glycolysis in Hepatocellular Carcinoma

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]
Zhang, Z., Tan, X., Luo, J., Yao, H., Si, Z., & Tong, J.-S. (2020). The miR-30a-5p/CLCF1 axis regulates sorafenib resistance and aerobic glycolysis in hepatocellular carcinoma. Cell Death & Disease, 11(10), 1–14. https://doi.org/10.1038/s41419-020-03123-3 Cite
Full Article
Bookmark

No account yet? Register

0
Share

Neddylation Blockade Induces HIF-1α Driven Cancer Cell Migration via Upregulation of ZEB1

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.
[Scientific Reports]
Park, J. B., Seo, J., Park, J.-W., & Chun, Y.-S. (2020). Neddylation blockade induces HIF-1α driven cancer cell migration via upregulation of ZEB1. Scientific Reports, 10(1), 18210. https://doi.org/10.1038/s41598-020-75286-0 Cite
Full Article
Bookmark

No account yet? Register

0
Share

Antileukemic Activity of the VPS34-IN1 Inhibitor in Acute Myeloid Leukemia

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.
[Oncogenesis]
Full Article
Bookmark

No account yet? Register

0
Share

Endothelial Dysfunction in Neuroprogressive Disorders- Causes and Suggested Treatments

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.
[BMC Medicine]
Morris, G., Puri, B. K., Olive, L., Carvalho, A., Berk, M., Walder, K., Gustad, L. T., & Maes, M. (2020). Endothelial dysfunction in neuroprogressive disorders—causes and suggested treatments. BMC Medicine, 18(1), 305. https://doi.org/10.1186/s12916-020-01749-w Cite
Abstract
Bookmark

No account yet? Register

0
Share

SPARC Promotes Insulin Secretion through Down-Regulation of RGS4 Protein in Pancreatic β Cells

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.
[Scientific Reports]
Hu, L., He, F., Huang, M., Zhao, Q., Cheng, L., Said, N., Zhou, Z., Liu, F., & Dai, Y.-S. (2020). SPARC promotes insulin secretion through down-regulation of RGS4 protein in pancreatic β cells. Scientific Reports, 10(1), 17581. https://doi.org/10.1038/s41598-020-74593-w Cite
Full Article
Bookmark

No account yet? Register

1+
Share

Pan-Cancer Analysis Reveals TAp63-Regulated Oncogenic lncRNAs that Promote Cancer Progression through AKT Activation

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.
[Nature Communications]
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
Full ArticlePress Release
Bookmark

No account yet? Register

0
Share
Share