Oncotarget is a bio-medical journal that makes its publications available on platforms including PubMed Central, PubMed, BIOSIS Previews, ISI/Web of Science, Biological Abstracts. It cooperates with the Medicine’s National Library hence becoming among the first to submit its publications to PubMed. It aims at making available scientific papers and increases the impact of research through its educative reviews. It nurtures the use of clinical and basic science to fight diseases. Through scientific experts, it helps researchers to contribute to the advancement of science. Follow Oncotarget on Twitter.
Oncotarget works closely with renowned scientific archives and indexes to make its publications public. It researches on oncology, aging, microbiology, immunology, pathology, chromosomes and Autophagy. It produces papers twice per week, is peer-reviewed and of the open access type. Since 2010, it has published 324 issues and currently is in its eight volume
Oncotarget focuses on growing more like a scholarly journal for biomedical research. The researchers of Oncotarget also focused on identifying a Molecular Trigger for Prostate Cancer Cells. According to a recent study, a small modification in proteins causes the migratory and insensitivity of prostate cancer cells. The analysis can help on the development of therapies since they involve the study of how the cancer cells migrate within the body and when the cells break free from the tumor and migrate through the bloodstream which can make them metastatic.
Learn more: https://www.ncbi.nlm.nih.gov/pmc/journals/1558/
The migration of the cells is through a process called epithelial-to-mesenchymal transition. Transforming growth factor beta is one of the proteins thought to activate the EMT. The mechanism behind the activation of the EMT can enable scientists to prevent cancer metastasis. Swedish researchers found out that modifying the protein building blocks could alter Snail1 and lead to more growth of cancer cells.
The modification involved other small protein attachment which could change the structure and function of Snail1. Preventing the modification called “sumoylation” of snail1 by genetically canceling the migration and invasion of prostate cancer cells. It also regulated the appearance of particular proteins and genes involved in EMT. The researchers found out that the sumoylated snail1 can enhance EMT and TGF-beta signaling in prostate cancer. The results indicated that snail1 Sumoylation might be the cause of the prostate cancer growth. Download output styles at Endnote.com