{"id":11086,"date":"2021-04-27T16:23:05","date_gmt":"2021-04-27T15:23:05","guid":{"rendered":"https:\/\/www.innovationnewsnetwork.com\/?p=11086"},"modified":"2021-04-27T16:23:05","modified_gmt":"2021-04-27T15:23:05","slug":"treating-cancer-preventing-cell-proliferation","status":"publish","type":"post","link":"https:\/\/www.innovationnewsnetwork.com\/treating-cancer-preventing-cell-proliferation\/11086\/","title":{"rendered":"Treating cancer by preventing the process of cell proliferation"},"content":{"rendered":"<h2>Scientists at the RIKEN Center for Biosystems Dynamics Research (BDR) have been researching the processes behind cell proliferation in hopes of better treating cancer.<\/h2>\n<p>The group found that decreased consumption of a particular protein building block inhibits the growth of cells that become cancerous.<\/p>\n<p>The team\u2019s findings, which were published in the journal <em>eLife<\/em>, could lead to the possibility of dietary therapy for cancer.<\/p>\n<p>A tumour is a group of <a href=\"https:\/\/www.innovationnewsnetwork.com\/heating-tumours-whilst-they-undergo-chemotherapy-can-kill-up-to-98-of-brain-cancer-cells\/8626\/\">cancer cells<\/a> that reproduce uncontrollably; they derive from single cells that become cancerous when genes that trigger cells to multiply are over-activated. However, these genes, known as oncogenes, can also cause cell death, so activation of one oncogene inside a cell is not a large enough quantity to become a cancer cell.<\/p>\n<p>This occurrence is considered to be a &#8220;fail-safe&#8221; mechanism that prohibits cells from turning into cancer too easily. In order for a cell to become cancer, numerous other oncogenes, along with cancer-suppressing genes, need to be stimulated in a multi-step process. The specifics of this process were the subject of the new study.<\/p>\n<p>The team centred their research on an oncogene called <em>Src<\/em> and examined how cell proliferation \u2014oncogenesis \u2014 and cell death are measured in the fruit fly. They demonstrated that <em>Src<\/em> does not stimulate cell death as a consequence of cell proliferation but pushes both processes independently and simultaneously. By hindering the function of specific genes through RNA interference, the team discovered that the gene <em>p38<\/em> was involved in cell proliferation and that another gene, <em>JNK<\/em> was implicated in cell death. On top of this, they uncovered a gene called <em>slpr<\/em> that concurrently activates <em>p38<\/em> and <em>JNK<\/em>.<\/p>\n<p>\u201cHow oncogenes simultaneously promote cell death and cell proliferation has been controversial,\u201d explained Sa Kan Yoo, of <a href=\"https:\/\/www.riken.jp\/en\/research\/labs\/bdr\/\">RIKEN BDR<\/a>. \u201cOur major finding was that the oncogene <em>Src<\/em> promotes cell death and cell proliferation via parallel pathways.\u201d<\/p>\n<p>One potential method of treating cancer utilises the fail-safe procedure by preventing cell proliferation, but not cell death. For this process to be successful, the researchers had to identify the molecular players involved in the process.<\/p>\n<p>After the research group figured out <em>p38<\/em> activation is a significant part of the process leading to cell proliferation, they realised they could make this concept a reality. After examining the gene, <em>p38<\/em> in greater detail, they understood that its activity can be controlled by nutrients in the diet.<\/p>\n<p>The team then tested their theory by examining the relationship between the food fed to fly larvae and cell proliferation. They discovered that by limiting the quantity of the amino acid methionine in the diet, p38-controlled oncogenesis was prohibited.<\/p>\n<p>\u201cWe were excited to find that manipulating the amount of dietary methionine can affect cell proliferation but not cell death,\u201d commented Yoo. \u201cCurrently we do not know whether our finding in flies will translate to cases of human cancer. But, we speculate that it will in particular cases because some human cancers also activate the <em>Src<\/em> gene.<\/p>\n<p>\u201cWe are curious to know how general the mechanism is that we found here. Aside from the <em>Src<\/em> signalling pathway, we also found that <em>slpr<\/em> can mediate the signalling pathways controlled by other oncogenes. Finding out how this happens is our next goal.\u201d<\/p>\n","protected":false},"excerpt":{"rendered":"<p>Scientists at the RIKEN Center for Biosystems Dynamics Research (BDR) have been researching the processes behind cell proliferation in hopes of better treating cancer.<\/p>\n","protected":false},"author":13,"featured_media":11087,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"_acf_changed":false,"_monsterinsights_skip_tracking":false,"_monsterinsights_sitenote_active":false,"_monsterinsights_sitenote_note":"","_monsterinsights_sitenote_category":0,"footnotes":""},"categories":[10551],"tags":[3475,768],"acf":[],"yoast_head":"\n<title>Treating cancer by preventing the process of cell proliferation<\/title>\n<meta name=\"description\" content=\"Scientists at RIKEN BDR have been researching the processes behind cell proliferation in hopes of better treating cancer.\" \/>\n<meta name=\"robots\" content=\"index, follow, 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