{"id":6766,"date":"2020-09-04T11:21:00","date_gmt":"2020-09-04T10:21:00","guid":{"rendered":"https:\/\/www.innovationnewsnetwork.com\/?p=6766"},"modified":"2020-09-04T11:21:00","modified_gmt":"2020-09-04T10:21:00","slug":"prostate-cancer-secondary-tumours","status":"publish","type":"post","link":"https:\/\/www.innovationnewsnetwork.com\/prostate-cancer-secondary-tumours\/6766\/","title":{"rendered":"New insight into how prostate cancer causes secondary tumours"},"content":{"rendered":"<h2>An increased awareness on a molecular level of the mechanisms prostate cancer cells use to become mobile and start spreading could provide new opportunities for treatment of aggressive prostate cancer in the future, according to a new study published in the scientific journal <em>iScience<\/em>.<\/h2>\n<p>Researchers at Ume\u00e5 University, Sweden, in collaboration with researchers in Uppsala and Tokyo, have <a href=\"https:\/\/www.cell.com\/iscience\/pdf\/S2589-0042(20)30662-3.pdf\" target=\"_blank\" rel=\"noopener noreferrer\">studied the growth factor TGF-\u03b2<\/a>, Transforming Growth Factor Beta, which regulates how cells grow and specialise, to gain an insight into how prostate cancer causes secondary tumours.<\/p>\n<p>\u201cWe can show that one specific amino acid in a signalling molecule plays an important role in mobilising the cancer cells and in that way increase the risk of metastases,\u201d explains Professor Mar\u00e9ne Landstr\u00f6m, Ume\u00e5 University.<\/p>\n<h3>TGF-\u03b2 and cancer growth<\/h3>\n<p>Previous studies have shown an overproduction of TGF-\u03b2 in many cancer forms, including <a href=\"https:\/\/www.innovationnewsnetwork.com\/eortc-driving-clinical-research-in-prostate-cancer\/6036\/\">prostate cancer<\/a>. High levels of TGF-\u03b2 have proven to be strongly linked with poor prognosis and low survival rates because of the growth factor stimulating cancer cells to spread in the human body and cause life-threatening secondary tumours \u2013 so-called metastases.<\/p>\n<p>TGF-\u03b2 regulates the expression of the protein Smad7 \u2013 an active component in the TGF-\u03b2 signalling chain. In healthy cells, Smad7 can prevent continued TGF-\u03b2 signalling via negative feedback.<\/p>\n<p>However, Mar\u00e9ne Landstr\u00f6m and her research group can now show, contrary to previous belief, that, in cancer cells, Smad7 can reinforce the <a href=\"https:\/\/www.innovationnewsnetwork.com\/prostate-cancer-diagnosis-treatment-and-research\/6093\/\">development of tumours<\/a> by regulating the gene expression of HDAC6 and c-Jun.<\/p>\n<p>The specific amino acid that has caught the researchers\u2019 attention, Lys102, is found in Smad7 and it binds to particular gene-regulating functions in DNA to increase production of the gene expression HDAC6 and c-Jun. This has the effect that cancer cells become more mobile and more prone to form metastases. Researchers have been able to see a clear connection between all these variables and a negative prognosis for prostate cancer.<\/p>\n<h3>Inhibiting secondary prostate cancer tumours<\/h3>\n<p>\u201cThe good news is that by using treatment with an HDAC6 inhibitor, we can make prostate cancer cells lose their mobility. In that way, novel opportunities can open up for treatments that reduce the risk of metastases,\u201d says Landstr\u00f6m.<\/p>\n<p>Clinical trials are now taking place in the UK with the goal of finding specific HDAC6 inhibitors in <a href=\"https:\/\/www.healtheuropa.eu\/ai-system-matches-professional-expertise-in-prostate-cancer-diagnosis\/96293\/\" target=\"_blank\" rel=\"noopener noreferrer\">patients with solid tumours<\/a>, in order to develop future treatments using HDAC6 inhibitors to be deployed alongside existing treatment protocols for patients with hard-to-treat forms of the disease.<\/p>\n<p>Future studies can explore the benefit of indicating expressions of Smad7, HDAC6 and c-Jun to enable new and more specific treatments for men with aggressive prostate cancer.<\/p>\n<p>The study also shows an entirely new function of Smad7 in the way that it can recruit Smad2 and Smad3 to the place of transcription for these genes. Previously, it has been thought that Smad7 held the role of inhibitor for TGF beta-Smad2\/3 transcriptional activity.<\/p>\n","protected":false},"excerpt":{"rendered":"<p>An increased awareness on a molecular level of the mechanisms prostate cancer cells use to become mobile and start spreading could provide new opportunities for treatment of aggressive prostate cancer in the future, according to a new study published in the scientific journal iScience. Researchers at Ume\u00e5 University, Sweden, in collaboration with researchers in Uppsala [&hellip;]<\/p>\n","protected":false},"author":3,"featured_media":6767,"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":[768],"acf":[],"yoast_head":"\n<title>New insight into how prostate cancer causes secondary tumours<\/title>\n<meta name=\"description\" content=\"Molecular awareness of the development of secondary tumours in prostate cancer cells could provide new opportunities for treatment.\" \/>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/www.innovationnewsnetwork.com\/prostate-cancer-secondary-tumours\/6766\/\" 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