{"id":20793,"date":"2018-11-08T00:00:29","date_gmt":"2018-11-08T08:00:29","guid":{"rendered":"https:\/\/vermont.salk.edu\/?post_type=disclosure&#038;p=20793"},"modified":"2024-01-30T15:04:52","modified_gmt":"2024-01-30T23:04:52","slug":"genetic-whodunnit-for-cancer-gene-solved","status":"publish","type":"disclosure","link":"https:\/\/www.salk.edu\/de\/news-release\/genetic-whodunnit-for-cancer-gene-solved\/","title":{"rendered":"Genetic &#8220;whodunnit&#8221; for cancer gene solved"},"content":{"rendered":"<p>LA JOLLA\u2014Long thought to suppress cancer by slowing cellular metabolism, the protein complex AMPK also seemed to help some tumors grow, confounding researchers. Now, Salk Institute researchers have solved the long-standing mystery around why AMPK can both hinder and help cancer.<\/p>\n<div class=\"row\" style=\"\"><div class=\"col-md-12 col-md-push-0\"><div class=\"video-anchor\" id=\"video-kIV3Lypsfo0\"><\/div><div class=\"embed-responsive embed-responsive-16by9\"> <iframe class=\"embed-responsive-item\" src=\"\/\/www.youtube.com\/embed\/kIV3Lypsfo0?rel=0\" webkitallowfullscreen mozallowfullscreen allowfullscreen><\/iframe><\/div><!-- .embed-responsive --><\/div><!-- .col-md-*size --><\/div><!-- .\/row -->\n<p>The lab of Salk Professor <a href=\"https:\/\/www.salk.edu\/de\/scientist\/reuben-shaw\/\">Reuben Shaw<\/a> showed that late-stage cancers can trigger AMPK\u2019s cellular recycling signal to cannibalize pieces of the cell, supplying large lung tumors with the nutrients they need to grow. The work, which appeared in <a href=\"https:\/\/www.cell.com\/cell-metabolism\/fulltext\/S1550-4131(18)30637-5\"><em>Cell Metabolism<\/em><\/a> on November 8, 2018, suggests that blocking AMPK in some conditions could stop the growth of advanced tumors in the most common type of lung cancer.<\/p>\n<figure id=\"attachment_20797\"  class=\"wp-caption alignright\"><img loading=\"lazy\" decoding=\"async\" width=\"458\" height=\"305\" class=\"img-responsive wp-image-20797 size-col-md-5\" src=\"https:\/\/www.salk.edu\/wp-content\/uploads\/2018\/11\/0X8C7152rt-1500-458x305.jpg\" alt=\"From left: Reuben Shaw and Lillian Eichner\" srcset=\"https:\/\/www.salk.edu\/wp-content\/uploads\/2018\/11\/0X8C7152rt-1500-458x305.jpg 458w, https:\/\/www.salk.edu\/wp-content\/uploads\/2018\/11\/0X8C7152rt-1500-300x200.jpg 300w, https:\/\/www.salk.edu\/wp-content\/uploads\/2018\/11\/0X8C7152rt-1500-768x512.jpg 768w, https:\/\/www.salk.edu\/wp-content\/uploads\/2018\/11\/0X8C7152rt-1500-1024x683.jpg 1024w, https:\/\/www.salk.edu\/wp-content\/uploads\/2018\/11\/0X8C7152rt-1500-147x98.jpg 147w, https:\/\/www.salk.edu\/wp-content\/uploads\/2018\/11\/0X8C7152rt-1500-585x390.jpg 585w, https:\/\/www.salk.edu\/wp-content\/uploads\/2018\/11\/0X8C7152rt-1500-553x369.jpg 553w, https:\/\/www.salk.edu\/wp-content\/uploads\/2018\/11\/0X8C7152rt-1500-750x500.jpg 750w, https:\/\/www.salk.edu\/wp-content\/uploads\/2018\/11\/0X8C7152rt-1500-767x511.jpg 767w, https:\/\/www.salk.edu\/wp-content\/uploads\/2018\/11\/0X8C7152rt-1500-945x630.jpg 945w, https:\/\/www.salk.edu\/wp-content\/uploads\/2018\/11\/0X8C7152rt-1500-1250x833.jpg 1250w, https:\/\/www.salk.edu\/wp-content\/uploads\/2018\/11\/0X8C7152rt-1500-400x267.jpg 400w, https:\/\/www.salk.edu\/wp-content\/uploads\/2018\/11\/0X8C7152rt-1500.jpg 1500w\" sizes=\"auto, (max-width: 458px) 100vw, 458px\" \/><figcaption class=\"wp-caption-text\">From left: Reuben Shaw and Lillian Eichner <\/p>\n<p><a href=\"https:\/\/www.salk.edu\/wp-content\/uploads\/2018\/11\/0X8C7152rt-1500.jpg\">Klicken Sie hier<\/a> f\u00fcr ein hochaufl\u00f6sendes Bild. <\/p>\n<p>Kredit: Salk Institut<\/figcaption><\/figure>\n<p>&#8220;Our study shows that the same dysfunction in a genetic circuit that causes non-small-cell lung cancer to begin with is necessary for more mature tumor cells to survive when they don&#8217;t have enough nutrients,&#8221; says Shaw, director of the Salk Cancer Center and the paper&#8217;s co-senior author. &#8220;It&#8217;s exciting because not only does it solve a genetic &#8216;whodunnit,&#8217; but it also points to a potential new therapeutic target for a cancer that is often diagnosed very late.&#8221;<\/p>\n<p>AMPK acts as a fuel gauge for the cell, overseeing energy input and output to keep the cell running smoothly. Similar to a car sensor flashing a low-gas signal or turning off a vehicle\u2019s AC to save energy, AMPK slows down cell growth and changes the cell\u2019s metabolism if the cell\u2019s fuel (nutrients) is low. Previously, Shaw discovered that AMPK could <a href=\"https:\/\/www.salk.edu\/de\/news-release\/how-cells-running-on-empty-trigger-fuel-recycling\/\">halt tumors\u2019 revved-up metabolism<\/a>, as well as restore normal function to the liver and other tissues in diabetics.<\/p>\n<p>But the Shaw lab&#8217;s new work suggests that AMPK actually helps large tumors grow. In the current study, the team observed groups of mice with and without the AMPK fuel gauge to see how tumors developed.<\/p>\n<p>&#8220;We found that tumors grew much more slowly when AMPK was not present,&#8221; says Research Associate Lillian Eichner, the paper&#8217;s co-first author. &#8220;That means that AMPK is not always functioning as a tumor suppressor, as we originally thought.&#8221;<\/p>\n<figure id=\"attachment_20798\"  class=\"wp-caption alignleft\"><img loading=\"lazy\" decoding=\"async\" width=\"300\" height=\"225\" class=\"img-responsive wp-image-20798 size-pr-300\" src=\"https:\/\/www.salk.edu\/wp-content\/uploads\/2018\/11\/Image-1-hr-300x225.jpg\" alt=\"Genetically engineered lung tumors (solid purple) within the native lung environment are shown.\" srcset=\"https:\/\/www.salk.edu\/wp-content\/uploads\/2018\/11\/Image-1-hr-300x225.jpg 300w, https:\/\/www.salk.edu\/wp-content\/uploads\/2018\/11\/Image-1-hr-768x576.jpg 768w, https:\/\/www.salk.edu\/wp-content\/uploads\/2018\/11\/Image-1-hr-147x110.jpg 147w, https:\/\/www.salk.edu\/wp-content\/uploads\/2018\/11\/Image-1-hr-458x344.jpg 458w, https:\/\/www.salk.edu\/wp-content\/uploads\/2018\/11\/Image-1-hr-585x439.jpg 585w, https:\/\/www.salk.edu\/wp-content\/uploads\/2018\/11\/Image-1-hr-553x415.jpg 553w, https:\/\/www.salk.edu\/wp-content\/uploads\/2018\/11\/Image-1-hr-750x563.jpg 750w, https:\/\/www.salk.edu\/wp-content\/uploads\/2018\/11\/Image-1-hr-767x576.jpg 767w, https:\/\/www.salk.edu\/wp-content\/uploads\/2018\/11\/Image-1-hr-400x300.jpg 400w, https:\/\/www.salk.edu\/wp-content\/uploads\/2018\/11\/Image-1-hr.jpg 798w\" sizes=\"auto, (max-width: 300px) 100vw, 300px\" \/><figcaption class=\"wp-caption-text\">Genetically engineered lung tumors (solid purple) within the native lung environment are shown. <\/p>\n<p><a href=\"https:\/\/www.salk.edu\/wp-content\/uploads\/2018\/11\/Image-1-hr.jpg\">Klicken Sie hier<\/a> f\u00fcr ein hochaufl\u00f6sendes Bild. <\/p>\n<p>Kredit: Salk Institut<\/figcaption><\/figure>\n<p>The team analyzed which genes in tumor cells from the same mouse models were being activated under various conditions. One gene that was particularly active was Tfe3, which is known to activate cellular recycling. It turned out that when tumors became large enough that cells in the middle were too far from easy access to nutrients, AMPK signaled Tfe3 to initiate recycling of cellular materials as nutrients\u2014effectively cannibalizing pieces of the cell\u2014for the tumor to use.<\/p>\n<p>&#8220;Previously we were focused on how we could activate AMPK,&#8221; says Eichner. &#8220;Now that we&#8217;ve identified this mechanism, we can shift to how to inhibit it in certain cancers.&#8221;<\/p>\n<p>Shaw, who holds the William R. Brody Chair, adds, &#8220;We\u2019re excited because more advanced tumors seem to rely on AMPK to survive, and understanding this mechanism means we may be able to treat them.&#8221;<\/p>\n<p>Other authors included Sonja N. Brun, S\u00e9bastien Herzig, Nathan P. Young, Stephanie D. Curtis, David B. Shackelford, Maxim N. Shokhirev, Mathias Leblanc, Liliana I. Vera, Amanda Hutchins, Debbie S. Ross and Robert U. Svensson, who was the paper&#8217;s co-first and co-senior author.<\/p>\n<p>The work was funded by the National Institutes of Health (R35CA220538, P01CA120964), the Samuel Waxman Cancer Research Foundation, The Leona M. and Harry B. Helmsley Charitable Trust (grant #2012-PG- MED002) and the American Cancer Society (ACS#124183-PF-13-023-01-CSM)(PF-15-037-01-DMC).<\/p>","protected":false},"featured_media":20794,"template":"","faculty":[45],"disease-research":[46],"class_list":["post-20793","disclosure","type-disclosure","status-publish","has-post-thumbnail","hentry","faculty-reuben-shaw","disease-research-cancer-biology"],"acf":[],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v27.3 - https:\/\/yoast.com\/product\/yoast-seo-wordpress\/ -->\n<title>Genetic &quot;whodunnit&quot; for cancer gene solved - Salk Institute for Biological Studies<\/title>\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.salk.edu\/de\/news-release\/genetic-whodunnit-for-cancer-gene-solved\/\" \/>\n<meta property=\"og:locale\" content=\"de_DE\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Genetic &quot;whodunnit&quot; for cancer gene solved - Salk Institute for Biological Studies\" \/>\n<meta property=\"og:description\" content=\"LA JOLLA\u2014Long thought to suppress cancer by slowing cellular metabolism, the protein complex AMPK also seemed to help some tumors grow, confounding researchers. 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