{"paper_id":"0f6ecbb3-aca7-47f8-a460-ac9dfcf71d02","body_text":"Poly-(A)-binding protein cytoplasmic 1 gene regulates cell proliferation via TP53 R273H hotspot activation in Japanese patients with common cancer types | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Research Article Poly-(A)-binding protein cytoplasmic 1 gene regulates cell proliferation via TP53 R273H hotspot activation in Japanese patients with common cancer types Shumpei Ohnami, Kouji Maruyama, Takeshi Nagashima, Keiichi Hatakeyama, and 13 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-7115778/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract Background Mutations in TP53 occur in approximately half of all common cancer types, and play a critical role in tumor progression and metastasis. However, because mutant TP53 can result in both loss and gain of function in cells, complicating the development of drugs that directly target TP53 . We screened for genes whose expression is directly/indirectly increased by specific TP53 mutations that affect cancer progression. Methods We explored potential effector molecules based on differences in gene expression between patients with colorectal (CRC, n = 370), lung (LC, n = 347), and stomach cancers (STC, n = 282) carrying wild-type TP53 , and patients with CRC (n = 902), LC (n = 349), and STC (n = 237) carrying TP53 mutations. Results Frequencies of TP53 mutations in CRC, LC, and STC were 70.9%, 50.1%, and 45.7%, respectively, and the most frequent TP53 missense mutation was TP53- R273H. Comprehensive gene expression analyses comparing patients with TP53 mutations and those with wild-type TP53 identified 24 genes whose expression was significantly increased in TP53 -mutated patients, and 20 genes whose expression was decreased across all three tumor types. Among these genes, poly-(A)-binding protein cytoplasmic 1 ( PABPC1 ) showed significantly increased expression in A549 LC and MCF7 breast cancer cell lines carrying wild-type TP53 transfected with TP53- R273H mutants, but not TP53 -R175H and TP53 -D49H mutants. Furthermore, transient transfection with a plasmid encoding small interfering RNA targeting PABPC1 significantly suppressed the proliferation of HT29 and SW480 colon cancer cell lines harboring the TP53- R273H mutation. Additionally, patients with CRC harboring the TP53 -R273H with high PABPC1 expression had poorer overall survival than those with low PABPC1 expression. Conclusion To our knowledge, this is the first report to demonstrate whether PABPC1 is upregulated by TP53- R273H mutation, suggesting that PABPC1 , which potentially functions as an oncogene, may be an effective therapeutic target for patients with TP53- R273H mutation. PABPC1 TP53-R273H mutation Colorectal cancer Targeting TP53 Gene expression Full Text Additional Declarations No competing interests reported. Supplementary Table 1 is not available with this version. Supplementary Table 1. Genes showing upregulated or downregulated expression in patients with TP53 mutation types compared with those with wild-type TP53 across three cancer types. Supplementary Files SuppleFig11.pdf SuppleFig12.pdf SuppleFig13.pdf SuppleFig14.pdf SuppleFig15.pdf Cite Share Download PDF Status: Posted Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. Our growing team is made up of researchers and industry professionals working together to solve the most critical problems facing scientific publishing. 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TP53 R273H hotspot activation in Japanese patients with common cancer types\",\"fulltext\":[],\"fulltextSource\":\"\",\"fullText\":\"\",\"funders\":[],\"hasAdminPriorityOnWorkflow\":false,\"hasManuscriptDocX\":false,\"hasOptedInToPreprint\":true,\"hasPassedJournalQc\":\"\",\"hasAnyPriority\":false,\"hideJournal\":true,\"highlight\":\"\",\"institution\":\"\",\"isAcceptedByJournal\":false,\"isAuthorSuppliedPdf\":true,\"isDeskRejected\":\"\",\"isHiddenFromSearch\":false,\"isInQc\":false,\"isInWorkflow\":false,\"isPdf\":true,\"isPdfUpToDate\":true,\"isWithdrawnOrRetracted\":false,\"journal\":{\"display\":true,\"email\":\"info@researchsquare.com\",\"identity\":\"researchsquare\",\"isNatureJournal\":false,\"hasQc\":true,\"allowDirectSubmit\":true,\"externalIdentity\":\"\",\"sideBox\":\"\",\"snPcode\":\"\",\"submissionUrl\":\"/submission\",\"title\":\"Research Square\",\"twitterHandle\":\"researchsquare\",\"acdcEnabled\":true,\"dfaEnabled\":false,\"editorialSystem\":\"\",\"reportingPortfolio\":\"\",\"inReviewEnabled\":false,\"inReviewRevisionsEnabled\":true},\"keywords\":\"PABPC1, TP53-R273H mutation, Colorectal cancer, Targeting TP53, Gene expression\",\"lastPublishedDoi\":\"10.21203/rs.3.rs-7115778/v1\",\"lastPublishedDoiUrl\":\"https://doi.org/10.21203/rs.3.rs-7115778/v1\",\"license\":{\"name\":\"CC BY 4.0\",\"url\":\"https://creativecommons.org/licenses/by/4.0/\"},\"manuscriptAbstract\":\"\\u003ch2\\u003eBackground\\u003c/h2\\u003e\\u003cp\\u003eMutations in \\u003cem\\u003eTP53\\u003c/em\\u003e occur in approximately half of all common cancer types, and play a critical role in tumor progression and metastasis. However, because mutant \\u003cem\\u003eTP53\\u003c/em\\u003e can result in both loss and gain of function in cells, complicating the development of drugs that directly target \\u003cem\\u003eTP53\\u003c/em\\u003e. We screened for genes whose expression is directly/indirectly increased by specific \\u003cem\\u003eTP53\\u003c/em\\u003e mutations that affect cancer progression.\\u003c/p\\u003e\\u003ch2\\u003eMethods\\u003c/h2\\u003e\\u003cp\\u003eWe explored potential effector molecules based on differences in gene expression between patients with colorectal (CRC, n\\u0026thinsp;=\\u0026thinsp;370), lung (LC, n\\u0026thinsp;=\\u0026thinsp;347), and stomach cancers (STC, n\\u0026thinsp;=\\u0026thinsp;282) carrying wild-type \\u003cem\\u003eTP53\\u003c/em\\u003e, and patients with CRC (n\\u0026thinsp;=\\u0026thinsp;902), LC (n\\u0026thinsp;=\\u0026thinsp;349), and STC (n\\u0026thinsp;=\\u0026thinsp;237) carrying \\u003cem\\u003eTP53\\u003c/em\\u003e mutations.\\u003c/p\\u003e\\u003ch2\\u003eResults\\u003c/h2\\u003e\\u003cp\\u003eFrequencies of \\u003cem\\u003eTP53\\u003c/em\\u003e mutations in CRC, LC, and STC were 70.9%, 50.1%, and 45.7%, respectively, and the most frequent \\u003cem\\u003eTP53\\u003c/em\\u003e missense mutation was \\u003cem\\u003eTP53-\\u003c/em\\u003eR273H. Comprehensive gene expression analyses comparing patients with \\u003cem\\u003eTP53\\u003c/em\\u003e mutations and those with wild-type \\u003cem\\u003eTP53\\u003c/em\\u003e identified 24 genes whose expression was significantly increased in \\u003cem\\u003eTP53\\u003c/em\\u003e-mutated patients, and 20 genes whose expression was decreased across all three tumor types. Among these genes, poly-(A)-binding protein cytoplasmic 1 (\\u003cem\\u003ePABPC1\\u003c/em\\u003e) showed significantly increased expression in A549 LC and MCF7 breast cancer cell lines carrying wild-type \\u003cem\\u003eTP53\\u003c/em\\u003e transfected with \\u003cem\\u003eTP53-\\u003c/em\\u003eR273H mutants, but not \\u003cem\\u003eTP53\\u003c/em\\u003e-R175H and \\u003cem\\u003eTP53\\u003c/em\\u003e-D49H mutants. Furthermore, transient transfection with a plasmid encoding small interfering RNA targeting \\u003cem\\u003ePABPC1\\u003c/em\\u003e significantly suppressed the proliferation of HT29 and SW480 colon cancer cell lines harboring the \\u003cem\\u003eTP53-\\u003c/em\\u003eR273H mutation. Additionally, patients with CRC harboring the \\u003cem\\u003eTP53\\u003c/em\\u003e-R273H with high \\u003cem\\u003ePABPC1\\u003c/em\\u003e expression had poorer overall survival than those with low \\u003cem\\u003ePABPC1\\u003c/em\\u003e expression.\\u003c/p\\u003e\\u003ch2\\u003eConclusion\\u003c/h2\\u003e\\u003cp\\u003eTo our knowledge, this is the first report to demonstrate whether \\u003cem\\u003ePABPC1\\u003c/em\\u003e is upregulated by \\u003cem\\u003eTP53-\\u003c/em\\u003eR273H mutation, suggesting that \\u003cem\\u003ePABPC1\\u003c/em\\u003e, which potentially functions as an oncogene, may be an effective therapeutic target for patients with \\u003cem\\u003eTP53-\\u003c/em\\u003eR273H mutation.\\u003c/p\\u003e\",\"manuscriptTitle\":\"Poly-(A)-binding protein cytoplasmic 1 gene regulates cell proliferation via TP53 R273H hotspot activation in Japanese patients with common cancer types\",\"msid\":\"\",\"msnumber\":\"\",\"nonDraftVersions\":[{\"code\":1,\"date\":\"2025-08-05 15:43:41\",\"doi\":\"10.21203/rs.3.rs-7115778/v1\",\"editorialEvents\":[{\"type\":\"communityComments\",\"content\":0}],\"status\":\"published\",\"journal\":{\"display\":true,\"email\":\"info@researchsquare.com\",\"identity\":\"researchsquare\",\"isNatureJournal\":false,\"hasQc\":true,\"allowDirectSubmit\":true,\"externalIdentity\":\"\",\"sideBox\":\"\",\"snPcode\":\"\",\"submissionUrl\":\"/submission\",\"title\":\"Research Square\",\"twitterHandle\":\"researchsquare\",\"acdcEnabled\":true,\"dfaEnabled\":false,\"editorialSystem\":\"\",\"reportingPortfolio\":\"\",\"inReviewEnabled\":false,\"inReviewRevisionsEnabled\":true}}],\"origin\":\"\",\"ownerIdentity\":\"ee233b44-2fb2-4e2a-b40e-ff745e45d025\",\"owner\":[],\"postedDate\":\"August 5th, 2025\",\"published\":true,\"recentEditorialEvents\":[],\"rejectedJournal\":[],\"revision\":\"\",\"amendment\":\"\",\"status\":\"posted\",\"subjectAreas\":[],\"tags\":[],\"updatedAt\":\"2025-10-08T14:09:02+00:00\",\"versionOfRecord\":[],\"versionCreatedAt\":\"2025-08-05 15:43:41\",\"video\":\"\",\"vorDoi\":\"\",\"vorDoiUrl\":\"\",\"workflowStages\":[]},\"version\":\"v1\",\"identity\":\"rs-7115778\",\"journalConfig\":\"researchsquare\"},\"__N_SSP\":true},\"page\":\"/article/[identity]/[[...version]]\",\"query\":{\"redirect\":\"/article/rs-7115778\",\"identity\":\"rs-7115778\",\"version\":[\"v1\"]},\"buildId\":\"8U1c8b4HqxoKbykW_rLl7\",\"isFallback\":false,\"isExperimentalCompile\":false,\"dynamicIds\":[84888],\"gssp\":true,\"scriptLoader\":[]}","source_license":"CC-BY-4.0","license_restricted":false}