{"title":"HTF4 可调节 GID2 的转录，从而促进胰腺癌的恶性生物学行为。","authors":"Wenyang Zhou, Xin Deng, Baosheng Wang, Yifeng Yuan, Jia Ma, Xiangpeng Meng","doi":"10.1016/j.pan.2024.08.008","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Helix-loop-helix transcription factor 4 (HTF4) as an anti-cancer target has been reported in many human cancers, but limited data exists regarding the effect of HTF4 in pancreatic cancer. In this study, we aimed to investigate the role of HTF4 in pancreatic cancer.</p><p><strong>Methods: </strong>The expression levels of HTF4 in clinical pancreatic cancer samples were measured. HTF4 was knocked down or overexpressed in pancreatic cancer cells and was subsequently tested for bio-function using in vitro assays and in vivo. The regulation of HTF4 on GID2 was assessed via bioinformatic tools and dual-luciferase reporter assay.</p><p><strong>Results: </strong>We found that HTF4 was highly expressed in pancreatic cancer tissues and correlated with poor patient prognosis. In addition, knocking down HTF4 expression inhibited cell proliferation, migration, and invasion, whereas HTF4 overexpression exerted the opposite effect. Moreover, HTF4 promoted tumor growth and metastasis in pancreatic cancer. Further, HTF4 bound to the GID2 promoter region and promoted transcriptional activation of GID2 in pancreatic cancer cells. GID2 knockdown suppressed HTF4-induced malignant behaviors of pancreatic cancer cells.</p><p><strong>Conclusions: </strong>Our findings suggest that the HTF4/GID2 axis accelerates the progression of pancreatic cancer, providing a potential therapeutic target and prognostic indicator for the treatment of pancreatic cancer patients.</p>","PeriodicalId":19976,"journal":{"name":"Pancreatology","volume":null,"pages":null},"PeriodicalIF":2.8000,"publicationDate":"2024-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"HTF4 modulates the transcription of GID2 to promote the malignant biological behavior of pancreatic cancer.\",\"authors\":\"Wenyang Zhou, Xin Deng, Baosheng Wang, Yifeng Yuan, Jia Ma, Xiangpeng Meng\",\"doi\":\"10.1016/j.pan.2024.08.008\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Helix-loop-helix transcription factor 4 (HTF4) as an anti-cancer target has been reported in many human cancers, but limited data exists regarding the effect of HTF4 in pancreatic cancer. In this study, we aimed to investigate the role of HTF4 in pancreatic cancer.</p><p><strong>Methods: </strong>The expression levels of HTF4 in clinical pancreatic cancer samples were measured. HTF4 was knocked down or overexpressed in pancreatic cancer cells and was subsequently tested for bio-function using in vitro assays and in vivo. The regulation of HTF4 on GID2 was assessed via bioinformatic tools and dual-luciferase reporter assay.</p><p><strong>Results: </strong>We found that HTF4 was highly expressed in pancreatic cancer tissues and correlated with poor patient prognosis. In addition, knocking down HTF4 expression inhibited cell proliferation, migration, and invasion, whereas HTF4 overexpression exerted the opposite effect. Moreover, HTF4 promoted tumor growth and metastasis in pancreatic cancer. Further, HTF4 bound to the GID2 promoter region and promoted transcriptional activation of GID2 in pancreatic cancer cells. GID2 knockdown suppressed HTF4-induced malignant behaviors of pancreatic cancer cells.</p><p><strong>Conclusions: </strong>Our findings suggest that the HTF4/GID2 axis accelerates the progression of pancreatic cancer, providing a potential therapeutic target and prognostic indicator for the treatment of pancreatic cancer patients.</p>\",\"PeriodicalId\":19976,\"journal\":{\"name\":\"Pancreatology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":2.8000,\"publicationDate\":\"2024-08-13\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Pancreatology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1016/j.pan.2024.08.008\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"GASTROENTEROLOGY & HEPATOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Pancreatology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1016/j.pan.2024.08.008","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"GASTROENTEROLOGY & HEPATOLOGY","Score":null,"Total":0}
HTF4 modulates the transcription of GID2 to promote the malignant biological behavior of pancreatic cancer.
Background: Helix-loop-helix transcription factor 4 (HTF4) as an anti-cancer target has been reported in many human cancers, but limited data exists regarding the effect of HTF4 in pancreatic cancer. In this study, we aimed to investigate the role of HTF4 in pancreatic cancer.
Methods: The expression levels of HTF4 in clinical pancreatic cancer samples were measured. HTF4 was knocked down or overexpressed in pancreatic cancer cells and was subsequently tested for bio-function using in vitro assays and in vivo. The regulation of HTF4 on GID2 was assessed via bioinformatic tools and dual-luciferase reporter assay.
Results: We found that HTF4 was highly expressed in pancreatic cancer tissues and correlated with poor patient prognosis. In addition, knocking down HTF4 expression inhibited cell proliferation, migration, and invasion, whereas HTF4 overexpression exerted the opposite effect. Moreover, HTF4 promoted tumor growth and metastasis in pancreatic cancer. Further, HTF4 bound to the GID2 promoter region and promoted transcriptional activation of GID2 in pancreatic cancer cells. GID2 knockdown suppressed HTF4-induced malignant behaviors of pancreatic cancer cells.
Conclusions: Our findings suggest that the HTF4/GID2 axis accelerates the progression of pancreatic cancer, providing a potential therapeutic target and prognostic indicator for the treatment of pancreatic cancer patients.
期刊介绍：
Pancreatology is the official journal of the International Association of Pancreatology (IAP), the European Pancreatic Club (EPC) and several national societies and study groups around the world. Dedicated to the understanding and treatment of exocrine as well as endocrine pancreatic disease, this multidisciplinary periodical publishes original basic, translational and clinical pancreatic research from a range of fields including gastroenterology, oncology, surgery, pharmacology, cellular and molecular biology as well as endocrinology, immunology and epidemiology. Readers can expect to gain new insights into pancreatic physiology and into the pathogenesis, diagnosis, therapeutic approaches and prognosis of pancreatic diseases. The journal features original articles, case reports, consensus guidelines and topical, cutting edge reviews, thus representing a source of valuable, novel information for clinical and basic researchers alike.
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