Reem Alkhayer, Viviane Ponath, Elke Pogge von Strandmann
{"title":"NKG2D配体MICA响应APTO253的细胞类型特异性上调。","authors":"Reem Alkhayer, Viviane Ponath, Elke Pogge von Strandmann","doi":"10.21037/atm-24-20","DOIUrl":null,"url":null,"abstract":"<p><p>One of the most important targets for natural killer (NK) cell-mediated therapy is the induction of natural killer group 2D ligand (NKG2D-L) expression. APTO253 is a small molecule that selectively kills acute myeloid leukemia (AML) cells, and it has been reported that APTO253 can induce Krüppel-like factor 4 (KLF4) expression and downregulate c-MYC expression. Recently, we discovered a novel role of APTO253 in modulating the NK cell response by inducing surface expression of NKG2D-Ls, especially MHC class I polypeptide-related sequence A (MICA), in AML cells. In this study, we extended the research to validate the effect of APTO253 in other cancer cell lines and found that the enhanced expression of NKG2D-Ls in response to APTO253 is limited in a tumor cell-specific manner. Here, we show that MICA induction upon treatment with APTO253 not only varies between ovarian and pancreatic cancer cell lines but also differs in two ovarian cancer cell lines for an unknown reason. Additionally, our data suggest a link between the induced expression of <i>MICA</i> and the regulation of both, <i>KLF4</i> and <i>c</i>-<i>MYC</i>, which might represent a mechanism underlying the induction of NKG2D-L expression upon treatment with APTO253. These results may contribute to the potential use of APTO253 as a treatment to improve tumor cell-mediated NK cell cytotoxicity in various cancers.</p>","PeriodicalId":8216,"journal":{"name":"Annals of translational medicine","volume":"12 6","pages":"113"},"PeriodicalIF":0.0000,"publicationDate":"2024-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11729809/pdf/","citationCount":"0","resultStr":"{\"title\":\"Cell type-specific upregulation of NKG2D ligand MICA in response to APTO253.\",\"authors\":\"Reem Alkhayer, Viviane Ponath, Elke Pogge von Strandmann\",\"doi\":\"10.21037/atm-24-20\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>One of the most important targets for natural killer (NK) cell-mediated therapy is the induction of natural killer group 2D ligand (NKG2D-L) expression. APTO253 is a small molecule that selectively kills acute myeloid leukemia (AML) cells, and it has been reported that APTO253 can induce Krüppel-like factor 4 (KLF4) expression and downregulate c-MYC expression. Recently, we discovered a novel role of APTO253 in modulating the NK cell response by inducing surface expression of NKG2D-Ls, especially MHC class I polypeptide-related sequence A (MICA), in AML cells. In this study, we extended the research to validate the effect of APTO253 in other cancer cell lines and found that the enhanced expression of NKG2D-Ls in response to APTO253 is limited in a tumor cell-specific manner. Here, we show that MICA induction upon treatment with APTO253 not only varies between ovarian and pancreatic cancer cell lines but also differs in two ovarian cancer cell lines for an unknown reason. Additionally, our data suggest a link between the induced expression of <i>MICA</i> and the regulation of both, <i>KLF4</i> and <i>c</i>-<i>MYC</i>, which might represent a mechanism underlying the induction of NKG2D-L expression upon treatment with APTO253. These results may contribute to the potential use of APTO253 as a treatment to improve tumor cell-mediated NK cell cytotoxicity in various cancers.</p>\",\"PeriodicalId\":8216,\"journal\":{\"name\":\"Annals of translational medicine\",\"volume\":\"12 6\",\"pages\":\"113\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-12-24\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11729809/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Annals of translational medicine\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.21037/atm-24-20\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/12/3 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Annals of translational medicine","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.21037/atm-24-20","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/12/3 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
Cell type-specific upregulation of NKG2D ligand MICA in response to APTO253.
One of the most important targets for natural killer (NK) cell-mediated therapy is the induction of natural killer group 2D ligand (NKG2D-L) expression. APTO253 is a small molecule that selectively kills acute myeloid leukemia (AML) cells, and it has been reported that APTO253 can induce Krüppel-like factor 4 (KLF4) expression and downregulate c-MYC expression. Recently, we discovered a novel role of APTO253 in modulating the NK cell response by inducing surface expression of NKG2D-Ls, especially MHC class I polypeptide-related sequence A (MICA), in AML cells. In this study, we extended the research to validate the effect of APTO253 in other cancer cell lines and found that the enhanced expression of NKG2D-Ls in response to APTO253 is limited in a tumor cell-specific manner. Here, we show that MICA induction upon treatment with APTO253 not only varies between ovarian and pancreatic cancer cell lines but also differs in two ovarian cancer cell lines for an unknown reason. Additionally, our data suggest a link between the induced expression of MICA and the regulation of both, KLF4 and c-MYC, which might represent a mechanism underlying the induction of NKG2D-L expression upon treatment with APTO253. These results may contribute to the potential use of APTO253 as a treatment to improve tumor cell-mediated NK cell cytotoxicity in various cancers.
期刊介绍:
The Annals of Translational Medicine (Ann Transl Med; ATM; Print ISSN 2305-5839; Online ISSN 2305-5847) is an international, peer-reviewed Open Access journal featuring original and observational investigations in the broad fields of laboratory, clinical, and public health research, aiming to provide practical up-to-date information in significant research from all subspecialties of medicine and to broaden the readers’ vision and horizon from bench to bed and bed to bench. It is published quarterly (April 2013- Dec. 2013), monthly (Jan. 2014 - Feb. 2015), biweekly (March 2015-) and openly distributed worldwide. Annals of Translational Medicine is indexed in PubMed in Sept 2014 and in SCIE in 2018. Specific areas of interest include, but not limited to, multimodality therapy, epidemiology, biomarkers, imaging, biology, pathology, and technical advances related to medicine. Submissions describing preclinical research with potential for application to human disease, and studies describing research obtained from preliminary human experimentation with potential to further the understanding of biological mechanism underlying disease are encouraged. Also warmly welcome are studies describing public health research pertinent to clinic, disease diagnosis and prevention, or healthcare policy. With a focus on interdisciplinary academic cooperation, ATM aims to expedite the translation of scientific discovery into new or improved standards of management and health outcomes practice.