Brooke L O'Donnell, Dan Stefan, Yu-Hsin Chiu, Michael Zeitz, Justin Tang, Danielle Johnston, Stephanie Leighton, Carlijn Van Kessell, Kevin Barr, Laszlo Gyenis, Taylor Freeman, John J Kelly, Samar Sayedyahossein, David W Litchfield, Kathryn Roth, James W Smyth, Matthew Hebb, John Ronald, Douglas A Bayliss, Silvia Penuela
{"title":"新型 Pannexin 1 同工酶在癌症中增加","authors":"Brooke L O'Donnell, Dan Stefan, Yu-Hsin Chiu, Michael Zeitz, Justin Tang, Danielle Johnston, Stephanie Leighton, Carlijn Van Kessell, Kevin Barr, Laszlo Gyenis, Taylor Freeman, John J Kelly, Samar Sayedyahossein, David W Litchfield, Kathryn Roth, James W Smyth, Matthew Hebb, John Ronald, Douglas A Bayliss, Silvia Penuela","doi":"10.1101/2024.09.09.612143","DOIUrl":null,"url":null,"abstract":"Pannexin 1 (PANX1) is upregulated in many cancers, where its activity and signalling promote tumorigenic properties. Here, we report a novel ~25 kDa isoform of human PANX1 (hPANX1-25K) which lacks the N-terminus and was detected in several human cancer cell lines including melanoma, osteosarcoma,breast cancer and glioblastoma multiforme. This isoform was increased upon hPANX1 CRISPR/Cas9 deletion targeting the first exon near M1, suggesting a potential alternative translation initiation (ATI) site. hPANX1-25K was confirmed to be a hPANX1 isoform via mass spectrometry, can be N-linked glycosylated at N254, and can interact with both β-catenin and full length hPANX1. A double deletion of hPANX1 and hPANX1-25K reduces cell growth and viability in cancer cells. hPANX1-25K is prevalent throughout melanoma progression, and its levels are increased in squamous cell carcinoma cells and patient-derived tumours, compared to keratinocytes and normal skin controls, indicating that it may be differentially regulated in normal and cancer cells.","PeriodicalId":501590,"journal":{"name":"bioRxiv - Cell Biology","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Novel Pannexin 1 isoform is increased in cancer\",\"authors\":\"Brooke L O'Donnell, Dan Stefan, Yu-Hsin Chiu, Michael Zeitz, Justin Tang, Danielle Johnston, Stephanie Leighton, Carlijn Van Kessell, Kevin Barr, Laszlo Gyenis, Taylor Freeman, John J Kelly, Samar Sayedyahossein, David W Litchfield, Kathryn Roth, James W Smyth, Matthew Hebb, John Ronald, Douglas A Bayliss, Silvia Penuela\",\"doi\":\"10.1101/2024.09.09.612143\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Pannexin 1 (PANX1) is upregulated in many cancers, where its activity and signalling promote tumorigenic properties. Here, we report a novel ~25 kDa isoform of human PANX1 (hPANX1-25K) which lacks the N-terminus and was detected in several human cancer cell lines including melanoma, osteosarcoma,breast cancer and glioblastoma multiforme. This isoform was increased upon hPANX1 CRISPR/Cas9 deletion targeting the first exon near M1, suggesting a potential alternative translation initiation (ATI) site. hPANX1-25K was confirmed to be a hPANX1 isoform via mass spectrometry, can be N-linked glycosylated at N254, and can interact with both β-catenin and full length hPANX1. A double deletion of hPANX1 and hPANX1-25K reduces cell growth and viability in cancer cells. hPANX1-25K is prevalent throughout melanoma progression, and its levels are increased in squamous cell carcinoma cells and patient-derived tumours, compared to keratinocytes and normal skin controls, indicating that it may be differentially regulated in normal and cancer cells.\",\"PeriodicalId\":501590,\"journal\":{\"name\":\"bioRxiv - Cell Biology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-09-11\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"bioRxiv - Cell Biology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1101/2024.09.09.612143\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"bioRxiv - Cell Biology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1101/2024.09.09.612143","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Pannexin 1 (PANX1) is upregulated in many cancers, where its activity and signalling promote tumorigenic properties. Here, we report a novel ~25 kDa isoform of human PANX1 (hPANX1-25K) which lacks the N-terminus and was detected in several human cancer cell lines including melanoma, osteosarcoma,breast cancer and glioblastoma multiforme. This isoform was increased upon hPANX1 CRISPR/Cas9 deletion targeting the first exon near M1, suggesting a potential alternative translation initiation (ATI) site. hPANX1-25K was confirmed to be a hPANX1 isoform via mass spectrometry, can be N-linked glycosylated at N254, and can interact with both β-catenin and full length hPANX1. A double deletion of hPANX1 and hPANX1-25K reduces cell growth and viability in cancer cells. hPANX1-25K is prevalent throughout melanoma progression, and its levels are increased in squamous cell carcinoma cells and patient-derived tumours, compared to keratinocytes and normal skin controls, indicating that it may be differentially regulated in normal and cancer cells.
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