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Transcriptional ITPR3 as potential targets and biomarkers for human pancreatic cancer
Inositol 1,4,5-Triphosphate Receptor Family (ITPRs) are necessary intracellular Ca2+-release channel encoders and participate in mammalian cell physiological and pathological processes. Previous studies have suggested that ITPRs participate in tumorigenesis of multiple cancers. Nevertheless, the div...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Impact Journals
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9186782/ https://www.ncbi.nlm.nih.gov/pubmed/35580861 http://dx.doi.org/10.18632/aging.204080 |
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author | Zheng, Wangyang Bai, Xue Zhou, Yongxu Yu, Liang Ji, Daolin Zheng, Yuling Meng, Nanfeng Wang, Hang Huang, Ziyue Chen, Wangming Yam, Judy Wai Ping Xu, Yi Cui, Yunfu |
author_facet | Zheng, Wangyang Bai, Xue Zhou, Yongxu Yu, Liang Ji, Daolin Zheng, Yuling Meng, Nanfeng Wang, Hang Huang, Ziyue Chen, Wangming Yam, Judy Wai Ping Xu, Yi Cui, Yunfu |
author_sort | Zheng, Wangyang |
collection | PubMed |
description | Inositol 1,4,5-Triphosphate Receptor Family (ITPRs) are necessary intracellular Ca2+-release channel encoders and participate in mammalian cell physiological and pathological processes. Previous studies have suggested that ITPRs participate in tumorigenesis of multiple cancers. Nevertheless, the diverse expression profiles and prognostic significance of three ITPRs in pancreatic cancer have yet to be uncovered. In this work, we examined the expression levels and survival dates of ITPRs in patients with pancreatic cancer. As a result, we identified that ITPR1 and ITPR3 expression levels are significantly elevated in cancerous specimens. Survival data revealed that over-expression of ITPR2 and ITPR3 resulted in unfavourable overall survival and pathological stage. The multivariate Cox logistic regression analysis showed that ITPR3 could be an independent risk factor for PAAD patient survival. Moreover, to investigate how ITPRs work, co-expressed genes, alterations, protein-protein interaction, immune infiltration, methylation, and functional enrichment of ITPRs were also analyzed. Then, we evaluated these findings in clinical samples. Moreover, the gain and loss of function of ITPR3 were also conducted. The electron microscope assay was employed to explore the role of ITPR3 in pancreatic cancer cell lines’ endoplasmic reticulum stress. In summary, our findings demonstrated that ITPR3 has the potential to be drug targets and biomarkers for human pancreatic cancer. |
format | Online Article Text |
id | pubmed-9186782 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Impact Journals |
record_format | MEDLINE/PubMed |
spelling | pubmed-91867822022-06-14 Transcriptional ITPR3 as potential targets and biomarkers for human pancreatic cancer Zheng, Wangyang Bai, Xue Zhou, Yongxu Yu, Liang Ji, Daolin Zheng, Yuling Meng, Nanfeng Wang, Hang Huang, Ziyue Chen, Wangming Yam, Judy Wai Ping Xu, Yi Cui, Yunfu Aging (Albany NY) Research Paper Inositol 1,4,5-Triphosphate Receptor Family (ITPRs) are necessary intracellular Ca2+-release channel encoders and participate in mammalian cell physiological and pathological processes. Previous studies have suggested that ITPRs participate in tumorigenesis of multiple cancers. Nevertheless, the diverse expression profiles and prognostic significance of three ITPRs in pancreatic cancer have yet to be uncovered. In this work, we examined the expression levels and survival dates of ITPRs in patients with pancreatic cancer. As a result, we identified that ITPR1 and ITPR3 expression levels are significantly elevated in cancerous specimens. Survival data revealed that over-expression of ITPR2 and ITPR3 resulted in unfavourable overall survival and pathological stage. The multivariate Cox logistic regression analysis showed that ITPR3 could be an independent risk factor for PAAD patient survival. Moreover, to investigate how ITPRs work, co-expressed genes, alterations, protein-protein interaction, immune infiltration, methylation, and functional enrichment of ITPRs were also analyzed. Then, we evaluated these findings in clinical samples. Moreover, the gain and loss of function of ITPR3 were also conducted. The electron microscope assay was employed to explore the role of ITPR3 in pancreatic cancer cell lines’ endoplasmic reticulum stress. In summary, our findings demonstrated that ITPR3 has the potential to be drug targets and biomarkers for human pancreatic cancer. Impact Journals 2022-05-17 /pmc/articles/PMC9186782/ /pubmed/35580861 http://dx.doi.org/10.18632/aging.204080 Text en Copyright: © 2022 Zheng et al. https://creativecommons.org/licenses/by/3.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/3.0/) (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Paper Zheng, Wangyang Bai, Xue Zhou, Yongxu Yu, Liang Ji, Daolin Zheng, Yuling Meng, Nanfeng Wang, Hang Huang, Ziyue Chen, Wangming Yam, Judy Wai Ping Xu, Yi Cui, Yunfu Transcriptional ITPR3 as potential targets and biomarkers for human pancreatic cancer |
title | Transcriptional ITPR3 as potential targets and biomarkers for human pancreatic cancer |
title_full | Transcriptional ITPR3 as potential targets and biomarkers for human pancreatic cancer |
title_fullStr | Transcriptional ITPR3 as potential targets and biomarkers for human pancreatic cancer |
title_full_unstemmed | Transcriptional ITPR3 as potential targets and biomarkers for human pancreatic cancer |
title_short | Transcriptional ITPR3 as potential targets and biomarkers for human pancreatic cancer |
title_sort | transcriptional itpr3 as potential targets and biomarkers for human pancreatic cancer |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9186782/ https://www.ncbi.nlm.nih.gov/pubmed/35580861 http://dx.doi.org/10.18632/aging.204080 |
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