Cargando…

Syntenin Regulated by miR-216b Promotes Cancer Progression in Pancreatic Cancer

Outcomes for patients with pancreatic cancer (PC) are poor; therefore, there is an urgent need to identify novel therapeutic targets involved in the progression of PC. We previously identified 161 differentially expressed proteins (DEPs) in PC. Syntenin (SDCBP) was identified as a survival-related p...

Descripción completa

Detalles Bibliográficos
Autores principales: Zu, Fuqiang, Chen, Hui, Liu, Qingfeng, Zang, Hui, Li, Zeyu, Tan, Xiaodong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8831246/
https://www.ncbi.nlm.nih.gov/pubmed/35155233
http://dx.doi.org/10.3389/fonc.2022.790788
_version_ 1784648463523250176
author Zu, Fuqiang
Chen, Hui
Liu, Qingfeng
Zang, Hui
Li, Zeyu
Tan, Xiaodong
author_facet Zu, Fuqiang
Chen, Hui
Liu, Qingfeng
Zang, Hui
Li, Zeyu
Tan, Xiaodong
author_sort Zu, Fuqiang
collection PubMed
description Outcomes for patients with pancreatic cancer (PC) are poor; therefore, there is an urgent need to identify novel therapeutic targets involved in the progression of PC. We previously identified 161 differentially expressed proteins (DEPs) in PC. Syntenin (SDCBP) was identified as a survival-related protein through integrated, survival, and Cox analyses. High expression of SDCBP was associated with a poor prognosis in PC tissue and promoted the proliferation, migration, and invasion of PC cells, and induced epithelial–mesenchymal transition (EMT) via the PI3K/AKT pathway. Additionally, we elucidated the regulatory mechanism underlying these roles of SDCBP at the post-transcriptional level. microRNAs (miRNAs) of SDCBP were predicted using bioinformatics. Low levels of miR-216b expression were confirmed in PC tissues and were negatively correlated with SDCBP expression. miR-216b was found to directly regulate SDCBP expression through luciferase reporter assays. Furthermore, agomiR-216b restrained PC proliferation, migration, invasion, and EMT via the PI3K/AKT pathway, whereas antagomiR-216b facilitated this process. Notably, the knockout of SDCBP counteracted the effect of antagomiR-216b in PC, which suggested that miR-216b and SDCBP represent molecular targets underlying PC progression and EMT. Finally, the results were validated in in vivo studies. These findings indicated that low expression of miR-216b and the oncogene SDCBP contributes to PC migration, invasion, and EMT, and that they have potential as future therapeutic targets for patients with PC.
format Online
Article
Text
id pubmed-8831246
institution National Center for Biotechnology Information
language English
publishDate 2022
publisher Frontiers Media S.A.
record_format MEDLINE/PubMed
spelling pubmed-88312462022-02-12 Syntenin Regulated by miR-216b Promotes Cancer Progression in Pancreatic Cancer Zu, Fuqiang Chen, Hui Liu, Qingfeng Zang, Hui Li, Zeyu Tan, Xiaodong Front Oncol Oncology Outcomes for patients with pancreatic cancer (PC) are poor; therefore, there is an urgent need to identify novel therapeutic targets involved in the progression of PC. We previously identified 161 differentially expressed proteins (DEPs) in PC. Syntenin (SDCBP) was identified as a survival-related protein through integrated, survival, and Cox analyses. High expression of SDCBP was associated with a poor prognosis in PC tissue and promoted the proliferation, migration, and invasion of PC cells, and induced epithelial–mesenchymal transition (EMT) via the PI3K/AKT pathway. Additionally, we elucidated the regulatory mechanism underlying these roles of SDCBP at the post-transcriptional level. microRNAs (miRNAs) of SDCBP were predicted using bioinformatics. Low levels of miR-216b expression were confirmed in PC tissues and were negatively correlated with SDCBP expression. miR-216b was found to directly regulate SDCBP expression through luciferase reporter assays. Furthermore, agomiR-216b restrained PC proliferation, migration, invasion, and EMT via the PI3K/AKT pathway, whereas antagomiR-216b facilitated this process. Notably, the knockout of SDCBP counteracted the effect of antagomiR-216b in PC, which suggested that miR-216b and SDCBP represent molecular targets underlying PC progression and EMT. Finally, the results were validated in in vivo studies. These findings indicated that low expression of miR-216b and the oncogene SDCBP contributes to PC migration, invasion, and EMT, and that they have potential as future therapeutic targets for patients with PC. Frontiers Media S.A. 2022-01-28 /pmc/articles/PMC8831246/ /pubmed/35155233 http://dx.doi.org/10.3389/fonc.2022.790788 Text en Copyright © 2022 Zu, Chen, Liu, Zang, Li and Tan https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Oncology
Zu, Fuqiang
Chen, Hui
Liu, Qingfeng
Zang, Hui
Li, Zeyu
Tan, Xiaodong
Syntenin Regulated by miR-216b Promotes Cancer Progression in Pancreatic Cancer
title Syntenin Regulated by miR-216b Promotes Cancer Progression in Pancreatic Cancer
title_full Syntenin Regulated by miR-216b Promotes Cancer Progression in Pancreatic Cancer
title_fullStr Syntenin Regulated by miR-216b Promotes Cancer Progression in Pancreatic Cancer
title_full_unstemmed Syntenin Regulated by miR-216b Promotes Cancer Progression in Pancreatic Cancer
title_short Syntenin Regulated by miR-216b Promotes Cancer Progression in Pancreatic Cancer
title_sort syntenin regulated by mir-216b promotes cancer progression in pancreatic cancer
topic Oncology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8831246/
https://www.ncbi.nlm.nih.gov/pubmed/35155233
http://dx.doi.org/10.3389/fonc.2022.790788
work_keys_str_mv AT zufuqiang synteninregulatedbymir216bpromotescancerprogressioninpancreaticcancer
AT chenhui synteninregulatedbymir216bpromotescancerprogressioninpancreaticcancer
AT liuqingfeng synteninregulatedbymir216bpromotescancerprogressioninpancreaticcancer
AT zanghui synteninregulatedbymir216bpromotescancerprogressioninpancreaticcancer
AT lizeyu synteninregulatedbymir216bpromotescancerprogressioninpancreaticcancer
AT tanxiaodong synteninregulatedbymir216bpromotescancerprogressioninpancreaticcancer