A glycogen derived from sea urchin- shifts macrophages to the M1 phenotype and enhances the anti-pancreatic cancer activity of gemcitabine.

Fuente: PubMed
Salvato in:
Dettagli Bibliografici
Autori principali: Deng, Zhenzhen, Yu, Haoyu, Wu, Ning, Wang, Qingchi, Wang, Jing, Yue, Yang, Geng, Lihua, Zhang, Quanbin
Natura: Artículo científico
Lingua:en
Pubblicazione: Frontiers in pharmacology 2025
Accesso online:
Tags: Aggiungi Tag
Nessun Tag, puoi essere il primo ad aggiungerne!!
_version_ 1868266167301308416
author Deng, Zhenzhen
Yu, Haoyu
Wu, Ning
Wang, Qingchi
Wang, Jing
Yue, Yang
Geng, Lihua
Zhang, Quanbin
author_facet Deng, Zhenzhen
Yu, Haoyu
Wu, Ning
Wang, Qingchi
Wang, Jing
Yue, Yang
Geng, Lihua
Zhang, Quanbin
Deng, Zhenzhen
Yu, Haoyu
Wu, Ning
Wang, Qingchi
Wang, Jing
Yue, Yang
Geng, Lihua
Zhang, Quanbin
collection PubMed - marine biology
contents A glycogen derived from sea urchin- shifts macrophages to the M1 phenotype and enhances the anti-pancreatic cancer activity of gemcitabine. Deng, Zhenzhen Yu, Haoyu Wu, Ning Wang, Qingchi Wang, Jing Yue, Yang Geng, Lihua Zhang, Quanbin One of the biggest obstacles to treating pancreatic ductal adenocarcinoma (PDAC) is chemotherapy resistance. Macrophages are an essential element of the innate immune system and are distributed in almost every tissue in the body. Among them, macrophages infiltrating into the tumor microenvironment negatively regulate tumor immunity and participate in the generation, invasion, migration and drug resistance of PDAC. In prior study, we isolated a polysaccharide from sea urchin-, which was identified as a high molecular weight, highly branched glycogen (MSGA). In this study, we found that MSGA increased the expression of iNOS, IL-6, TNFα, IL-12 and triggered macrophage differentiation to the CD86 M1 phenotype. MSGA-induced M1 macrophages decreased the cell viabilities and induced apoptosis of PDAC cells. When combined with gemcitabine (GEM), MSGA significantly enhanced the pro-apoptotic activity of GEM. Mechanistically, MSGA transformed macrophages to the M1 phenotype through the stimulation of the JAK1/3-STAT1 signaling pathway and the suppression of STAT3 activity. Overall, our research showed that MSGA has profound potential for tumor immunotherapy. And as an "immune stimulator", MSGA could assist GEM in the treatment of PDAC.
format Artículo científico
id pubmed_40786029
institution PubMed
language en
publishDate 2025
publisher Frontiers in pharmacology
record_format pubmed
spellingShingle A glycogen derived from sea urchin- shifts macrophages to the M1 phenotype and enhances the anti-pancreatic cancer activity of gemcitabine.
Deng, Zhenzhen
Yu, Haoyu
Wu, Ning
Wang, Qingchi
Wang, Jing
Yue, Yang
Geng, Lihua
Zhang, Quanbin
A glycogen derived from sea urchin- shifts macrophages to the M1 phenotype and enhances the anti-pancreatic cancer activity of gemcitabine. Deng, Zhenzhen Yu, Haoyu Wu, Ning Wang, Qingchi Wang, Jing Yue, Yang Geng, Lihua Zhang, Quanbin One of the biggest obstacles to treating pancreatic ductal adenocarcinoma (PDAC) is chemotherapy resistance. Macrophages are an essential element of the innate immune system and are distributed in almost every tissue in the body. Among them, macrophages infiltrating into the tumor microenvironment negatively regulate tumor immunity and participate in the generation, invasion, migration and drug resistance of PDAC. In prior study, we isolated a polysaccharide from sea urchin-, which was identified as a high molecular weight, highly branched glycogen (MSGA). In this study, we found that MSGA increased the expression of iNOS, IL-6, TNFα, IL-12 and triggered macrophage differentiation to the CD86 M1 phenotype. MSGA-induced M1 macrophages decreased the cell viabilities and induced apoptosis of PDAC cells. When combined with gemcitabine (GEM), MSGA significantly enhanced the pro-apoptotic activity of GEM. Mechanistically, MSGA transformed macrophages to the M1 phenotype through the stimulation of the JAK1/3-STAT1 signaling pathway and the suppression of STAT3 activity. Overall, our research showed that MSGA has profound potential for tumor immunotherapy. And as an "immune stimulator", MSGA could assist GEM in the treatment of PDAC.
title A glycogen derived from sea urchin- shifts macrophages to the M1 phenotype and enhances the anti-pancreatic cancer activity of gemcitabine.
url https://pubmed.ncbi.nlm.nih.gov/40786029/