ArticleCancer science2024
Potential of Mac-2-binding protein glycan isomer as a new therapeutic target in pancreatic cancer.
Article in Cancer science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Role of mac-2 binding protein glycosylation isomer in predicting fibrosis in patients with metabolic dysfunction-associated steatotic liver disease.World journal of hepatology · 2025Article
- Serum Mac2-binding protein glycosylated isomer (M2BPGi) as a prognostic biomarker in pancreatic ductal adenocarcinoma: iCAFs-derived M2BPGi drives tumor invasion.Journal of gastroenterology · 2025Article
- Leveraging glycosylation for early detection and therapeutic target discovery in pancreatic cancer.Cell death & disease · 2025Review
- Utility of Mac-2 binding protein glycosylation isomer as an excellent biomarker for the prediction of liver fibrosis, activity, and hepatocellular carcinoma onset: an expert review.Journal of gastroenterology · 2025Review
- Disease modifiers and novel markers in hepatitis B virus-related hepatocellular carcinoma.Journal of liver cancer · 2024Article
- Potential of Mac-2-binding protein glycan isomer as a new therapeutic target in pancreatic cancer.Cancer science · 2024Article
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 2 countries.
Funding
Abstract
Pancreatic cancer (PC) is a challenging malignancy to treat. Mac-2-binding protein glycan isomer (M2BPGi) is a novel serum marker of liver fibrosis and hepatocellular carcinoma and is secreted by hepatic stellate and stroma cells. Serum M2BPGi levels are upregulated in PC patients. We measured the expression of M2BPGi in the serum of 27 PC patients and determined whether M2BPGi affects the malignant potential of PC cells in vitro. We also examined the effect of M2BP on PC tumor growth and gemcitabine sensitivity in vivo. Serum M2BPGi levels in PC patients were higher compared with those of healthy subjects. M2BPGi extraction in cancer-associated fibroblasts (CAFs) was higher compared with that of PC cells. M2BPGi treatment promoted the proliferation and invasion of PC cells. The suppression of galectin-3, which binds to M2BPGi, did not affect the proliferation-promoting effect of M2BPGi in PC cells. The suppression of M2BP reduced tumor growth and enhanced gemcitabine sensitivity in PC-bearing xenograft mice. CAF-derived M2BPGi promotes the proliferation and invasion of PC cells. Targeting M2BPGi may represent a new therapeutic strategy to circumvent refractory PC.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.