ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016
Suppression of CD26 inhibits growth and metastasis of pancreatic cancer.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- DNA methylation-mediated ADA overexpression drives pancreatic cancer progression.Discover oncology · 2025Article
- Down-regulation of DPP4 by TGFβ1/miR29a-3p inhibited proliferation and promoted migration of ovarian cancer cells.Discover oncology · 2023Article
- DPP inhibition alters the CXCR3 axis and enhances NK and CD8+ T cell infiltration to improve anti-PD1 efficacy in murine models of pancreatic ductal adenocarcinoma.Journal for immunotherapy of cancer · 2021Article
- CD26 as a Promising Biomarker for Predicting Prognosis in Patients with Pancreatic Tumors.OncoTargets and therapy · 2020Article
- Review
- Effects of a DPP4 Inhibitor on Progression of NASH-related HCC and the p62/ Keap1/Nrf2-Pentose Phosphate Pathway in a Mouse Model.Liver cancer · 2019Article
- Predictive significance of serum dipeptidyl peptidase-IV in papillary thyroid carcinoma.Cancer biomarkers : section A of Disease markers · 2019Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CD26/DPPIV is a glycosylated transmembrane type II protein and has a multitude of biological functions, while its impact on the malignant phenotypes of cancer cells has not been fully understood. This study aimed to investigate the effect of CD26 on growth and metastasis of pancreatic cancer cells in vitro and in vivo. We found in this study that CD26 expression was higher in cell lines that derived from the metastatic sites than those from the primary tumor sites. In specimens of pancreatic cancer patients, CD26 expression was higher in cancerous tissues than in paired normal tissues. In in vitro experiments, knockdown of CD26 expression inhibited cell growth, migration, invasion, colony formation, and increased cell apoptosis of pancreatic cancer cells. Knockdown of CD26 also decreased tumor growth and liver metastasis in vivo by using xenograft animal models. Suppression of CD26 could inhibit expression of epithelial-mesenchymal transition (EMT) regulatory genes. Our results indicated that CD26 may represent a new therapeutic target for pancreatic cancer.
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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 Socratic graph.