ArticleJournal of endocrinological investigation2021
DPP4 gene silencing inhibits proliferation and epithelial-mesenchymal transition of papillary thyroid carcinoma cells through suppression of the MAPK pathway.
Article in Journal of endocrinological investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Integrated Cytokine, Metabolic, and Proliferative Profiling Reveals Divergent Metabolic and Proliferative Responses in Papillary Thyroid Cancer Cells.International journal of molecular sciences · 2026Article
- Anti-fibrotic effects of evogliptin in fibroblasts derived from post-burn hypertrophic scars.Scientific reports · 2026Article
- Quercetin suppresses the proliferation of thyroid cancer cells by reducing the expression level of DPP4 and inhibiting its enzyme activity.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Sitagliptin Mitigates Diabetic Cardiomyopathy Through Oxidative Stress Reduction and Suppression of VEGF and FLT-1 Expression in Rats.Biomolecules · 2025Article
- Blood leukocytes as a non-invasive diagnostic tool for thyroid nodules: a prospective cohort study.BMC medicine · 2024Article
- Exploring the clinical utility of DPP-IV and SGLT2 inhibitors in papillary thyroid cancer: a literature review.Frontiers in pharmacology · 2024Review
- Glucagon-like peptide 1 receptor agonists and thyroid cancer: is it the time to be concerned?Endocrine connections · 2023Review
- Down-regulation of DPP4 by TGFβ1/miR29a-3p inhibited proliferation and promoted migration of ovarian cancer cells.Discover oncology · 2023Article
- DPP3 expression promotes cell proliferation and migrationOncology reports · 2023Article
- Drug repositioning in thyroid cancer treatment: the intriguing case of anti-diabetic drugs.Frontiers in pharmacology · 2023Review
- Article
- Dipeptidyl Peptidase 4 (DPP4) as A Novel Adipokine: Role in Metabolism and Fat Homeostasis.Biomedicines · 2022Review
- Validating Cell Surface Proteases as Drug Targets for Cancer Therapy: What Do We Know, and Where Do We Go?Cancers · 2022Review
- DPP4 Is a Potential Prognostic Marker of Thyroid Carcinoma and a Target for Immunotherapy.International journal of endocrinology · 2022Article
- Identification of Immune-Cell-Related Prognostic Biomarkers of Esophageal Squamous Cell Carcinoma Based on Tumor Microenvironment.Frontiers in oncology · 2021Article
- Comprehensive Analysis of Ferroptosis Regulators With Regard to PD-L1 and Immune Infiltration in Clear Cell Renal Cell Carcinoma.Frontiers in cell and developmental biology · 2021Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposePapillary thyroid carcinoma (PTC) is characterized by epithelial malignancy and is the most prevalent thyroid neoplasm with the best overall prognosis. Notably, recently published studies have indicated remarkably high expression of dipeptidyl peptidase 4 (DPP4) in PTC. However, the underlying molecular mechanism and regulatory factors of PTC progression remain unknown. Therefore, the current study aimed to elucidate the effects of DPP4 gene silencing on PTC and further investigated whether the mechanism of PTC progression is related to the mitogen-activated protein kinase (MAPK) pathway.
methodsHerein, microarray-based gene expression profiling of PTC was conducted to identify the differentially expressed genes between tumor thyroid tissue and normal thyroid tissue as well as the underlying signaling pathway involved in PTC pathogenesis. Moreover, protein quantification was performed to assess the protein expression of DPP4 in PTC tissues collected from 65 patients. In addition, DPP4 was silenced in PTC cell lines (GLAG-66 and TPC-1) through siRNA-mediated DPP4 knockdown or sitagliptin (inhibitor of DPP4)-mediated inhibition to assess the effects of DPP4 on the MAPK pathway and cellular processes, including proliferation, apoptosis, and epithelial-to-mesenchymal transition (EMT).
resultsIntriguingly, our data revealed markedly high expression of DPP4 in PTC tissues. However, in GLAG-66 and TPC-1 cells, the silencing of DPP4 resulted in significantly reduced expression of ERK1/2, JNK1, P38 MAPK, VEGF, FGFR-1, TGF-β1, Snail, HIF-1α, N-cadherin, and Bcl-2 along with reduced phosphorylation of ERK1/2, JNK1, and P38 MAPK, whereas the expression of E-cadherin and Bax was increased. Furthermore, DPP4 silencing was found to hinder cell proliferation and potentiate cell apoptosis.
conclusionCollectively, the present study demonstrated that DPP4 gene silencing inhibits PTC cell proliferation and EMT and promotes cell apoptosis via suppression of the MAPK pathway, thus highlighting a possible regulatory pathway in PTC progression.
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