Role of fibroblast growth factors in pancreatic cancer

Gnatenko, D. A.; Копанцев, Е. П.

doi:10.18097/pbmc20166206622

Cited by 5 publications

(1 citation statement)

References 51 publications

(61 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Общая характеристика FGF/FGFR сигнального пути и роль FGF факторов в канцерогенезе были рассмотрены нами ранее [8]. Вкратце, семейство ростовых факторов FGF включает в себя 23 белка (рис.…”

Section: краткая характеристика Fgf/fgfr сигнального путиunclassified

Fibroblast growth factors and their effects in pancreas organogenesis

Gnatenko

Kopantzev

2017

BIOMED KHIM

Self Cite

View full text Add to dashboard Cite

Fibroblast growth factors (FGF) - growth factors that regulate many important biological processes, including proliferation and differentiation of embryonic cells during organogenesis. In this review, we will summarize current information about the involvement of FGFs in the pancreas organogenesis. Pancreas organogenesis is a complex process, which involves constant signaling from mesenchymal tissue. This orchestrates the activation of various regulator genes at specific stages, determining the specification of progenitor cells. Alterations in FGF/FGFR signaling pathway during this process lead to incorrect activation of the master genes, which leads to different pathologies during pancreas development. Understanding the full picture about role of FGF factors in pancreas development will make it possible to more accurately understand their role in other pathologies of this organ, including carcinogenesis.

show abstract

Section: краткая характеристика Fgf/fgfr сигнального путиunclassified

Fibroblast growth factors and their effects in pancreas organogenesis

Gnatenko

Kopantzev

2017

BIOMED KHIM

Self Cite

View full text Add to dashboard Cite

show abstract

FGFBP1-mediated crosstalk between fibroblasts and pancreatic cancer cells via FGF22/FGFR2 promotes invasion and metastasis of pancreatic cancer

Zhang

Qin

et al. 2021

ABBS

View full text Add to dashboard Cite

Fibroblast growth factor–binding protein 1 (FGFBP1) promotes fibroblast growth factor (FGF) activity by releasing FGFs from extracellular matrix storage. We previously reported that the tumor suppressor F-box and WD repeat domain-containing 7 suppresses FGFBP1 by reducing expression of c-Myc, which inhibits the proliferation and migration of pancreatic cancer cells. However, the potential mechanism by which FGFBP1 facilitates pancreatic ductal adenocarcinoma (PDAC) remains unexplored. In this study, we focused on the function of FGFBP1 in the interplay between cancer-associated fibroblasts (CAFs) and pancreatic cancer cells (PCCs). Decreased FGF22 expression was detected in CAF cocultured with PCCs with FGFBP1 abrogation, which was verified in the cell culture medium by enzyme-linked immunosorbent assay. Active cytokine FGF22 significantly facilitated the migration and invasion of PANC-1 and Mia PaCa-2 cells. The number of penetrating PCCs cocultured with CAFs with FGF22 abrogation was significantly less than that of the control group. Interestingly, higher expressions of FGF22 and fibroblast growth factor receptor 2 (FGFR2) were associated with worse prognosis of patients with PDAC and FGFR2, an independent prognostic marker of PDAC. The PANC-1 and Mia PaCa-2 cells with silenced FGFR2 showed weaker invasion and metastasis, even if these cells were simultaneously treated with cytokine FGF22. These results revealed that FGFBP1-mediated interaction between CAFs and PCCs via FGF22/FGFR2 facilitates the migration and invasion of PCCs. FGFR2 could act as a prognostic marker for patients with PDAC.

show abstract

NF-κB Mediated Disruption of Pancreatic Signaling Pathways and its Implications for the Risk of Pancreatic Adenocarcinoma: a systematic review

Shafi,

Rajpar,

Aakash

et al. 2024

Preprint

View full text Add to dashboard Cite

ObjectiveThe objective of this study is to determine how NF-κB-mediated inflammation disrupts pancreatic signaling pathways and the resultant increase in the risk of Pancreatic Adenocarcinoma.BackgroundPancreatic adenocarcinoma’s severity and poor prognosis underscore the critical role of NF-κB-mediated inflammation in disease progression. NF-κB activation disrupts key pancreatic signaling pathways by promoting cell proliferation, inhibiting differentiation, and facilitating oncogenic transformation. Understanding these mechanisms is essential for developing targeted therapies that mitigate NF-κB-induced damage, improve early detection through biomarkers, and enhance treatment outcomes for pancreatic cancer patients.MethodsDatabases, including PubMed, MEDLINE, Google Scholar, and open access/ subscription-based journals were searched for published articles without any date restrictions, to investigate how NF-κB-mediated inflammation disrupts pancreatic signaling pathways and the resultant increase in the risk of Pancreatic Adenocarcinoma. Based on the criteria mentioned in the methods section, studies were systematically reviewed to investigate the research question. This study adheres to relevant PRISMA guidelines (Preferred Reporting Items for Systematic Reviews and Meta-Analyses).ResultsNF-κB-mediated inflammation significantly disrupts several critical pancreatic signaling pathways, leading to oncogenic transformations and increased risk of pancreatic adenocarcinoma. Specifically, NF-κB activation alters Notch signaling, causing abnormal cell differentiation; disrupts Wnt and Shh pathways, enhancing cellular proliferation; and perturbs FGF and TGF-β pathways, leading to impaired cellular homeostasis. Additionally, NF-κB interferes with BMP signaling, contributing to dysregulated cell growth; modulates the PI3K/Akt/mTOR pathway, promoting cell survival and tumor growth; affects JAK/STAT signaling, resulting in enhanced inflammatory responses and tumor progression; and disrupts Hippo pathway components, which normally regulate organ size and inhibit tumorigenesis.ConclusionNF-κB-mediated inflammation disrupts critical pancreas signaling pathways—Notch, Wnt, Hippo, JAK/STAT, and others—promoting cell survival, proliferation, and oncogenic transformation. This dysregulation, seen in chronic inflammation, elevates pancreatic adenocarcinoma risk by fostering a tumorigenic microenvironment. These interactions highlight NF-κB as a central player in pancreatic cancer pathogenesis. Targeting NF-κB and associated pathways emerges as crucial for therapeutic strategies aimed at mitigating inflammatory damage and improving outcomes in pancreatic adenocarcinoma treatment.

show abstract

Role of fibroblast growth factors in pancreatic cancer

Cited by 5 publications

References 51 publications

Fibroblast growth factors and their effects in pancreas organogenesis

Fibroblast growth factors and their effects in pancreas organogenesis

FGFBP1-mediated crosstalk between fibroblasts and pancreatic cancer cells via FGF22/FGFR2 promotes invasion and metastasis of pancreatic cancer

NF-κB Mediated Disruption of Pancreatic Signaling Pathways and its Implications for the Risk of Pancreatic Adenocarcinoma: a systematic review

Contact Info

Product

Resources

About