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EPLIN, a prospective oncogenic molecule with contribution to growth, migration and drug resistance in pancreatic cancer
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EPLIN, a prospective oncogenic molecule with contribution to growth, migration and drug resistance in pancreatic cancer
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Journal Article
EPLIN, a prospective oncogenic molecule with contribution to growth, migration and drug resistance in pancreatic cancer
2024
Overview
Most pancreatic cancer patients are diagnosed at advanced stages, with poor survival rates and drug resistance making pancreatic cancer one of the highest causes of cancer death in the UK. Understanding the underlying mechanism behind its carcinogenesis, metastasis and drug resistance has become an essential task for researchers. We have discovered that a well-established tumour suppressor, EPLIN, has an oncogenic rather than suppressive role in pancreatic cancer. Notably, upregulation of EPLIN was observed in pancreatic cancer samples compared to normal samples at RNA and protein levels. Moreover, the presence of EPLIN resulted in poor clinical outcomes in patients. We also report that inhibition of EPLIN led to reduced cellular growth and migration in pancreatic cancer cells. EPLIN regulates expression and phosphorylation levels of several key players in MAPK and PIK3CA-AKT signalling pathways, as well as key contributors of EMT. Furthermore, EPLIN mediates the inhibitory ability PIK3 kinases, MEK and ERK inhibitors have on cell migration. EPLIN was also found to have an impact on pancreatic cancer cells response to chemotherapeutic and EGFR/HER2 targeted therapeutic agents, namely gemcitabine, fluorouracil (5FU) and neratinib (Nerlynx).
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ Antineoplastic Agents - pharmacology
/ Antineoplastic Agents - therapeutic use
/ Cell Movement - drug effects
/ Cell Proliferation - drug effects
/ Drug Resistance, Neoplasm - genetics
/ Epithelial-Mesenchymal Transition - drug effects
/ EPLIN
/ Fluorouracil - therapeutic use
/ Gene Expression Regulation, Neoplastic - drug effects
/ Humanities and Social Sciences
/ Humans
/ Kinases
/ MAPK
/ Pancreatic Neoplasms - drug therapy
/ Pancreatic Neoplasms - genetics
/ Pancreatic Neoplasms - metabolism
/ Pancreatic Neoplasms - pathology
/ PIK3s
/ Science
