ArticleCancer genomics & proteomics2025
Noggin Promotes Cell Proliferation Through Up-regulating EGFR/HER2 in Pancreatic Cancer Cells.
Article in Cancer genomics & proteomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
BACKGROUND/
aimNoggin is a secreted antagonist of bone morphogenetic proteins (BMPs) and plays a key role in regulating various developmental and homeostatic biological processes. BMPs have been linked to the development of several types of cancers. However, the impact of Noggin on cellular functions and its role in pancreatic cancer remain unclear. This study aimed to investigate the role of Noggin in pancreatic cancer and its underlying molecular mechanisms. MATERIALS AND
methodsNoggin expression in both normal and cancerous pancreatic tissues was assessed using both quantitative and conventional PCR methods, alongside an analysis of publicly available gene expression array datasets. Correlations between Noggin expression and patient survival, TNM staging, tumor/stroma subtypes, and the expression of other cancer-related genes were examined. The influence of Noggin on cellular functions was evaluated in pancreatic cancer cell lines Mia PaCa-2 and PANC-1, which were genetically modified to overexpress Noggin.
resultsNoggin expression was found to be significantly higher in tumor tissues compared to normal pancreatic tissues. Elevated Noggin expression was associated with shorter overall survival in patients. Overexpression of Noggin led to increased proliferation of pancreatic cancer cells. Furthermore, elevated levels of EGFR and HER2 proteins were observed in the PANC-1 and Mia PaCa-2 cell lines, respectively. Treatment with EGFR and HER2 inhibitors reduced Noggin-induced proliferation in these cell lines.
conclusionNoggin is overexpressed in pancreatic cancer tissues and is linked to poor patient survival. Noggin promotes the proliferation of pancreatic cancer cells by up-regulating EGFR and HER2.
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