Related Experiment Video For Pancreatic ductal adenocarcinoma
Updated: Aug 19, 2025

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
Published on: October 27, 2020
Intracellular C3 Modulates EMT via the Akt/Smad Pathway in Pancreatic Cancer Cells
Rei Suzuki1, Tadayuki Takagi2, Mitsuru Sugimoto2
1Department of Gastroenterology, Fukushima Medical University School of Medicine, Fukushima, Japan; subaru@fmu.ac.jp.
Background/Aim:
We aimed to explore the role of intracellular C3 in pancreatic ductal adenocarcinoma (PDAC).
Materials And Methods:
We evaluated C3 expression in PDAC using a gene expression database and tissue microarray. To clarify the role of C3 expression in PDAC, we conducted knockdown experiments using C3 short hairpin RNA (shRNA) in BxPC-3 cells. Differences in protein expression and cell behaviours were analysed.
Results:
C3 was highly expressed in PDAC and correlated with cancer metastasis. In vitro experiments using BxPX-3 cells showed that C3 and its active form, C3a, were expressed in tumour cells. C3 knockdown reduced cell migration and invasion by inhibiting Akt/Smad pathway activation. TNF-α, not IL-6, enhanced C3 expression in this PDAC cell line.
Conclusion:
Intracellular C3 may regulate epithelial-mesenchymal transition in pancreatic cancer.
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