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Updated: Dec 15, 2025

Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
C-phycocyanin inhibits epithelial-to-mesenchymal transition in Caski cells
Huanhuan Ji1, Guoxiang Liu1, Jingjing Han1
1Department of Genetics and Cell Biology, Basic Medical College, Qingdao University, 308 Ningxia Road, Qingdao, 266071 People's Republic of China.
Background:
In cervical cancer, most patients die of metastasis. The epithelial-to-mesenchymal transition (EMT) is a pivotal and intricate process that increases the metastatic potential of cervical cancer. C-phycocyanin (C-PC) is a natural marine product isolated and purified from Spirulina platensis, has been investigated that has anti-cancer function. The aim of this study was to explore the inhibitory effect of C-phycocyanin on the migration and invasion of cervical cancer cells induced by transforming growth factor-β1 (TGF-β1), so as to provide a new idea for the treatment and prognosis of cervical cancer.
Methods:
A wound-healing assay, an invasion assay, immunofluorescence assay, western blot, flow cytometry and real-time reverse transcriptione polymerase chain reaction were explored in cervical cancer Caski cell lines. TGF-β/smad signaling pathway was evaluated of in Caski cell lines.
Results:
Our study indicated that TGF-β1 induced EMT in cervical cancer cells. C-phycocyanin inhibited EMT in Caski cells by down-regulating N-cadherin and up-regulating E-cadherin protein expression. Furthermore, C-phycocyanin could inhibit the expression and proteins Twist, Snail and Zeb1 transcription factors related to EMT. In addition, C-phycocyanin could inhibit the migration and invasion of Caski cells induced by TGF-β1. Besides, C-phycocyanin inhibited EMT through TGF-β/smads signaling pathway. We also found C-phycocyanin induced cell cycle G0/G1 arrest by decreasing protein expression levels of Cyclin D1 and p27.
Conclusions:
C-phycocyanin reversed TGF-β1-induced epithelial-to-mesenchymal transition in cervical cancer cells and down-regulated the TGF-β/samd signaling pathway induced G0/G1 arrest of tumor cell cycle.
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