Abstract
BackgroundIn 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.MethodsA 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.ResultsOur 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.ConclusionsC-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.
Highlights
IntroductionThe epithelial-to-mesenchymal transition (EMT) is a pivotal and intricate process that increases the metastatic potential of cervical cancer
In cervical cancer, most patients die of metastasis
We found that C-phycocyanin inhibited the expression of epithelial-to-mesenchymal transition (EMT)-related N-cadherin, Twist, Snail and Zeb1, promoted the expression of E-cadherin, and inhibited the migration and invasion of Caski cells
Summary
The epithelial-to-mesenchymal transition (EMT) is a pivotal and intricate process that increases the metastatic potential of cervical cancer. Infiltration and metastasis are still the main causes of death in EMT refers to the biological process by which epithelial cells are transformed into mesenchymal phenotype cells by a specific procedure. Phosphorylation of Smad2/3 binds to Smad to form trimer and translocated to the nucleus [10] It interacts with transcription factors, co-activating factors and co-inhibitors in the nucleus to inhibit epithelial genes expression but promote the expression of stroma genes. The gene expression mediated by smad 3/4 induced by TGF-β drives the gene reprogramming in the EMT process [11]. In addition to Smad signals, TGF-β1 can activate other signaling pathways, such as phosphoinositide 3-kinase (PI3K)–AKT, extracellular signal-regulated kinase (ERK)-mitogenactivated protein kinase (MAPK) and p38MAPK [12]
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