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Published:
Jun 9, 2023DOI:
10.4314/tjpr.v22i2.2Keywords:
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Main Article Content
KLK4 affects the biological behavior of oral squamous cell carcinoma through Wnt/β catenin and PI3K/Akt signaling pathways
Abstract
Purpose: To investigate the effect of kallikrein 4 (KLK4) on oral squamous cell carcinoma (OSCC), and its mechanism of action.
Method: Human tongue SCC cell line TCA-8113 was cultured, and the interference fragment and irrelevant sequence fragment of KLK4 gene were designed and synthesized. These fragments were constructed into pgcsi-h1 plasmid. Then, the TCA-8113 cells were cultured for 24 h, followed by transfection, after which TCA-8113-NC and TCA-8113-siKLK4 cells were obtained. The mRNA expression of KLK4 was determined using quantitative real-time-polymerase chain reaction (PCR). Proliferative potential was assessed using MTT method, while apoptosis was determined by flow cytometry. Furthermore, cell migration was evaluated by scratch test, and Transwell cell invasion experiment was used to determine cell invasion. Immunoblot assay was applied to determine the expressions of E- and N-cadherins, vimentin, uPA, Wnt1, β-Catenin, p-pi3k and p-Akt.
Result: Compared with TCA-8113-nc, the expression of KLK4 in TCA-8113-siKLK4 cells was significantly down-regulated, while, relative to TCA-8113-NC, TCA-8113-siKLK4 cells had significantly reduced cell proliferation, invasion and migration, and enhanced apoptosis (p < 0.05). Moreover, there was significant up-regulation of E- and N-cadherins, vimentin, uPA, Wnt1, β-Catenin, p-pi3k and p-Akt in TCA-8113-siKLK4 group, relative to TCA-8113-NC (p < 0.05).
Conclusion: KLK4 enhances the multiplication, metastasis and invasive potential of OSCC cells, but suppresses apoptotic changes via activation of Wnt/β-catenin/PI3K/Akt signal route. The potential of Kallikrein-4 as biomarker for OSCC cells should be determined in suitable animal models.
