Purpose: At present, the global incidence of lung cancer is still high. Exploring its effective treatment is still a crucial research direction. Trefoil factor 3 (TFF3) was found to be related to the proliferation and apoptosis of many tumor cells. Therefore, this article focuses on the effect of TFF3 on SPC-A1 lung cancer cells.
Methods: The tissue samples of lung cancer patients were collected, and the expression level of TFF3 was detected by Western blot (WB) and Quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) techniques. After transfection technique was used to silence the expression of TFF3 in SPC-A1 cells, the proliferation activity of SPC-A1 cells was detected by CCK-8 assay and EdU staining, and the cell cycle and related factor expression levels were also detected. The apoptosis rate of SPC-A1 cells was detected by Tunel staining and flow cytometry, and the expression levels of apoptosis-related factors were also detected.
Results: TFF3 in lung cancer tissues was obviously higher than that in para-carcinoma tissue. At the same time, similar results were found in SPC-A1 lung cancer cells. CCK-8 assay and EdU staining found that silencing TFF3 gene expression can effectively inhibit the proliferation of SPC-A1 cells. Flow cytometry detection of SPC-A1 cell cycle showed that cells were blocked in G0/G1 phase, and the number of cells in S+G2/M phase was obviously reduced. Cyclin D1 expression was also obviously reduced. At the same time, silencing TFF3 gene expression can promote the increase of Bax expression and inhibit the expression of Bcl-2, thereby increasing the apoptosis rate of SPC-A1 cells. Furthermore, silencing the TFF3 gene can effectively inhibit the excessive activation of the Wnt/β-catenin pathway in SPC-A1 cells.
Conclusions: Our results show that the expression of TFF3 in lung cancer was obviously increased. Silencing TFF3 in SPC-A1 cells can inhibit the cell proliferation and promote cell apoptosis. At the same time, we confirmed that silencing TFF3 gene can inhibit the abnormal activation of Wnt/β-catenin signaling pathway in SPC-A1 cells.