Research on the mechanism of targeting CD59 to inhibit proliferation， migration， and induce apoptosis in oral squamous cell carcinoma

doi:10.3760/cma.j.cn371439-20250530-00002

Abstract

Abstract:

Objective To investigate the effects and mechanisms of targeting CD59 on the proliferation， migration， and apoptosis of oral squamous cell carcinoma （OSCC） cells. Methods Thirty patients with OSCC admitted to Qingdao Stomatological Hospital Affiliated to Qingdao University from September 2020 to September 2022 were selected as the research subjects. The expression of CD59 in their tumor tissues and paired adjacent normal tissues was detected by immunohistochemistry. CD59 expression was knocked down or overexpressed in HOK （normal oral keratinocytes） and SCC-9 （human tongue squamous cell carcinoma） cells via lentiviral transduction. Cells were divided into four groups： siCD59-C group （knockdown control）， siCD59 group （CD59 knockdown）， CD59 group （CD59 overexpression）， and CD59-C group （overexpression control）. Apoptosis was detected by flow cytometry； proliferation was evaluated via colony formation and CCK-8 assays； migration was examined by wound healing assay； and PI3K， Akt， and mTOR phosphorylation levels were detected by Western blotting. Results The immunohistochemical results showed that the expression of CD59 in OSCC tissues （334.06±72.50） was significantly higher than that in adjacent normal tissues （125.77±56.60； t=3.20， P=0.033）. The results of flow cytometry showed that the apoptosis rates of HOK cells in the siCD59-C group and the siCD59 group were 5.67%±0.83% and 6.92%±0.51%， respectively， with no statistically significant difference （t=2.23， P=0.089）. Compared with the siCD59-C group （17.79%±0.45%）， the apoptosis rate of SCC-9 cells in the siCD59 group （38.03%±0.64%） increased significantly （t=13.09， P<0.001）. The apoptosis rates of HOK cells in the CD59-C group and the CD59 group were 4.57%±0.31% and 5.25%±0.65%， respectively， with no statistically significant difference （t=1.66， P=0.172）. Compared with the CD59-C group （18.19%±0.45%）， the apoptosis rate of SCC-9 cells in the CD59 group （7.26%±0.28%） was significantly decreased （t=35.76， P<0.001）. The results of colony formation assay showed that the numbers of HOK cells clones formed in the siCD59-C group and the siCD59 group were 350.53±6.31 and 367.01±7.36， respectively， with no statistically significant difference （t=1.48， P=0.214）. Compared with the siCD59-C group （418.46±6.75）， the clone formation ability of SCC-9 cells in the siCD59 group （326.02±5.15） was significantly decreased （t=3.46， P=0.026）. The results of CCK-8 assay showed that the viability of HOK cells in the CD59-C group and the CD59 group were 2.72%±0.43% and 2.60%±0.66%， respectively， with no statistically significant difference （t=2.54， P=0.064）. Compared with the CD59-C group （1.21%±0.77%）， the proliferation ability of SCC-9 cells in the CD59 group （2.09%±0.45%） increased significantly （t=16.97， P<0.001）. The results of wound healing assay showed that 24 h after the scratch， the migration rates of HOK cells in the siCD59-C group and the siCD59 group were 15.01%±1.56% and 13.32%±2.08%， respectively， with no statistically significant difference （t=1.25， P=0.279）. Compared with the siCD59-C group （17.67%±1.53%）， the migration ability of SCC-9 cells in the siCD59 group （7.13%±1.22%） decreased significantly （t=9.17， P<0.001）. The results of Western blotting showed that there was no statistically significant difference in the phosphorylation levels of PI3K， Akt， and mTOR in HOK cells between the siCD59-C group and the siCD59 group （all P>0.05）. Compared with the siCD59-C group， the phosphorylation levels of PI3K， Akt， and mTOR in SCC-9 cells in the siCD59 group were significantly decreased （all P<0.001）. Conclusions CD59 expression is significantly upregulated in OSCC tissues. Knockdown of CD59 can promote apoptosis of OSCC cells， inhibit their proliferation and migration. The mechanism may be related to the inhibition of the activation of the PI3K/Akt/mTOR signaling pathway.

Key words: Mouth neoplasms, CD59 antigens, Apoptosis, Cell proliferation, PI3K/Akt/mTOR signaling pathway

Yang Xinting, Ma Tengyu, Guan Shulong, Yang Mei, Jiang Zhou, Yang Xinru, Jiang Liangqian, Gao Meihua, Xu Yingjie, Cong Beibei. Research on the mechanism of targeting CD59 to inhibit proliferation， migration， and induce apoptosis in oral squamous cell carcinoma[J]. Journal of International Oncology, 2026, 53(1): 16-23.

Figures/Tables 9

References 27

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组别	p-PI3K/PI3K	p-Akt/Akt	p-mTOR/mTOR
siCD59-C组	0.46±0.11	0.34±0.13	1.71±0.09
siCD59组	0.47±0.14	0.36±0.12	1.73±0.15
t值	1.71	1.80	2.00
P值	0.163	0.146	0.116

组别	p-PI3K/PI3K	p-Akt/Akt	p-mTOR/mTOR
siCD59-C组	0.69±0.09	0.65±0.04	1.89±0.13
siCD59组	0.39±0.17	0.33±0.19	0.65±0.06
t值	65.73	56.62	56.68
P值	<0.001	<0.001	<0.001