Inhibiting SNX10 induces autophagy to suppress invasion and EMT and inhibits the PI3K/AKT pathway in cervical cancer

被引:1
|
作者
Liao, Dan [1 ]
He, Yanxian [1 ]
He, Bin [2 ]
Zeng, Saitian [1 ]
Cui, Yejia [3 ]
Li, Cuifen [1 ]
Huang, Haohai [2 ,4 ]
机构
[1] Guangdong Med Univ, Affiliated Dongguan Songshan Lake Cent Hosp, Dept Gynaecol, 1, Huangzhou Xianglong Rd Shilong Town, Dongguan 523326, Guangdong, Peoples R China
[2] Guangdong Med Univ, Affiliated Dongguan Songshan Lake Cent Hosp, Clin Translat Med Ctr, Dongguan, Guangdong, Peoples R China
[3] Guangdong Med Univ, Affiliated Dongguan Songshan Lake Cent Hosp, Dept Clin Lab, Dongguan, Guangdong, Peoples R China
[4] Guangdong Med Univ, Affiliated Dongguan Songshan Lake Cent Hosp, Dept Clin Pharm, 1, Huangzhou Xianglong Rd Shilong Town, Dongguan 523326, Guangdong, Peoples R China
基金
中国国家自然科学基金;
关键词
SNX10; Cervical cancer; Autophagy; Migration; Invasion; PI3K/AKT;
D O I
10.1007/s12094-024-03715-x
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
PurposeCervical cancer (CC) is a prevalent malignancy among women with high morbidity and poor prognosis. Sorting nexin 10 (SNX10) is a newly recognized cancer regulatory factor, while its action on CC progression remains elusive. Hence, this study studied the effect of SNX10 on CC development and investigated the mechanism.MethodsThe SNX10 level in CC and the overall survival of CC cases with different SNX10 expressions were determined by bioinformatics analysis in GEPIA. The SNX10 expression in tumor tissues and clinical significance were studied in 64 CC cases. The overall survival was assessed using Kaplan-Meier analysis. The formation of LC3 was evaluated using immunofluorescence. Cell invasion was measured using the Transwell assay. Epithelial-to-mesenchymal transition (EMT) was determined by observing cell morphology and assessing EMT marker levels. A xenograft tumor was constructed to evaluate tumor growth.ResultsSNX10 was elevated in CC tissues and cells, and the CC cases with high SNX10 levels exhibited poor overall survival. Besides, SNX10 correlated with the FIGO stage, lymph node invasion, and stromal invasion of CC. SNX10 silencing induced CC cell autophagy and suppressed CC cell invasion and EMT. Meanwhile, silenced SNX10 could suppress invasion and EMT via inducing autophagy. Furthermore, SNX10 inhibition suppressed the PI3K/AKT pathway. Moreover, silenced SNX10 restrained the tumor growth, autophagy, and EMT of CC in vivo.ConclusionSNX10 was enhanced in CC and correlated with poor prognosis. Silenced SNX10 induced autophagy to suppress invasion and EMT and inhibited the PI3K/AKT pathway in CC, making SNX10 a valuable molecule for CC therapy.
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页数:11
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