Liao Dan, He Yanxian, He Bin, Zeng Saitian, Cui Yejia, Li Cuifen, Huang Haohai
Department of Gynaecology, Affiliated Dongguan Songshan Lake Central Hospital, Guangdong Medical University, No.1, Huangzhou Xianglong Road of Shilong Town, Dongguan, 523326, Guangdong, China.
Clinical Translational Medical Center, Affiliated Dongguan Songshan Lake Central Hospital, Guangdong Medical University, Dongguan, Guangdong, China.
Clin Transl Oncol. 2025 May;27(5):2084-2094. doi: 10.1007/s12094-024-03715-x. Epub 2024 Oct 5.
Cervical 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.
The 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.
SNX10 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.
SNX10 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.
宫颈癌（CC）是女性中一种常见的恶性肿瘤，发病率高且预后较差。分选连接蛋白10（SNX10）是一种新发现的癌症调节因子，但其对CC进展的作用仍不清楚。因此，本研究探讨了SNX10对CC发展的影响并研究其机制。
通过GEPIA中的生物信息学分析确定CC中SNX10水平以及不同SNX10表达的CC病例的总生存期。研究了64例CC病例中肿瘤组织中SNX10的表达及其临床意义。采用Kaplan-Meier分析评估总生存期。使用免疫荧光评估LC3的形成。使用Transwell试验测量细胞侵袭。通过观察细胞形态和评估EMT标志物水平来确定上皮-间质转化（EMT）。构建异种移植肿瘤以评估肿瘤生长。
SNX10在CC组织和细胞中升高，SNX10水平高的CC病例总生存期较差。此外，SNX10与CC的FIGO分期、淋巴结侵袭和间质侵袭相关。SNX10沉默诱导CC细胞自噬并抑制CC细胞侵袭和EMT。同时，沉默的SNX10可通过诱导自噬抑制侵袭和EMT。此外，SNX10抑制抑制了PI3K/AKT途径。此外，沉默的SNX10在体内抑制了CC的肿瘤生长、自噬和EMT。
SNX10在CC中增强且与预后不良相关。沉默的SNX10诱导自噬以抑制侵袭和EMT，并抑制CC中的PI3K/AKT途径，使SNX10成为CC治疗的有价值分子。
