Liu Wenfeng, Wu Zuoli, Wang Lijuan, Wang Qijun, Sun Xiuhua, Niu Shufeng
Department of Gynecology, Jinan City People's Hospital, Jinan People's Hospital Affiliated to Shandong First Medical University Jinan, Shandong Province, China.
Anaesthesia Recovery Room, People's Hospital of Rizhao Rizhao, Shandong Province, China.
Am J Transl Res. 2021 Sep 15;13(9):10328-10340. eCollection 2021.
To detect the expression pattern of TRIM11 in CC and to investigate the effect of TRIM11 knockdown on CC progression.
First, the expression pattern and function of TRIM11 in CC were inferred by GEPIA database. The expression of TRIM11 in CC tissues and cells was verified by RT-qPCR and Western blot assays. TRIM11 shRNA was transfected into CC cells. The effect of TRIM11 knockdown on CC cell proliferation and cell apoptosis was assessed by CCK-8 assay, clone formation test and flow cytometry (FCM). Furthermore, the effect of TRIM11 knockdown on cell migration and invasion was measured by Transwell assay. The apoptosis-related proteins (Bax, Bcl-2 and Cleaved caspase 3) and PI3K/AKT pathway-related proteins (PI3K, p-PI3K, AKT and p-Akt) were examined by Western blot assay.
TRIM11 was found to be dramatically upregulated in CC tissues and cells. Besides this, TRIM11 was closely related to FIGO stage, infiltration depth and metastasis. Moreover, high expression of TRIM11 was found to be associated with poor prognosis of CC patients. Functional experiments showed that knockdown of TRIM11 obviously suppressed CC cell proliferation, migration and invasion, while accelerated cell apoptosis. In addition, the PI3K inhibitor (LY294002) was used to assess the connection between PI3K/AKT pathway and TRIM11 in CC cells. We found that TRIM11 overexpression suppressed the phosphorylation of PI3K and AKT in CC cells.
Hence, TRIM11 regulates CC cell progression by modulating PI3K/AKT pathway. The results suggested that TRIM11 might be a possible target for the diagnosis and prognosis of CC patients.
检测TRIM11在宫颈癌（CC）中的表达模式，并研究敲低TRIM11对CC进展的影响。
首先，通过GEPIA数据库推断TRIM11在CC中的表达模式和功能。采用逆转录定量聚合酶链反应（RT-qPCR）和蛋白质免疫印迹法（Western blot）验证TRIM11在CC组织和细胞中的表达。将TRIM11短发夹RNA（shRNA）转染至CC细胞中。通过细胞计数试剂盒-8（CCK-8）检测、克隆形成试验和流式细胞术（FCM）评估敲低TRIM11对CC细胞增殖和细胞凋亡的影响。此外，采用Transwell试验检测敲低TRIM11对细胞迁移和侵袭的影响。通过蛋白质免疫印迹法检测凋亡相关蛋白（Bax、Bcl-2和裂解的半胱天冬酶3）和磷脂酰肌醇-3激酶/蛋白激酶B（PI3K/AKT）信号通路相关蛋白（PI3K、磷酸化PI3K、AKT和磷酸化Akt）。
发现TRIM11在CC组织和细胞中显著上调。除此之外，TRIM11与国际妇产科联盟（FIGO）分期、浸润深度和转移密切相关。此外，发现TRIM11高表达与CC患者预后不良相关。功能实验表明，敲低TRIM11明显抑制CC细胞增殖、迁移和侵袭，同时加速细胞凋亡。此外，使用PI3K抑制剂（LY294002）评估PI3K/AKT信号通路与CC细胞中TRIM11之间的联系。我们发现TRIM11过表达抑制CC细胞中PI3K和AKT的磷酸化。
因此，TRIM11通过调节PI3K/AKT信号通路调控CC细胞进展。结果表明，TRIM11可能是CC患者诊断和预后的一个潜在靶点。
