Qin Yanzi, Zhao Wenjun, Li Qicai, Cai Zhaogeng, Wang Guowen, Wang Nan, Ma Li
Department of Pathology, The First Affiliated Hospital of Bengbu Medical University, Bengbu 233000, China.
Department of Emergency Internal Medicine, The Third the People's Hospital of Bengbu, Bengbu 233000, China.
Iran J Biotechnol. 2024 Jul 1;22(3):e3693. doi: 10.30498/ijb.2024.394737.3693. eCollection 2024 Jul.
Oesophageal cancer (EC) is one of the common malignant tumors, and the prognosis of patients is poor. Further exploration of EC pathogenesis remains warranted.
The relationship between vascular epithelial cadherin (VE-cadherin) and chitinase-3-like protein 1 (CHI3L1) in EC is currently unknown. To further explore the relationship, immunohistochemical staining was performed to detect the expression level of CHI3L1 and VE-cadherin in oesophageal squamous cell carcinoma ( ESCC).
Small interfering RNAs (siRNAs) inhibited CHI3L1 expression in KYSE-150 and TE1 cells. Western blot and quantitative fluorescence polymerase chain reaction were used to detect the levels of CHI3L1, VE-cadherin and epithelial-mesenchymal transition (EMT)-related proteins and , and KYSE-150 cells were used to establish an model and observe tumour growth.
High levels of CHI3L1 and VE-cadherin expression were closely associated with the progression of ESCC; the pathologic tumour-node-metastasis stage was also closely related with the progression of ESCC ( < 0.05). High levels of CHI3L1 and VE-cadherin expression led to poor prognosis in patients with EC. In KYSE-150 and TE1 EC cell lines, the invasion, migration and proliferation of cells decreased, and the apoptotic rate increased after CHI3L1 expression was decreased using siRNA. The CHI3L1, VE-cadherin, Snail, Twist1 protein and mRNA expression levels decreased, whereas the E-cadherin levels increased.
Chitinase-3-like protein 1 could promote the EMT of ESCC, and the inhibition of CHI3L1 decreases the expression of VE-cadherin, which inhibits tumour angiogenesis and tumour progression in ESCC.
食管癌(EC)是常见的恶性肿瘤之一,患者预后较差。仍有必要进一步探索EC的发病机制。
目前尚不清楚血管内皮钙黏蛋白(VE-钙黏蛋白)与几丁质酶-3样蛋白1(CHI3L1)在EC中的关系。为进一步探究二者关系,采用免疫组化染色检测食管鳞状细胞癌(ESCC)中CHI3L1和VE-钙黏蛋白的表达水平。
小干扰RNA(siRNA)抑制KYSE-150和TE1细胞中CHI3L1的表达。采用蛋白质免疫印迹法和定量荧光聚合酶链反应检测CHI3L1、VE-钙黏蛋白及上皮-间质转化(EMT)相关蛋白E-钙黏蛋白和波形蛋白的水平,并利用KYSE-150细胞建立裸鼠模型观察肿瘤生长情况。
CHI3L1和VE-钙黏蛋白的高表达水平与ESCC的进展密切相关;病理肿瘤-淋巴结-转移分期也与ESCC的进展密切相关(P<0.05)。CHI3L1和VE-钙黏蛋白的高表达水平导致EC患者预后不良。在KYSE-150和TE1食管癌细胞系中,使用siRNA降低CHI3L1表达后,细胞的侵袭、迁移和增殖能力下降,凋亡率增加。CHI3L1、VE-钙黏蛋白、Snail、Twist1蛋白及mRNA表达水平降低,而E-钙黏蛋白水平升高。
几丁质酶-3样蛋白1可促进ESCC的EMT,抑制CHI3L1可降低VE-钙黏蛋白的表达,从而抑制ESCC的肿瘤血管生成和肿瘤进展。