| 柳 叶,蒋 超,程洪英,等.食管鳞癌中Apelin表达的临床意义及其对肿瘤侵袭和迁移的影响[J].肿瘤学杂志,2025,31(2):134-143. |
| 食管鳞癌中Apelin表达的临床意义及其对肿瘤侵袭和迁移的影响 |
| Clinical Significance of Apelin Expression and Its Effects on Invasion and Migration of Esophageal Squamous Cell Carcinoma |
| 投稿时间：2024-10-24 |
| DOI：10.11735/j.issn.1671-170X.2025.02.B008 |
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| 中文关键词: 食管肿瘤 鳞癌 apelin（APLN） 预后 侵袭 转移 |
| 英文关键词:esophageal neoplasms squamous cell carcinoma apelin(APLN) prognosis invasion metastasis |
| 基金项目:国家自然科学基金（82102969）；南京医科大学附属淮安第一医院“转化医学研究创新团队、创新人才”项目（YZHR201904） |
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| 中文摘要: |
| 摘 要： ［目的］ 探讨食管鳞癌（esophageal squamous cell carcinoma，ESCC）中apelin（APLN）的表达意义及其对肿瘤恶性表型侵袭和迁移的影响。［方法］ 收集公共数据库中ESCC患者的临床病理资料，分析APLN在ESCC中的表达及对预后的影响。选取2016年1月至2017年12月南京医科大学附属淮安第一医院163例ESCC患者作为研究对象，收集患者的临床资料、随访相关资料，同时将病理标本制作成组织芯片。采用免疫组织化学染色对APLN的表达及其与患者病理特征和预后关系进行验证分析。进一步在ESCC细胞和动物模型中分析APLN对ESCC的生物行为学影响。［结果］ 数据库分析结果显示，APLN在ESCC中的表达水平显著高于癌旁组织（P＜0.05），且高表达患者预后较差（P=0.015）。临床样本RT-PCR结果显示APLN在ESCC中的表达水平显著高于癌旁组织（9.355±3.110 vs 1.016±0.110，t=16.673，P＜0.001），组织芯片免疫组化结果显示，APLN在ESCC中表达显著高于癌旁组织（0.277±0.110 vs 0.251±0.150，t=12.072，P＜0.001），且ESCC患者肿瘤组织中APLN表达与N分期（χ2=2.435，P=0.049）及神经脉管侵犯（χ2=8.320，P=0.004）显著相关。单因素及多因素Logistic回归分析显示，较高的N分期及APLN的高表达均与ESCC患者较差的预后相关。在ESCC细胞株中，APLN在KYSE-150和KYSE-30细胞的基因相对表达水平（2.153±0.014，6.246±1.214）高于人正常食管上皮细胞（0.124±0.012）（P=0.012，0.002），Western blot分析表现出相似的结果。在KYSE-30细胞中，抑制APLN表达可以显著降低细胞的侵袭和迁移能力，过表达APLN表达可以显著增强细胞的侵袭和迁移能力。在动物模型中，敲低APLN后，肿瘤重量明显低于对照组［（0.023±0.012） g vs （0.391±0.111） g，t=5.798，P=0.001］，而过表达APLN则可以挽救这一现象［（0.123±0.014） g vs （0.051±0.025） g，t=2.524，P=0.031］。［结论］ ESCC中APLN的表达显著增高，且与患者预后不良相关。APLN能够促进ESCC细胞的恶性表型。 |
| 英文摘要: |
| Abstract：［Objective］ To investigate the effect of apelin (APLN) expression on invasion and migration of esophageal squamous cell carcinoma (ESCC). ［Methods］ The clinical and pathological data of ESCC were obtained from public data bases of TCGA and GEPIS. The relationship of APLN expression with the prognosis of ESCC patients was analyzed. Clinical and follow-up data of 163 ESCC patients admitted to the the Affiliated Huai’an No.1 People’s Hospital of Nanjing Medical University from January 2016 to December 2017 were collected. The expression of APLN in tissue chips was detected with immunohistochemical staining. The effects of APLN expression on biological phenotypes of ESCC were studied using ESCC cell lines and animal model. ［Results］ Data from public databases showed that the expression level of APLN in ESCC was significantly higher than that in adjacent tissues (P<0.05)， and patients with high APLN expression had poor prognosis (P=0.015). RT-PCR results of clinical samples showed that the expression level of APLN in ESCC was significantly higher than that in the adjacent tissues (9.355±3.110 vs 1.016±0.110， t=16.673， P<0.001)， Immunhistochemistry results showed that APLN expression in ESCC was significantly higher than that in adjacent tissues (0.277±0.110 vs 0.251±0.15， t=12.072， P<0.001). The expression of APLN in ESCC was significantly correlated with N stage (χ2=2.435， P=0.049) and neurovascular invasion (χ2=8.320， P=0.004). Univariate and multivariate Logistic regression analysis showed that higher N stage and high APLN expression were associated with poorer prognosis of ESCC patients. In ESCC cell line studies， RT-PCR analysis showed APLN gene expression levels in KYSE-150 and KYSE-30 cells (2.153±0.014， 6.246±1.214) were significantly higher than those in human normal esophageal epithelial cells (0.124±0.012) (P=0.012， 0.002)， and Western blot showed similar results. In KYSE-30 cells， inhibition of APLN expression significantly reduced cell invasion and migration capacity， and overexpression of APLN expression significantly enhanced cell invasion and migration capacity. In the animal model， compared to control group knocking down APLN expression significantly reduced tumor weight ［(0.023±0.012) g vs (0.391±0.111) g， t=5.798， P=0.001］， while APLN overexpression reversed the effect ［(0.123±0.014) g vs (0.051±0.025) g， t=2.524， P=0.031］. ［Conclusion］ The expression of APLN is significantly increased and is associated with poor prognosis in ESCC patients. APLN can promote the malignant phenotype of ESCC cells. |
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