目的 分析长链非编码RNA LINC02038的表达与子宫内膜癌发生、发展的关联性,并探讨其潜在的生物学调控机制,为子宫内膜癌的精准诊治提供科学线索。方法 采用荧光定量PCR技术检测LINC02038 在2019年—2020年期间于我院收集的42例子宫内膜癌标本及相应癌旁正常组织中的表达差异。构建LINC02038过表达载体并转染子宫内膜癌Ishikawa 细胞系,通过CCK-8、Transwell等功能实验验证其对肿瘤细胞增殖、侵袭能力的影响。利用TCGA公共数据库分析LINC02038与子宫内膜癌预后的相关性,并通过基因本体论（GO）、京都基因组百科全书（KEGG）及基因集富集分析（GSEA）等生物信息学方法预测其潜在的下游调控机制。结果 LINC02038在子宫内膜癌组织中的表达高于癌旁正常组织（P<0.001）。过表达LINC02038可促进子宫内膜癌细胞Ishikawa的增殖和迁移。生物信息学分析提示LINC02038可能通过调控细胞分化、激素分泌、细胞外基质重塑等过程,激活NF-κB、细胞外基质受体等信号通路影响子宫内膜癌的发生。结论 LINC02038的异常表达与子宫内膜癌的发生、发展相关联,可作为评估子宫内膜癌发病风险的候选生物标志物。

Objective To analyze the expression of long non-coding RNA LINC02038 and its relationship with the occurrence and development of endometrial carcinoma（EC）,explore its potential biological mechanisms,and provide potential biomarkers for targeted therapy of EC．Methods Quantitative real-time PCR was used to detect the expression levels of LINC02038 in 42 EC tissues and their adjacent tissues．The LINC02038 overexpressin vector was constructed and transfected into EC Ishikawa cells．CCK-8,Transwell migration and invasion assays were performed to examine the effects of LINC02038 overexpression on cancer cell proliferation,migration and invasion．Public TCGA data were analyzed to investigate the associations between LINC02038 and EC pathogenesis and prognosis．GO,KEGG and GSEA enrichment analyses were conducted to elucidate the potential biological mechanisms of LINC02038．Results LINC02038 expression was significantly upregulated in EC tissues compared to adjacent non-tumor tissues（P<0.001）．Overexpression of LINC02038 markedly promoted the proliferation and migration of Ishikawa cells．Bioinformatics analysis suggested that LINC02038 may participate in regulating cell differentiation,hormone secretion,extracellular matrix remodeling and other processes,as well as activating NF-κB,extracellular matrix receptor and other signaling pathways involved in endometrial carcinogenesis．Conclusions The aberrant expression of LINC02038 is associated with EC occurrence and may serve as a potential biomarker for assessing the risk of this cancer．

目的 探讨子宫内膜癌构成及临床病理特征。方法 以南平市第一医院2020年1月—2022年6月期间收治的82例子宫内膜癌患者为研究对象,收集其临床资料,通过免疫组织化学染色法检测4种错配修复蛋白表达,并分析错配修复蛋白表达与临床病理特征的关系。结果 82例患者中,70例（85.37%）为子宫内膜样癌,病理组织学类型以G1级30例（42.86%）为主,其他类型较为少见。错配修复蛋白表达总缺失率为35.71%,其中MUTL同源物1（MLH1）单独缺失率为2.86%,错配修复蛋白2抗体（MSH2）为4.29%,错配修复蛋白6抗体（MSH6）为14.29%,肿瘤错配修复基因PMS2抗体（PMS2）为14.29%;错配修复表达缺失（dMMR）组患者年龄50岁以上、伴脉管侵犯和淋巴结转移、组织学G3级和FIGO分期Ⅲ期占比高于错配修复表达正常（pMMR）组患者（P<0.05）;MSH6蛋白表达缺失易发生在年龄50岁以上、有家族相关疾病史的患者（P<0.05）;PMS2蛋白表达缺失易发生在组织学G2级、FIGO分期Ⅲ期、妊娠1次及以上、脉管内癌栓和淋巴结转移的患者（P<0.05）。结论 子宫内膜癌错配修复蛋白表达与其部分临床病理特征存在密切关联,可为患者后续治疗提供有价值的指导。

Objective To investigate the composition and clinicopathological features of endometrial carcinoma．Methods A total of 82 cases of endometrial carcinoma patients admitted to the First Hospital of Nanping City from January 2020 to June 2022 were studied．Epidemiological data were collected,and the expression of 4 mismatch repair proteins were detected by immunohistochemical staining,and their relationship with clinicopathological features was analyzed．Results Among 82 patients,70 cases（85.37%）were endometrioid carcinoma,and 30 cases（42.86%）were mainly G1 grade,other types were rare．The total deletion rate of mismatch repair proteins expression was 35.71%,in which MLH1 alone was 2.86%,MSH2 was 4.29%,MSH6 was14.29% and PMS2 was14.29%．The proportions of dMMR patients over 50 years old,with vascular invasion and lymph node metastasis,G3 grade histology and FIGO stage Ⅲ were significantly higher than those of the pMMR group（P<0.05）．The loss of MSH6 protein expression was more likely to occur in patients over 50 years old with a family history of related diseases（P<0.05）．The deletion of PMS2 protein expression was more likely to occur in patients with histological G2 grade,FIGO stage III,pregnancy of once or more and intravascular cancer thrombin and lymph node metastasis（P<0.05）．Conclusions The expression of mismatch repair proteins in endometrial carcinoma is closely related to some clinicopathological features,which provides valuable guidance for follow-up treatment．