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[1]耿彦南,邵 睿,张黎龙,等.ICAM1通过PI3K/Akt信号通路促进骨肉瘤细胞生长和侵袭[J].天津医科大学学报,2026,32(02):126-132.[doi:10.20135/j.issn.1006-8147.2026.02.0126]
　GENG Yannan,SHAO Rui,ZHANG Lilong,et al.ICAM1 promotes osteosarcoma cell growth and invasion through the PI3K/Akt signaling pathway[J].Journal of Tianjin Medical University,2026,32(02):126-132.[doi:10.20135/j.issn.1006-8147.2026.02.0126]
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ICAM1通过PI3K/Akt信号通路促进骨肉瘤细胞生长和侵袭(PDF)

《天津医科大学学报》[ISSN:1006-8147/CN:12-1259/R]

卷:
32卷
期数:
2026年02期
页码:
126-132
栏目:
肿瘤疾病专题
出版日期:
2026-03-20

文章信息/Info

Title:
ICAM1 promotes osteosarcoma cell growth and invasion through the PI3K/Akt signaling pathway
文章编号:
1006-8147(2026)02-0126-07
作者:
耿彦南; 邵 睿; 张黎龙; 徐天同
（天津市人民医院，南开大学第一附属医院脊柱六科，天津300121）
Author(s):
GENG Yannan;  SHAO Rui;  ZHANG Lilong;  XU Tiantong
（Department of the Sixth Spinal Surgery， Tianjin Union Medical Center， The First Affiliated Hospital of Nankai University， Tianjin 300121， China）
关键词:
骨肉瘤; ICAM1; 细胞外基质; 细胞生长; 转移; PI3K/Akt信号通路
Keywords:
osteosarcoma;  ICAM1;  extracellular matrix;  cell growth;  migration;  PI3K/Akt signaling pathway
分类号:
R738.1
DOI:
10.20135/j.issn.1006-8147.2026.02.0126
文献标志码:
A
摘要:
目的：探讨骨肉瘤微环境相关蛋白细胞间黏附分子1（ICAM1）通过磷脂酰肌醇3激酶（PI3K）/蛋白激酶B（Akt）信号通路对骨肉瘤细胞生长和侵袭的调控作用和机制。方法：使用GEO数据库数据GSE126209分析骨肉瘤组织和癌旁组织差异基因的GO功能注释和关键蛋白。通过实时PCR和Western印迹实验，比较正常成骨细胞系和不同骨肉瘤细胞系之间ICAM1的表达差异，选取ICAM1表达较高的U2OS细胞进一步研究。在U2OS细胞系中，通过MTT、Transwell和胶原收缩实验，检测对照组si-NC和不同si-ICAM1转染组之间骨肉瘤细胞生长和侵袭表型的差异。此外，通过GEO数据差异基因的KEGG信号通路富集结果分析、Western印迹、MTT、Transwell和胶原收缩实验，探讨ICAM1对PI3K/Akt信号通路的影响。结果：GEO数据的GO注释结果显示，骨肉瘤组织中细胞外基质相关信号通路显著富集，且ICAM1可能为其中的关键蛋白。ICAM1在骨肉瘤细胞系中显著高表达（F=76.15，P<0.001）。同时，ICAM1敲低显著抑制骨肉瘤细胞的生长（F=61.59，P<0.001）、迁移（F=55.21，P<0.001）和细胞外胶原收缩（F=83.61，P<0.005）。GEO数据的KEGG信号通路富集分析和Western 印迹实验证实，PI3K/Akt信号通路在骨肉瘤中异常激活，然而，加入PI3K抑制剂Wortmannin后，ICAM1敲低对骨肉瘤细胞生长（t=0.36，P=0.74）、迁移（t=2.31，P=0.08）和细胞外胶原收缩（t=0.19，P=0.86）无显著影响。结论：在骨肉瘤组织中，细胞外基质相关功能和信号通路显著富集，且ICAM1与这一现象相关。ICAM1通过PI3K/Akt信号通路显著促进骨肉瘤细胞的生长和侵袭。
Abstract:
Objective： To investigate the regulatory effect and mechanism of microenvironment-associated protein intercellular adhesion molecule-1 （ICAM1） on cell growth and invasion in osteosarcoma via the phosphatidylinositol 3-kinase （PI3K）/protein kinase B（Akt） signaling pathway. Methods： The GEO dataset GSE126209 was utilized to analyze GO functional annotation and key protein analysis of differentially expressed genes between osteosarcoma and adjacent tissues. ICAM1 expression differences was compared by real time PCR and Western blotting in normal osteoblasts versus different osteosarcoma cell lines， and U2OS cells with the higher ICAM1 expression were selected for further investigation. In U2OS cell lines， MTT assays， Transwell and collagen contraction experiments were conducted to evaluate phenotypic differences in osteosarcoma cell growth and invasion between si-NC control and various si-ICAM1 transfection groups. Furthermore， KEGG signal pathway enrichment analysis of differentially expressed genes in GEO data， Western blotting analyses， MTT， Transwell and collagen contraction assays were employed to explore the impact of ICAM1 on the PI3K/Akt signaling pathway. Results： GO annotation of GEO data indicated significant enrichment of extracellular matrix-related pathways in osteosarcoma tissues. ICAM1 maybe a key protein among them. ICAM1 was significantly upregulated in osteosarcoma cell lines （F=76.15，P<0.001）. Meanwhile， knockdown of ICAM1 suppressed osteosarcoma cell growth（F=61.59， P<0.001）， migration （F=55.21， P<0.001）， and collagen contraction （F=83.61，P<0.005）. Meanwhile， KEGG pathway enrichment analysis of GEO data and Western blotting confirmed that the PI3K/Akt signaling pathway was abnormally activated in osteosarcoma. In osteosarcoma cells treated with the PI3K inhibitor Wortmannin， the inhibitory effect of ICAM1 knockdown on osteosarcoma cell growth（t=0.36， P=0.74）， migration （t=2.31， P=0.08）， and collagen contraction （t=0.19， P=0.86） were blocked. Conclusion： In osteosarcoma tissue， extracellular matrix related functions and signaling pathways are significantly enriched， with ICAM1 potentially involved. ICAM1 promotes osteosarcoma cell growth and invasion via the PI3K/Akt signaling pathway.

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备注/Memo

备注/Memo:
基金项目 天津市医学重点学科（专科）建设项目资助（TJYXZDXK-064B）；天津市人民医院院级课题（2021YJ009）
作者简介 耿彦南（1987-），男，主治医师，硕士，研究方向：脊柱外科；通信作者：徐天同，E-mail：xtt1114@sina.com。
更新日期/Last Update: 2026-03-20