Extracellular vesicles isolated from SphK1 inhibitor SKI II-medium restrain the migration of colorectal cancer.

IF 1.5 4区医学 Q4 ONCOLOGY

Translational cancer research Pub Date : 2025-05-30 Epub Date: 2025-05-07 DOI:10.21037/tcr-24-2152

Chunyan Xu, Yingbin Hu, Guodong Dai, Yan Chen, Chengxia Liu

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引用次数: 0

Abstract

Background: Colorectal cancer is a chronic disease particularly detrimental to human health. Although there have been many studies on colorectal cancer and extracellular vesicles (EVs), it is unknown whether SKI II, an inhibitor of sphingosine kinase 1 (SphK1), uses EVs as transporters to inhibit colorectal cancer migration. This research aimed to investigate whether EVs, which were isolated from SphK1 inhibitor SKI II-medium, affected on E-cadherin and vimentin and the cell migration of colorectal cancer cells.

Methods: EVs were extracted from RKO cells using an exosome extraction and purification kit, and the extracted EVs were identified to evaluate whether the EVs extracted by this kit met the experimental requirements. ^RKOEVs were extracted from RKO exosom-free serum culture medium, and ^RKO-SKEVs were extracted from RKO exosom-free serum culture medium with SKI II intervention. PKH67-labeled EVs were added to the cells. EVs inhibitor GW4869, ^RKOEVs, and ^RKO-SKEVs were used to intervene in RKO cells, and ^RKOEVs and ^RKO-SKEVs were used to intervene in HT29 cells. The E-cadherin and vimentin expression were tested by western blotting. Transwell assay was used to detect cell migration ability.

Results: Compared with the control group, after GW4869 treatment, E-cadherin was increased, vimentin was decreased, and the number of migrating cells was decreased. After ^RKOEVs intervention, the expression of E-cadherin, vimentin and cell migration number were opposite. Compared with ^RKOEVs intervention in RKO cells, E-cadherin was increased, vimentin was decreased and the number of migrating cells decreased after ^RKO-SKEVs intervention. Similarly, compared with ^RKOEVs intervention in HT29 cells, after ^RKO-SKEVs intervention, E-cadherin was increased, vimentin was decreased, and the number of migrating cells decreased.

Conclusions: EVs isolated from SphK1 inhibitor SKI II-medium affect E-cadherin and vimentin expression in colorectal cancer and inhibit cell migration.

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SphK1抑制剂SKI ii -培养基中分离的细胞外囊泡抑制结直肠癌的迁移。

背景：结直肠癌是一种危害人体健康的慢性疾病。虽然对结直肠癌和细胞外囊泡（EVs）的研究较多，但鞘氨酸激酶1 （SphK1）抑制剂SKI II是否利用EVs作为转运体抑制结直肠癌的迁移尚不清楚。本研究旨在探讨从SphK1抑制剂SKI ii培养基中分离的ev是否影响E-cadherin和vimentin以及结直肠癌细胞的细胞迁移。方法：采用外泌体提取纯化试剂盒从RKO细胞中提取EVs，并对提取的EVs进行鉴定，评价该试剂盒提取的EVs是否符合实验要求。在无RKO外泌体的血清培养基中提取rkoev，在SKI II干预下，在无RKO外泌体的血清培养基中提取RKO- skev。将pkh67标记的ev添加到细胞中。使用ev抑制剂GW4869、rkoev和RKO- skev干预RKO细胞，使用rkoev和RKO- skev干预HT29细胞。western blotting检测E-cadherin和vimentin的表达。Transwell法检测细胞迁移能力。结果：与对照组比较，GW4869处理后，E-cadherin升高，vimentin降低，迁移细胞数量减少。RKOEVs干预后，E-cadherin、vimentin的表达和细胞迁移数量相反。与RKOEVs干预RKO细胞相比，RKO- skevs干预后，E-cadherin升高，vimentin降低，迁移细胞数量减少。同样，与rkoev干预HT29细胞相比，rko - skev干预后，E-cadherin升高，vimentin降低，迁移细胞数量减少。结论：SphK1抑制剂SKI ii培养基中分离的ev可影响结直肠癌组织中E-cadherin和vimentin的表达，抑制细胞迁移。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Translational cancer research ONCOLOGY-

CiteScore

2.10

自引率

0.00%

发文量

252

期刊介绍： Translational Cancer Research (Transl Cancer Res TCR; Print ISSN: 2218-676X; Online ISSN 2219-6803; http://tcr.amegroups.com/) is an Open Access, peer-reviewed journal, indexed in Science Citation Index Expanded (SCIE). TCR publishes laboratory studies of novel therapeutic interventions as well as clinical trials which evaluate new treatment paradigms for cancer; results of novel research investigations which bridge the laboratory and clinical settings including risk assessment, cellular and molecular characterization, prevention, detection, diagnosis and treatment of human cancers with the overall goal of improving the clinical care of cancer patients. The focus of TCR is original, peer-reviewed, science-based research that successfully advances clinical medicine toward the goal of improving patients'' quality of life. The editors and an international advisory group of scientists and clinician-scientists as well as other experts will hold TCR articles to the high-quality standards. We accept Original Articles as well as Review Articles, Editorials and Brief Articles.