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阿托伐他汀通过调节miR-125a-5p/TXLNA轴抑制胶质瘤糖酵解和免疫逃逸。

Atorvastatin inhibits glioma glycolysis and immune escape by modulating the miR-125a-5p/TXLNA axis.

作者信息

Gao Kang, Zhou Tao, Yin YingChun, Sun XiaoJie, Jiang HePing, Li TangYue

机构信息

Department of Neurosurgery, Central Hospital of Zibo, Zibo City, Shandong Province, 255000, China.

Department of Pathology, Central Hospital of Zibo, No.54, Communist Youth League West Road, Zhangdian District, Zibo City, Shandong Province, 255000, China.

出版信息

Hereditas. 2024 Dec 26;161(1):54. doi: 10.1186/s41065-024-00349-5.

DOI:10.1186/s41065-024-00349-5
PMID:39726023
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11670371/
Abstract

BACKGROUND

Conventional treatments, including surgery, radiotherapy and chemotherapy, have many limitations in the prognosis of glioma patients. Atorvastatin (ATOR) has a significant inhibitory effect on glioma malignancy. Thus, ATOR may play a key role in the search for new drugs for the effective treatment of gliomas.

METHODS

U87 cells were treated with different doses of ATOR and transfected. Viability was assessed using MTT, proliferative ability was determined using the colony formation test, Bax and Bcl-2 were identified using Western blot, apoptosis was identified using flow cytometry, and U87 cell migration and invasion were detected using the Transwell assay. Glucose uptake, lactate secretion, and ATP production in U87 cell culture medium were quantified. The positive rates of IFN-γ and TNF-α in CD8T were measured through flow cytometry. Subcutaneous injection of U87 cells was carried out to construct an in vivo mouse model of gliom, followed by HE staining to assess the effects of ATOR and miR-125a-5p on tumor development.

RESULTS

ATOR blocked the viability, proliferation, migration, and invasion of U87 cells through the miR-125a-5p/TXLNA axis, and suppressed glycolysis and immune escape of glioma cells. Furthermore, overexpressing miR-125a-5p enhanced the anti-tumor effect of ATOR in vivo.

CONCLUSION

ATOR blocks glioma progression by modulating the miR-125a-5p/TXLNA axis, further demonstrating that ATOR provides an effective therapeutic target for the treatment of glioma.

摘要

背景

包括手术、放疗和化疗在内的传统治疗方法在胶质瘤患者的预后方面存在诸多局限性。阿托伐他汀（ATOR）对胶质瘤恶性肿瘤具有显著的抑制作用。因此，ATOR可能在寻找有效治疗胶质瘤的新药方面发挥关键作用。

方法

用不同剂量的ATOR处理U87细胞并进行转染。使用MTT评估细胞活力，使用集落形成试验测定增殖能力，使用蛋白质免疫印迹法鉴定Bax和Bcl-2，使用流式细胞术鉴定细胞凋亡，使用Transwell试验检测U87细胞的迁移和侵袭。对U87细胞培养基中的葡萄糖摄取、乳酸分泌和ATP产生进行定量。通过流式细胞术测量CD8T中IFN-γ和TNF-α的阳性率。皮下注射U87细胞以构建胶质瘤小鼠体内模型，随后进行苏木精-伊红染色以评估ATOR和miR-125a-5p对肿瘤发展的影响。

结果

ATOR通过miR-125a-5p/TXLNA轴阻断U87细胞的活力、增殖、迁移和侵袭，并抑制胶质瘤细胞的糖酵解和免疫逃逸。此外，过表达miR-125a-5p增强了ATOR在体内的抗肿瘤作用。

结论

ATOR通过调节miR-125a-5p/TXLNA轴阻断胶质瘤进展，进一步证明ATOR为胶质瘤治疗提供了一个有效的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8952/11670371/9054c83cdb7c/41065_2024_349_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8952/11670371/e3761ad05644/41065_2024_349_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8952/11670371/5be2404eff8f/41065_2024_349_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8952/11670371/997f03134814/41065_2024_349_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8952/11670371/832e850825e6/41065_2024_349_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8952/11670371/1b2204bced13/41065_2024_349_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8952/11670371/7d8e587df453/41065_2024_349_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8952/11670371/c3e73be1c3dc/41065_2024_349_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8952/11670371/9054c83cdb7c/41065_2024_349_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8952/11670371/e3761ad05644/41065_2024_349_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8952/11670371/5be2404eff8f/41065_2024_349_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8952/11670371/997f03134814/41065_2024_349_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8952/11670371/832e850825e6/41065_2024_349_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8952/11670371/1b2204bced13/41065_2024_349_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8952/11670371/7d8e587df453/41065_2024_349_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8952/11670371/c3e73be1c3dc/41065_2024_349_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8952/11670371/9054c83cdb7c/41065_2024_349_Fig8_HTML.jpg

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