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阿托伐他汀在伯基特淋巴瘤模型的I-RTX治疗期间对HIF-1α的抑制作用

Inhibition of HIF-1α by Atorvastatin During I-RTX Therapy in Burkitt's Lymphoma Model.

作者信息

Kim Eun-Ho, Ko Hae Young, Yu A Ram, Kim Hyeongi, Zaheer Javeria, Kang Hyun Ji, Lim Young-Cheol, Cho Kyung Deuk, Joo Hyun-Yoo, Kang Min Kyoung, Lee Jae Jun, Lee Seung-Sook, Kang Hye Jin, Lim Sang Moo, Kim Jin Su

机构信息

Division of Radiation Biomedical Research, Korea Institute of Radiological and Medical Sciences, 75 Nowon-ro, Nowon-gu, Seoul 01812, Korea.

Department of Biochemistry, School of Medicine, Catholic University of Daegu, 33, 17-gil, Duryugongwon-ro, Nam-gu, Daegu 705-718, Korea.

出版信息

Cancers (Basel). 2020 May 11;12(5):1203. doi: 10.3390/cancers12051203.

DOI:10.3390/cancers12051203
PMID:32403237
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7281655/
Abstract

BACKGROUNDS

Radioimmunotherapy (RIT) serves as a targeted therapy for non-Hodgkin lymphomas (NHL). Although HIF(Hypoxia-inducible factors)-1α is an important biomarker during radiation therapy, its role in NHL is unclear. Atorvastatin (ATV) is used as a combination drug for chemotherapy.

METHODS

We investigated whether ATV downregulated tumor radio-resistance and enhanced the anticancer effect of I-RTX (rituximab) in Raji xenograft mouse models. First, the increased uptake and enhanced therapeutic effect of I-RTX by ATV was confirmed using molecular imaging in Raji xenograft subcutaneous model and orthotropic model with SPECT and IVIS images. Second, we examined the profile of differentially expressed miRNAs using miRNA array.

RESULTS

We found that miR-346 inhibited HIF-1α/VEGF (Vascular endothelial growth factor) during ATV combination therapy with I-RTX. The underlying mechanism of ATV involved induction of anti-angiogenesis and radiosensitivity by downregulating HIF-1α in Raji cells.

CONCLUSION

Our findings suggested that combination therapy with ATV and I-RTX is a promising strategy for enhancing the potency of I-RTX therapy in poorly responding patients and those with radio-resistance.

摘要

背景

放射免疫疗法（RIT）是非霍奇金淋巴瘤（NHL）的一种靶向治疗方法。虽然缺氧诱导因子（HIF）-1α是放射治疗期间的一种重要生物标志物，但其在NHL中的作用尚不清楚。阿托伐他汀（ATV）用作化疗的联合用药。

方法

我们在Raji异种移植小鼠模型中研究了ATV是否下调肿瘤放射抗性并增强I-RTX（利妥昔单抗）的抗癌效果。首先，在Raji异种移植皮下模型和原位模型中，使用SPECT和IVIS图像通过分子成像确认了ATV对I-RTX摄取的增加和治疗效果的增强。其次，我们使用miRNA阵列检查了差异表达miRNA的概况。

结果

我们发现，在ATV与I-RTX联合治疗期间，miR-346抑制HIF-1α/血管内皮生长因子（VEGF）。ATV的潜在机制包括通过下调Raji细胞中的HIF-1α诱导抗血管生成和放射敏感性。

结论

我们的研究结果表明，ATV与I-RTX联合治疗是一种有前景的策略，可增强I-RTX疗法对反应不佳患者和放射抗性患者的疗效。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f487/7281655/752d5b67465e/cancers-12-01203-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f487/7281655/35254e00b39e/cancers-12-01203-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f487/7281655/75364972a73f/cancers-12-01203-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f487/7281655/82968504c0ec/cancers-12-01203-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f487/7281655/a57b13292102/cancers-12-01203-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f487/7281655/7fafc4b6291d/cancers-12-01203-g005a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f487/7281655/752d5b67465e/cancers-12-01203-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f487/7281655/35254e00b39e/cancers-12-01203-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f487/7281655/75364972a73f/cancers-12-01203-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f487/7281655/82968504c0ec/cancers-12-01203-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f487/7281655/a57b13292102/cancers-12-01203-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f487/7281655/7fafc4b6291d/cancers-12-01203-g005a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f487/7281655/752d5b67465e/cancers-12-01203-g006.jpg

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