MicroRNA-101 inhibits angiogenesis via COX-2 in endometrial carcinoma

Abnormal angiogenesis is critically involved in tumor progression and metastasis including endometrial cancer and is regulated by microRNAs such as microRNA-101 (miR-101). We hypothesize that miR-101 expression is disrupted in endometrial cancer and modulation of miR-101 levels is sufficient to regu...

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Bibliographic Details
Published in:Molecular and cellular biochemistry 2018-11, Vol.448 (1-2), p.61-69
Main Authors: Liu, Ying, Li, Haiyan, Zhao, Congying, Jia, Hanbing
Format: Article
Language:English
Subjects:
Angiogenesis
Aromatase
Biochemistry
Biomedical and Life Sciences
Cancer
Carcinoma
Cardiology
COX-2 inhibitors
Cyclooxygenase-2
Cytochrome P-450
Development and progression
Endometrial cancer
Endometrium
Life Sciences
Medical Biochemistry
Metastases
MicroRNA
MicroRNAs
miRNA
Modulation
Oncology
Prostaglandin E2
Prostaglandins E
Ribonucleic acid
RNA
Thrombospondin
Toxicity
Tumorigenesis
Tumors
Uterine cancer
Vascular endothelial growth factor
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Summary:Abnormal angiogenesis is critically involved in tumor progression and metastasis including endometrial cancer and is regulated by microRNAs such as microRNA-101 (miR-101). We hypothesize that miR-101 expression is disrupted in endometrial cancer and modulation of miR-101 levels is sufficient to regulate tumor growth through angiogenesis. We examined the expression levels of miR-101 and factors involved in angiogenesis in the patients with endometrial cancer. We also overexpressed or inhibited miR-101 in RL-95-2 cells and examined their effects on cell toxicity and tumor growth. Finally, we determined if miR-101 regulated tumorigenesis through cyclooxygenase-2 (COX-2). We found that miR-101 levels were significantly reduced. Factors involved in angiogenesis included vascular endothelial growth factor-A (VEGF-A), thrombospondin-1 (TSP-1), cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), and aromatase (P450arom), which were increased in endometrial carcinoma. Modulation of miR-101 level was sufficient to affect tumor growth. Finally, we found that the effects of miR-101 inhibition on tumor growth were suppressed by COX-2 inhibition. Our results suggest that modulating miR-101 and COX-2 levels or their activity may be a potential therapeutic strategy for endometrial cancer.
ISSN:0300-8177
1573-4919
DOI:10.1007/s11010-018-3313-0