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Onco Targets Ther. 2019 Feb 14;12:1215-1223. doi: 10.2147/OTT.S194064. eCollection 2019.

Combined silencing of VEGF-A and angiopoietin-2, a more effective way to inhibit the Ishikawa endometrial cancer cell line.

Xu X1, Yan Y1,2, Xun Q3, Shi J1,4, Kong X1, Wu J1, Zhou H1.

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Department of Gynecology, Nanjing Drum Tower Hospital, Nanjing University Medical School, Nanjing, Jiangsu 210008, China,
Department of Gynecology, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, Guangxi 530021, China.
Department of Physiology, Medical College, Southeast University, Nanjing, Jiangsu 210009, China.
Department of Obstetrics and Gynecology, The First Affiliated Hospital of Henan University of Traditional Chinese Medicine, Zhengzhou, Henan 450008, China.



Angiogenesis is critical for the growth and metastasis of solid tumors and is, therefore, an important therapeutic target. Despite the great research advances in tumor therapies targeting vascular endothelial growth factor (VEGF), drug resistance frequently occurs, and further strategies targeting the tumor vasculature are of primary concern.


The present study aimed to determine whether a combination of small interfering RNAs (siRNAs) targeting VEGF-A and angiopoietin-2 (Ang-2) inhibited the biologic mechanisms of endometrial cancer more effectively compared to either one alone, in vitro and in vivo.


VEGF-A and Ang-2 were silenced by siRNA in Ishikawa endometrial cancer cells. Cell growth, apoptosis, metastasis, and tumor angiogenesis were measured in vitro and in vivo.


There was no difference observed in cell apoptosis rate; however, combined silencing of VEGF-A and Ang-2 resulted in a stronger inhibition of cell proliferation and invasion (P<0.05). Similarly, a greater reduction of tumor size and angiogenesis was seen with the concurrent administration of siRNAs targeting VEGF-A and Ang-2 in nude mice (P<0.05).


Our data indicated that simultaneous blockade of VEGF-A and Ang-2 may serve as a novel and effective therapeutic strategy in endometrial cancer.


Ang-2; angiogenesis; drug resistance; siRNA

Conflict of interest statement

Disclosure The authors report no conflicts of interest in this work.

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