6-sialyllactose ameliorates dihydrotestosterone-induced benign prostatic hyperplasia through suppressing VEGF-mediated angiogenesis

Benign prostatic hyperplasia (BPH), a common disease in elderly males, is accompanied by non-malignant growth of prostate tissues, subsequently causing hypoxia and angiogenesis. Although VEGF-related angiogenesis is one of the therapeutic targets of prostate cancer, there is no previous study target...

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Published inBMB reports Vol. 52; no. 9; pp. 560 - 565
Main Authors Kim, Eun-Yeong, Jin, Bo-Ram, Chung, Tae-Wook, Bae, Sung-Jin, Park, Hyerin, Ryu, Dongryeol, Jin, Ling, An, Hyo-Jin, Ha, Ki-Tae
Format Journal Article
LanguageEnglish
Published Korea (South) 생화학분자생물학회 01.09.2019
Korean Society for Biochemistry and Molecular Biology
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ISSN1976-6696
1976-670X
1976-670X
DOI10.5483/BMBRep.2019.52.9.113

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Summary:Benign prostatic hyperplasia (BPH), a common disease in elderly males, is accompanied by non-malignant growth of prostate tissues, subsequently causing hypoxia and angiogenesis. Although VEGF-related angiogenesis is one of the therapeutic targets of prostate cancer, there is no previous study targeting angiogenesis for treatment of BPH. Dihydrotestosterone (DHT)- induced expressions of vascular endothelial growth factor (VEGF) in prostate epithelial RWPE-1 cells and human umbilical vascular endothelial cells (HUVECs). Conditioned media (CM) from DHT-treated RWPE-1 cells were transferred to HUVECs. Then, 6SL inhibited proliferation, VEGFR-2 activation, and tube formation of HUVECs transferred with CM from DHT-treated RWPE-1 cells. In the rat BPH model, 6SL reduced prostate weight, size, and thickness of the prostate tissue. Formation of vessels in prostatic tissues were also reduced with 6SL treatment. We found that 6SL has an ameliorative effect on in vitro and in vivo the BPH model via inhibition of VEGFR-2 activation and subsequent angiogenesis. These results suggest that 6SL might be a candidate for development of novel BPH drugs. [BMB Reports 2019; 52(9): 560-565]
Bibliography:Korean Society for Biochemistry and Molecular Biology
KISTI1.1003/JNL.JAKO201928462661300
These authors contributed equally to this work.
ISSN:1976-6696
1976-670X
1976-670X
DOI:10.5483/BMBRep.2019.52.9.113