Rosa hybrida Petal Extract Exhibits Antitumor Effects by Abrogating Tumor Progression and Angiogenesis in Bladder Cancer Both In Vivo and In Vitro

Author:

Hwang Byungdoo1,Gho Yujeong1,Kim Hoon1,Lee Sanghyun2,Hong Soon Auck3,Lee Tae Jin3,Myung Soon Chul4,Yun Seok-Joong5,Choi Yung Hyun6,Kim Wun-Jae5,Moon Sung-Kwon1ORCID

Affiliation:

1. Department of Food and Nutrition, Chung-Ang University, Anseong, South Korea

2. Dpartment of Plant Science and Technology, Chung-Ang University, Anseong, South Korea

3. Department of Pathology, College of Medicine, Chung-Ang University, Seoul, South Korea

4. Department of Urology, College of Medicine, Chung-Ang University, Seoul, South Korea

5. Department of Urology, Chungbuk National University, Cheongju, Chungbuk, South Korea

6. Department of Biochemistry, College of Oriental Medicine, Dong-Eui University, Busan, South Korea

Abstract

The edible Rosa hybrida (RH) petal is utilized in functional foods and cosmetics. Although the biological function of RH petal extract is known, mechanism of action studies involving tumor-associated angiogenesis have not yet been reported. Herein, we investigated the regulatory effect of the ethanol extract of RH petal (EERH) on tumor growth and tumor angiogenesis against bladder cancer. EERH treatment inhibited the bladder carcinoma T24 cell and 5637 cell proliferation because of G1-phase cell cycle arrest by inducing p21WAF1 expression and reducing cyclins/CDKs level. EERH regulated signaling pathways differently in both cells. EERH-stimulated suppression of T24 and 5637 cell migration and invasion was associated with the decline in transcription factor-mediated MMP-9 expression. EERH oral administration to xenograft mice reduced tumor growth. Furthermore, no obvious toxicity was observed in acute toxicity test. Decreased CD31 levels in EERH-treated tumor tissues led to examine the angiogenic response. EERH alleviated VEGF-stimulated tube formation and proliferation by downregulating the VEGFR2/eNOS/AKT/ERK1/2 cascade in HUVECs. EERH impeded migration and invasion of VEGF-induced HUVECs, which is attributed to the repressed MMP-2 expression. Suppression of neo-microvessel sprouting, induced by VEGF, was verified by treatment with EERH using the ex vivo aortic ring assay. Finally, kaempferol was identified as the main active compound of EERH. The present study demonstrated that EERH may aid the development of antitumor agents against bladder cancer.

Funder

Chung-Ang University

National Research Foundation of Korea

Publisher

SAGE Publications

Subject

Complementary and alternative medicine,Oncology

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