Growth and Migration Blocking Effect of Nanaomycin K, a Compound Produced by Streptomyces sp., on Prostate Cancer Cell Lines In Vitro and In Vivo-Reference-Cited by-同舟云学术

Growth and Migration Blocking Effect of Nanaomycin K, a Compound Produced by Streptomyces sp., on Prostate Cancer Cell Lines In Vitro and In Vivo

Published:2023-05-10 Issue:10 Volume:15 Page:2684
ISSN:2072-6694
Container-title:Cancers
language:en
Short-container-title:Cancers

Author:

Hirata Yuto¹,Shigemura Katsumi¹²³⁴^ORCID,Moriwaki Michika¹,Iwatsuki Masato⁵⁶^ORCID,Kan Yuki¹,Ooya Tooru³⁴⁷^ORCID,Maeda Koki²^ORCID,Yang Youngmin²,Nakashima Takuji⁸,Matsuo Hirotaka⁹,Nakanishi Jun¹⁰^ORCID,Fujisawa Masato²

Affiliation:

1. Department of Public Health, Kobe University Graduate School of Health Sciences, 7-10-2 Tomogaoka, Suma-Ku, Kobe 654-0142, Japan

2. Department of Urology, Kobe University Graduate School of Medicine, 7-5-2 Kusunoki-Cho, Chuo-Ku, Kobe 650-0017, Japan

3. Department of Medical Device Engineering, Graduate School of Medicine, 7-5-2 Kusunoki-Cho, Chuo-Ku, Kobe 650-0017, Japan

4. Center for Advanced Medical Engineering Research & Development (CAMED), Kobe University, 1-5-1 Minatojima-minamimachi, Chuoku, Kobe 657-0047, Japan

5. Ōmura Satoshi Memorial Institute, Kitasato University, 5-9-1 Shirokane, Minato-Ku, Tokyo 108-8641, Japan

6. Graduate School of Infection Control Sciences, Kitasato University, 5-9-1 Shirokane, Minato-Ku, Tokyo 108-8641, Japan

7. Graduate School of Engineering Kobe University, 1-1 Rokkodai-Cho, Nada-Ku, Kobe 657-8501, Japan

8. Research Organization for Nano and Life Innovation, Waseda University, 513 Waseda Tsurumakicho, Shinjuku-Ku, Tokyo 162-0041, Japan

9. Research Center for Medicinal Plant Resources, National Institutes of Biomedical Innovation, Health and Nutrition, 1-2 Hachimandai, Tsukuba 305-8043, Japan

10. Research Center for Macromolecules and Biomaterials, National Institute for Materials Science (NIMS), 1-1 Namiki, Tsukuba 305-0044, Japan

Abstract

Since castration-resistant prostate cancer (CRPC) acquires resistance to molecularly targeted drugs, discovering a class of drugs with different mechanisms of action is needed for more efficient treatment. In this study, we investigated the anti-tumor effects of nanaomycin K, derived from “Streptomyces rosa subsp. notoensis” OS-3966. The cell lines used were LNCaP (non-CRPC), PC-3 (CRPC), and TRAMP-C2 (CRPC). Experiments included cell proliferation analysis, wound healing analysis, and Western blotting. In addition, nanaomycin K was administered intratumorally to TRAMP-C2 carcinoma-bearing mice to assess effects on tumor growth. Furthermore, immuno-histochemistry staining was performed on excised tissues. Nanaomycin K suppressed cell proliferation in all cell lines (p < 0.001) and suppressed wound healing in TRAMP-C2 (p = 0.008). Nanaomycin K suppressed or showed a tendency to suppress the expression of N-cadherin, Vimentin, Slug, and Ras in all cell lines, and suppressed the phosphorylation of p38, SAPK/JNK, and Erk1/2 in LNCaP and TRAMP-C2. In vivo, nanaomycin K safely inhibited tumor growth (p = 0.001). In addition, suppression of phospho-Erk1/2 and increased expression of E-cadherin and cleaved-Caspase3 were observed in excised tumors. Nanaomycin K inhibits tumor growth and suppresses migration by inhibiting epithelial-mesenchymal transition in prostate cancer. Its mechanism of action is related to the inhibition of phosphorylation of the MAPK signaling pathway.

Publisher

MDPI AG

Subject

Cancer Research,Oncology

Link

https://www.mdpi.com/2072-6694/15/10/2684/pdf

Reference42 articles.

1. Global Cancer Statistics 2020: GLOBOCAN Estimates of Incidence and Mortality Worldwide for 36 Cancers in 185 Countries;Sung;CA A Cancer J. Clin.,2021

2. The Diagnosis and Treatment of Prostate Cancer: A Review;Litwin;JAMA,2017

3. Wade, C.A., and Kyprianou, N. (2018). Profiling Prostate Cancer Therapeutic Resistance. Int. J. Mol. Sci., 19.

4. Kaszak, I., Witkowska-Piłaszewicz, O., Niewiadomska, Z., Dworecka-Kaszak, B., Ngosa Toka, F., and Jurka, P. (2020). Role of Cadherins in Cancer—A Review. Int. J. Mol. Sci., 21.

5. Du, B., and Shim, J.S. (2016). Targeting Epithelial–Mesenchymal Transition (EMT) to Overcome Drug Resistance in Cancer. Molecules, 21.

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