徳島大学 教育・研究者情報データベース(EDB)

1. (英) Dondoo Tsogt-Ochir

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2. 福森 知治

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3. (英) Daizumoto Kei

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4. 布川 朋也([徳島大学.大学院医歯薬学研究部.医学域.医科学部門.外科系.泌尿器科学]/[徳島大学.病院.診療科.外科.泌尿器科])

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5. (英) Kohzuki Miho

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6. (英) Kowada Minoru

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7. 楠原 義人([徳島大学.病院.診療科.外科.泌尿器科])

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8. 森 英恭

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9. 中逵 弘能

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10. 高橋 正幸([徳島大学.大学院医歯薬学研究部.医学域.医科学部門.外科系.泌尿器科学]/[徳島大学.病院.診療科.外科.泌尿器科])

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11. 金山 博臣

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(英) Galectin-3 Is Implicated in Tumor Progression and Resistance to Anti-androgen Drug Through Regulation of Androgen Receptor Signaling in Prostate Cancer.

(英) Castration-resistant prostate cancer (CRPC)-related deaths are increasing worldwide. Therefore, clarification of the mechanisms of hormone-related tumor progression and resistance to anti-androgen drugs is useful in order to develop strategies for appropriate treatment of CRPC. Galectin-3 has been shown to be correlated with tumor progression in a variety of cancer types through the regulation of tumor proliferation, angiogenesis, and apoptosis. We examined tumor cell invasion and migration using the xCELLigence system. Control LNCaP and galectin-3-expressing LNCaP (LNCaP-Gal-3) cells were cultured with androgen-depleted medium with 5% charcoal-stripped serum. Cells were treated for 24 h with or without dihydrotestosterone alone or combined with MDV3100 and bicalutamide; gene profile was then analyzed by microarray analysis and mRNA expression was confirmed by quantitative real-time polymerase chain reaction (qRT-PCR). We evaluated tumor growth using spheroids and xenograft tumor growth in a mouse model. In vitro, LNCaP-Gal-3 cells promoted both cell migration and invasion in an androgen-independent manner compared to control LNCaP cells. Galectin-3 also enhanced anchorage-independent growth and xenograft tumor growth even after castration. Importantly, galectin-3 greatly enhanced transcriptional activity of the androgen receptor (AR), especially on treatment with dihydrotestosterone. In microarray and qRT-PCR analyses, galectin-3 increased the expression of several AR-target genes, such as kallikrein-related peptidase 3 (KLK3), and transmembrane protease, serine 2 (TMPRSS2). These AR-target genes were not fully suppressed by anti-androgen drugs such as bicalutamide or MDV3100. Galectin-3 significantly inhibited the effect induced by anti-androgen drugs MDV3100 and bicalutamide, suggesting that galectin-3 may be involved in resistance to anti-androgen drug through enhancement of transcriptional activity of AR and expression of AR-related genes. These results suggest that galectin-3 is a potential target molecule for future treatment of anti-androgen drug-resistant prostate cancer.

1. (英) Androgen Antagonists
2. (英) Anilides
3. (英) Animals
4. (英) Antineoplastic Agents, Hormonal
5. (英) Cell Line, Tumor
6. (英) Cell Movement
7. (英) Cell Proliferation
8. (英) Disease Progression
9. (英) Drug Resistance, Neoplasm
10. (英) Galectin 3
11. (英) Gene Expression Profiling
12. (英) Gene Expression Regulation, Neoplastic
13. (英) Humans
14. (英) Male
15. (英) Mice, Inbred BALB C
16. (英) Mice, Nude
17. (英) Neoplasm Invasiveness
18. (英) Nitriles
19. (英) Oligonucleotide Array Sequence Analysis
20. (英) Phenylthiohydantoin
21. (英) Prostatic Neoplasms, Castration-Resistant
22. (英) Real-Time Polymerase Chain Reaction
23. (英) Receptors, Androgen
24. (英) Signal Transduction
25. (英) Tosyl Compounds
26. (英) Transcription, Genetic
27. (英) Xenograft Model Antitumor Assays

1. (英) Article.PublicationTypeList.PublicationType: Journal Article

2. (英) KeywordList.Keyword: Prostate cancer

3. (英) KeywordList.Keyword: anti-androgen resistance

4. (英) KeywordList.Keyword: galectin-3 gene