التفاصيل البيبلوغرافية
| العنوان: |
Imatinib mesylate inhibits androgen-independent PC-3 cell viability, proliferation, migration, and tumor growth by targeting platelet-derived growth factor receptor-α. |
| المؤلفون: |
Nayeem, Md Junayed1 (AUTHOR), Yamamura, Aya1 (AUTHOR), Hayashi, Hisaki1 (AUTHOR), Muramatsu, Hiroyuki2 (AUTHOR), Nakamura, Kogenta2 (AUTHOR), Sassa, Naoto2 (AUTHOR), Sato, Motohiko1 (AUTHOR) motosato@aichi-med-u.ac.jp |
| المصدر: |
Life Sciences. Jan2022, Vol. 288, pN.PAG-N.PAG. 1p. |
| مصطلحات موضوعية: |
*PLATELET-derived growth factor, *PLATELET-derived growth factor receptors, *ANDROGEN receptors, *IMATINIB, *TUMOR growth, *SMALL interfering RNA |
| مستخلص: |
The abnormal expression of oncogenic tyrosine kinase receptors such as platelet-derived growth factor receptors (PDGFRs) has been reported in cancer progression. However, the role of PDGFRs in the human androgen-independent prostate cancer PC-3 cell line is not well understood. Thus, this study examined the role of PDGFRs in androgen-independent PC-3 cells. PDGFR mRNA and protein expression was determined by quantitative real-time PCR and western blotting, respectively. The effects of the tyrosine kinase inhibitor imatinib (imatinib mesylate) and small interfering RNAs (siRNAs) were determined by a Cell Counting Kit-8 assay, bromodeoxyuridine assay, and Transwell migration assay. The in vivo effect of imatinib was analyzed using a tumor formation assay in nude mice. PDGFRα was upregulated in androgen-independent PC-3 cells compared with normal prostate epithelial cells. PDGF-BB induced the phosphorylation of PDGFRα and downstream signaling molecules, including Akt, in a dose-dependent manner. Imatinib reduced the phosphorylation of the PDGFRα/Akt axis. Imatinib also suppressed the viability, proliferation, migration, and tumor growth of PC-3 cells. PDGFRα knockdown by siRNA decreased the viability and migration of PC-3 cells. These results demonstrated the distinct contribution of PDGFRα signaling to the proliferation and migration of PC-3 cells and suggested the potential for PDGFRα as a therapeutic target for metastatic and androgen-independent prostate cancer. [ABSTRACT FROM AUTHOR] |
| قاعدة البيانات: |
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