Overexpression of spindle and kinetochore–associated protein 1 contributes to the progression of prostate cancer
Spindle and kinetochore–associated protein 1 is a microtubule-binding subcomplex of the outer kinetochore that is essential for proper chromosome segregation. Recently, spindle and kinetochore–associated protein 1 has been highlighted as a biomarker in various cancers; however, the precise role of s...
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Veröffentlicht in: | Tumor biology 2017-06, Vol.39 (6), p.1010428317701918-1010428317701918 |
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Zusammenfassung: | Spindle and kinetochore–associated protein 1 is a microtubule-binding subcomplex of the outer kinetochore that is essential for proper chromosome segregation. Recently, spindle and kinetochore–associated protein 1 has been highlighted as a biomarker in various cancers; however, the precise role of spindle and kinetochore–associated protein 1 in prostate cancer remains unknown. This study aims to evaluate whether spindle and kinetochore–associated protein 1 affects the biological behaviors of prostate cancer. We investigated the expression of spindle and kinetochore–associated protein 1 in a series of prostate cancer tissues as well as in a panel of prostate cancer cell lines. Cell proliferation, migration, and invasion were evaluated in spindle and kinetochore–associated protein 1 knockdown prostate cancer cell lines by MTT and Transwell assays. Our results showed that the expression of spindle and kinetochore–associated protein 1 was remarkably upregulated in prostate cancer at both messenger RNA and protein levels compared with non-cancerous tissue. Knockdown of spindle and kinetochore–associated protein 1 repressed the ability of cell proliferation, migration, and invasion of prostate cancer cells. Moreover, inhibition of spindle and kinetochore–associated protein 1 could inhibit the activity of AKT and ERK pathway. In conclusion, our findings suggest that spindle and kinetochore–associated protein 1 could serve as a potential therapeutic target in prostate cancer patients. |
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ISSN: | 1010-4283 1423-0380 |
DOI: | 10.1177/1010428317701918 |