ABSTRACT
Objective To observe the impacts of sulforaphane on proliferation, apoptosis and Wnt/β-catenin pathway of cultured retinoblastoma cells. Methods Retinoblastoma Y79 cells were cultured with varying concentrations of sulforaphane (10, 20, 40 mg/L) for 24 and 48 h. Cell proliferation and apoptosis were measured by CCK8 assay and flow cytometry. Apoptosis related proteins Bax and Bcl-2, as well as the expression levels of related proteins in Wnt/β-catenin signaling pathway were determined using Western Blot. Results Sulforaphane suppressed cell proliferation and stimulate apoptosis (12.47％ ± 2.24％, 24.63％ ± 3.44％, 57.49％ ± 5.41％ vs. 3.47％ ± 0.74％) in a dose- and time-dependent manner, respectively. Furthermore, 40 mg/L of sulforaphane increased the expression of Bax (0.57 ± 0.03 vs. 0.12 ± 0.01), but decreased the Bcl-2 (0.16 ± 0.01 vs. 0.81 ± 0.03) protein expression. The results of Western Blot displayed that sulforaphane decreased the expression levels of Wnt (0.19 ± 0.01 vs. 0.74 ± 0.02), β-catenin protein (0.22 ± 0.02 vs. 0.82 ± 0.03), indicating that sulforaphane can inhibit the activation of Wnt/β-catenin signaling pathway. Conclusions The sulforaphane could inhibit the proliferation and induce the apoptosis of retinoblastoma Y79 cells, probably regulating by the Wnt/β-catenin signaling pathway.
ABSTRACT
Kinesin-2 family proteins, including KIF3A, KIF3B, KIF3C and KIF17, are members of the kinesin superfamily motor proteins , which transport various proteins and vesicles in the cell and play diverse biological functions . Recently, studies on members of kinesin-2 family proteins suggest that they play fundamental roles during ciliary transport , whose defects can lead to abnormal cilia development , the major cause of human ciliopathies .In this review , we will sum-marize the functions of this motor protein family during ciliogenesis and focus mainly on their roles in the development of model organisms .