Graduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Taoyuan, Taiwan, R.O.C.
Department of Neurosurgery, Chang Gung Memorial Hospital at Linkou Medical Center, Taoyuan, Taiwan, R.O.C.
Anticancer Res. 2021 Dec;41(12):6135-6145. doi: 10.21873/anticanres.15433.
BACKGROUND/AIM: This study aimed to explore RGS2 as a regulator of melanoma cell growth.
Effect of RGS2 over-expression was analyzed in three melanoma cell lines, and Rgs2 knockdown was performed in zebrafish.
RGS2 was differentially expressed among the cell lines. In B16F10 cells, RGS2 over-expression inhibited MAPK and AKT activation, and prevented cell growth. A similar outcome was observed in A375 cells, but the MAPK signals were not suppressed. In A2058 cells, RGS2 repressed AKT activation, but without affecting cell growth. Moreover, MAPK and AKT constitutive activation abolished the RGS2 inhibitory effect on B16F10 cell growth. Rgs2 knockdown caused ectopic melanocyte differentiation, and promoted MAPK and AKT activation in zebrafish embryos.
RGS2 prevents melanoma cell growth by inhibiting MAPK and AKT, but this effect depends on the overall cell genetic landscape. Further studies are warranted to investigate the anticancer therapeutic potential of RGS2 for melanoma.
背景/目的：本研究旨在探索 RGS2 作为黑色素瘤细胞生长的调节剂。
在三种黑色素瘤细胞系中分析了 RGS2 过表达的效果，并在斑马鱼中进行了 Rgs2 敲低。
RGS2 在细胞系中表达差异。在 B16F10 细胞中，RGS2 过表达抑制了 MAPK 和 AKT 的激活，阻止了细胞生长。在 A375 细胞中也观察到类似的结果，但 MAPK 信号未被抑制。在 A2058 细胞中，RGS2 抑制了 AKT 的激活，但对细胞生长没有影响。此外，MAPK 和 AKT 的组成性激活消除了 RGS2 对 B16F10 细胞生长的抑制作用。Rgs2 敲低导致斑马鱼胚胎中异位黑素细胞分化，并促进了 MAPK 和 AKT 的激活。
RGS2 通过抑制 MAPK 和 AKT 来阻止黑色素瘤细胞生长，但这种作用取决于整体细胞遗传背景。需要进一步研究以探讨 RGS2 对黑色素瘤的抗癌治疗潜力。
