Wang Wu-Qing, Wu Jin-Feng, Xiao Xiao-Qing, Xiao Qin, Wang Jing, Zuo Fu-Guo
Department of Dermatology, The Central Hospital of Minhang, Shanghai 201199, P.R. China.
Department of Dermatology, Huashan Hospital, Fudan University, Shanghai 200040, P.R. China.
Mol Clin Oncol. 2013 Sep;1(5):858-862. doi: 10.3892/mco.2013.145. Epub 2013 Jul 11.
Melanocytes are found scattered throughout the basal layer of the epidermis. Following hormone or ultraviolet (UV) light stimulation, the melanin pigments contained in melanocytes are transferred through the dendrites to the surrounding keratinocytes to protect against UV light damage or carcinogenesis. This has been considered as a morphological indicator of melanocytes and melanoma cells. Small GTPases of the Rho family have been implicated in the regulation of actin reorganization underlying dendrite formation in melanocytes and melanoma cells. It has been proven that ultraviolet light plays a pivotal role in melanocyte dendrite formation; however, the molecular mechanism underlying this process has not been fully elucidated. The effect of small GTPases, such as Rac1 and RhoA, on the morphology of B16 melanoma cells treated with narrow-band UVB radiation was investigated. The morphological changes were observed under a phase contrast microscope and the F-actin microfilament of the cytoskeleton was observed under a laser scanning confocal microscope. The pull-down assay was performed to detect the activity of the small GTPases Rac1 and RhoA. The morphological changes were evident, with globular cell bodies and increased numbers of tree branch-like dendrites. The cytoskeletal F-actin appeared disassembled following narrow-band UVB irradiation of B16 melanoma cells. Treatment of B16 melanoma cells with narrow-band UVB radiation resulted in the activation of Rac1 in a time-dependent manner. In conclusion, the present study may provide a novel method through which narrow-band UVB radiation may be used to promote dendrite formation by activating the Rac1 signaling pathway, resulting in F-actin rearrangement in B16 melanoma cells.
黑素细胞散在于表皮的基底层。在激素或紫外线（UV）光刺激后，黑素细胞中所含的黑色素通过树突转移至周围的角质形成细胞，以防止紫外线损伤或致癌作用。这一直被视为黑素细胞和黑色素瘤细胞的一种形态学指标。Rho家族的小GTP酶参与了黑素细胞和黑色素瘤细胞中树突形成所依赖的肌动蛋白重组的调节。已证实紫外线在黑素细胞树突形成中起关键作用；然而，这一过程的分子机制尚未完全阐明。研究了小GTP酶，如Rac1和RhoA，对经窄带UVB辐射处理的B16黑色素瘤细胞形态的影响。在相差显微镜下观察形态变化，在激光扫描共聚焦显微镜下观察细胞骨架的F-肌动蛋白微丝。进行下拉试验以检测小GTP酶Rac1和RhoA的活性。形态变化明显，细胞体呈球形，树枝状树突数量增加。B16黑色素瘤细胞经窄带UVB照射后，细胞骨架F-肌动蛋白出现解聚。用窄带UVB辐射处理B16黑色素瘤细胞导致Rac1以时间依赖性方式激活。总之，本研究可能提供一种新方法，通过激活Rac1信号通路，利用窄带UVB辐射促进树突形成，从而导致B16黑色素瘤细胞中的F-肌动蛋白重排。
