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首页> 外文期刊>Medical Science Monitor Basic Research >The Role of p21 in Apoptosis, Proliferation, Cell Cycle Arrest, and Antioxidant Activity in UVB-Irradiated Human HaCaT Keratinocytes
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The Role of p21 in Apoptosis, Proliferation, Cell Cycle Arrest, and Antioxidant Activity in UVB-Irradiated Human HaCaT Keratinocytes

机译：p21在UVB照射的人HaCaT角质形成细胞的凋亡，增殖，细胞周期阻滞和抗氧化活性中的作用。

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BACKGROUND Skin cancer is the most common cancer in the United States, and ultraviolet B (UVB) radiation-induced DNA damage is the major environmental factor underlying skin cancer development. p21, a p53-inducible protein, plays a key role in the cellular response to UVB-induced DNA damage. MATERIAL AND METHODS Through p21 silencing and overexpression, we investigated the role of p21 in apoptosis, proliferation, cell cycle arrest, and oxidative stress in UVB-irradiated HaCaT keratinocytes. RESULTS We found that UVB exposure induced significant p21 downregulation (p<0.05) and was associated with significantly increased apoptosis, significantly decreased proliferation, and significantly increased G2 phase arrest (p<0.05) in UVB-irradiated HaCaT keratinocytes. p21 silencing significantly promoted apoptosis, significantly inhibited G2 phase arrest, and significantly inhibited proliferation ([i]p[/i]<0.05), but after UVB irradiation, p21 silencing demonstrated a less significant pro-apoptotic effect and a more significant inhibition of G2 phase arrest ([i]p[/i]<0.05), which was reflected in significantly higher proliferative activity ([i]p[/i]<0.05). p21 overexpression acted in an anti-apoptotic manner in the absence of UVB-induced DNA damage but acted in a pro-apoptotic manner in the presence of UVB-induced DNA damage, displaying an “antagonistic duality” similar to other growth-promoting oncoproteins. p53 expression mirrored p21 expression, suggesting a regulatory feedback mechanism between p21 and p53 expression. p21 overexpression significantly downregulated glutathione peroxidase and superoxide dismutase antioxidant activity ([i]p[/i]<0.05) while significantly upregulating hydrogen peroxide and malondialdehyde content ([i]p[/i]<0.05), suggesting a role in decreasing antioxidant defense capabilities in UVB-irradiated HaCaT keratinocytes. CONCLUSIONS These findings reveal that p21 may play a key role in HaCaT keratinocytes’ response to UVB exposure.
机译：背景技术皮肤癌是美国最常见的癌症，紫外线B（UVB）辐射诱导的DNA损伤是皮肤癌发展的主要环境因素。 p21是p53诱导蛋白，在细胞对UVB诱导的DNA损伤的反应中起关键作用。材料和方法通过p21沉默和过表达，我们研究了p21在UVB照射的HaCaT角质形成细胞的凋亡，增殖，细胞周期停滞和氧化应激中的作用。结果我们发现，UVB照射的HaCaT角质形成细胞中，UVB暴露可诱导p21明显下调（p <0.05），并与凋亡显着增加，增殖显着降低和G2期停滞（p <0.05）显着相关。 p21沉默可显着促进细胞凋亡，显着抑制G2期停滞并显着抑制增殖（[i] p [/ i] <0.05），但在UVB照射后，p21沉默显示出较不明显的促凋亡作用和更显着的抑制作用。 G2期阻滞（[i] p [/ i] <0.05），这反映在增殖活性显着更高（[i] p [/ i] <0.05）上。在不存在UVB诱导的DNA损伤的情况下，p21过表达以抗凋亡的方式起作用，但是在存在UVB诱导的DNA损伤的情况下以促凋亡的方式起作用，表现出与其他促进生长的癌蛋白相似的“拮抗对偶性”。 p53表达与p21表达相对应，表明p21和p53表达之间存在调节反馈机制。 p21过表达显着下调了谷胱甘肽过氧化物酶和超氧化物歧化酶的抗氧化活性（[i] p [/ i] <0.05），同时显着上调了过氧化氢和丙二醛的含量（[i] p [/ i] <0.05），表明在降低抗氧化性方面有作用UVB照射的HaCaT角质形成细胞的防御能力。结论这些发现表明p21可能在HaCaT角质形成细胞对UVB暴露的反应中起关键作用。

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