RIG-I acts as a tumor suppressor in melanoma via regulating the activation of the MKK/p38MAPK signaling pathway.
RIG-I acts as a tumor suppressor in melanoma via regulating the activation of the MKK/p38MAPK signaling pathway.
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RIG-I 通过调节 MKK/p38MAPK 信号通路的激活在黑色素瘤中充当肿瘤抑制因子
DOI：
10.1007/s13577-022-00698-1
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发表时间：
2022-07
期刊：
影响因子：
4.3
通讯作者：
Zhang, Hong-Xin
中科院分区：
文献类型：
--
作者：
Guo, Rui;Lu, Shun-Yuan;Ma, Jin-Xia;Wang, Qian-Lan;Zhang, Lu;Tang, Ling-Yun;Shen, Yan;Shen, Chun-Ling;Wang, Jin-Jin;Lu, Li-Ming;Wang, Zhu-Gang;Zhang, Hong-Xin
研究表明，RIG-Ⅰ可能作为一种肿瘤抑制因子，参与某些恶性疾病的发生。然而，RIG-I根据细胞类型通过不同的下游信号传导途径诱导不同的细胞应答。为了探讨RIG-I在黑色素瘤发生中的生物学功能及其分子机制，我们构建了RIG-I敲除、RIG-I过表达的B16-F10和RIG-I敲减的A375黑色素瘤细胞系，并分析了RIG-I介导的自发和poly（I：C）诱导的RIG-I激活对肿瘤细胞生物学行为的影响。CCK-8法检测细胞增殖，BrdU掺入法检测细胞周期，Annexin V-PI染色法检测细胞凋亡，Transwell法检测细胞迁移。通过裸鼠中的肿瘤异种移植物生长以及随后通过Ki 67染色和TUNEL测定来评价体内致瘤性。此外，蛋白质印迹法用于探讨RIG-I在黑色素瘤细胞中的潜在机制。我们的数据表明，RIG-I促进细胞凋亡和抑制细胞增殖的G1期细胞周期阻滞在黑色素瘤细胞系。在机制上，RIG-I诱导p38 MAPK和MAPK激酶MKK 3和MKK 4的磷酸化。总之，目前的研究表明，RIG-I抑制黑色素瘤的发展，通过调节MKK/p38 MAPK信号通路的活性，这是相关的新的治疗靶点，这种恶性疾病的研究。在线版本包含补充材料，可通过10.1007/s13577-022-00698-1获得。
Studies have indicated that RIG-I may act as a tumor suppressor and participate in the tumorigenesis of some malignant diseases. However, RIG-I induces distinct cellular responses via different downstream signaling pathways depending on the cell type. To investigate the biological function and underlying molecular mechanism of RIG-I in the tumorigenesis of melanoma, we constructed RIG-I knockout, RIG-I-overexpressing B16-F10 and RIG-I knockdown A375 melanoma cell lines, and analyzed the RIG-I-mediated change in the biological behavior of tumor cells in spontaneous and poly (I:C)-induced RIG-I activation. Cell proliferation, cell cycling, apoptosis and migration were detected by CCK-8 assay, BrdU incorporation assay, Annexin V–PI staining assay and Transwell assay, respectively. In vivo tumorigenicity was evaluated by tumor xenograft growth in nude mice and subsequently by Ki67 staining and TUNEL assays. Furthermore, Western blotting was utilized to explore the underlying mechanism of RIG-I in melanoma cells. Our data showed that RIG-I promotes apoptosis and inhibits proliferation by G1 phase cell cycle arrest in the melanoma cell lines. Mechanistically, RIG-I induced the phosphorylation of p38 MAPK and MAPK kinases MKK3 and MKK4. In conclusion, the current study demonstrated that RIG-I suppressed the development of melanoma by regulating the activity of the MKK/p38 MAPK signaling pathway, which is relevant to research on novel therapeutic targets for this malignant disease. The online version contains supplementary material available at 10.1007/s13577-022-00698-1.
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影响因子：
5.2
作者：
Leonardi GC;Falzone L;Salemi R;Zanghì A;Spandidos DA;Mccubrey JA;Candido S;Libra M
通讯作者：
Libra M
干扰素-α 通过上调头颈鳞状细胞癌中的 RIG-I 增强 EGFR 靶向治疗的抗肿瘤活性
影响因子：
8.8
作者：
Ma H;Jin S;Yang W;Zhou G;Zhao M;Fang S;Zhang Z;Hu J
通讯作者：
Hu J
RIG-I：一种超越模式识别受体的多功能蛋白质
影响因子：
21.1
作者：
Xu XX;Wan H;Nie L;Shao T;Xiang LX;Shao JZ
通讯作者：
Shao JZ
RNA 病毒受体 Rig-I 监测肠道微生物群并抑制结肠炎相关结直肠癌
DOI：
10.1186/s13046-016-0471-3
发表时间：
2017-01-05
期刊：
Journal of experimental & clinical cancer research : CR
影响因子：
--
作者：
Zhu H;Xu WY;Hu Z;Zhang H;Shen Y;Lu S;Wei C;Wang ZG
通讯作者：
Wang ZG
影响因子：
16.6
作者：
Marie, Kerrie L.;Sassano, Antonella;Mishra, Pravin J.
通讯作者：
Mishra, Pravin J.