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RIT1通过调控PI3K/AKT/c-Myc信号通路促进胶质瘤增殖。

RIT1 Promotes the Proliferation of Gliomas Through the Regulation of the PI3K/AKT/c-Myc Signalling Pathway.

作者信息

Liu Zhen, Jiang Hao-Dong, Kan Hao-Yuan, Zhang Li, Rao Yu-Xin, Jiang Xiao-Bing, Li Ming-Hui, Wang Qi

机构信息

Department of Neurosurgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.

Department of Anesthesiology, Hubei University of Chinese Medicine Affiliated Hubei Hospital of Chinese Medicine, Wuhan, China.

出版信息

J Cell Mol Med. 2025 Jan;29(2):e70362. doi: 10.1111/jcmm.70362.

DOI:10.1111/jcmm.70362
PMID:39833023
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11745823/
Abstract

Recently, RIT1 has been implicated in a range of neurological disorders; however, its precise function in glioma pathogenesis is not yet well-defined. This study employed quantitative reverse transcription PCR (qRT-PCR), Western blotting (WB), immunohistochemistry (IHC) and additional methodologies to assess RIT1 expression levels in glioma tissues. Furthermore, the study investigated its influence on glioma progression through a series of functional experiments. Animal models were also utilised to elucidate the mechanistic role of RIT1, with a particular focus on its effects on the PI3K/AKT signalling pathway. Research findings showcased that RIT1 is significantly overexpressed in gliomas and exhibits a strong correlation with tumour grade and unfavourable clinical outcomes. Furthermore, RIT1 serves as an independent prognostic marker of poor prognosis. Functional assays demonstrate that RIT1 facilitates the aggressiveness of glioma cells by activating the PI3K/AKT signalling. Additionally, it promotes tumour proliferation by inhibiting apoptosis and accelerating cell cycle progression. This study demonstrates that RIT1 significantly contributes to the aggressive phenotype and unfavourable prognosis of glioma, indicating its ability as a therapeutic target for glioma treatment.

摘要

最近,RIT1已被发现与一系列神经疾病有关;然而,其在胶质瘤发病机制中的精确功能尚未明确界定。本研究采用定量逆转录PCR(qRT-PCR)、蛋白质免疫印迹法(WB)、免疫组织化学(IHC)及其他方法评估胶质瘤组织中RIT1的表达水平。此外,该研究通过一系列功能实验研究了其对胶质瘤进展的影响。还利用动物模型来阐明RIT1的作用机制,特别关注其对PI3K/AKT信号通路的影响。研究结果表明,RIT1在胶质瘤中显著过表达,且与肿瘤分级和不良临床结果密切相关。此外,RIT1是预后不良的独立预后标志物。功能分析表明,RIT1通过激活PI3K/AKT信号促进胶质瘤细胞的侵袭性。此外,它通过抑制细胞凋亡和加速细胞周期进程来促进肿瘤增殖。本研究表明,RIT1对胶质瘤的侵袭性表型和不良预后有显著影响,表明其有能力作为胶质瘤治疗的靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7883/11745823/ea9d4eaa5ba4/JCMM-29-e70362-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7883/11745823/1f3e9a2cd30f/JCMM-29-e70362-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7883/11745823/c940e50d1951/JCMM-29-e70362-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7883/11745823/7722f1f35710/JCMM-29-e70362-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7883/11745823/588ccdbe60d3/JCMM-29-e70362-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7883/11745823/83c8de891741/JCMM-29-e70362-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7883/11745823/f04d644700f1/JCMM-29-e70362-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7883/11745823/ea9d4eaa5ba4/JCMM-29-e70362-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7883/11745823/1f3e9a2cd30f/JCMM-29-e70362-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7883/11745823/c940e50d1951/JCMM-29-e70362-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7883/11745823/7722f1f35710/JCMM-29-e70362-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7883/11745823/588ccdbe60d3/JCMM-29-e70362-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7883/11745823/83c8de891741/JCMM-29-e70362-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7883/11745823/f04d644700f1/JCMM-29-e70362-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7883/11745823/ea9d4eaa5ba4/JCMM-29-e70362-g007.jpg

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