激酶d相互作用的220 kDa底物在胃癌中过表达并与局部侵袭有关。

IF 2.6 4区 医学 Q2 GENETICS & HEREDITY Cancer Genomics & Proteomics Pub Date : 2023-12-01 DOI:10.21873/cgp.20420
Shuo Cai, Zhiwei Sun, Xiangyu Gao, K E Ji, Fiona Ruge, Deepa Shankla, Xiangyi Liu, Wen G Jiang, Lin Ye
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引用次数: 0

摘要

背景/目的:220 kDa的激酶d相互作用底物(Kidins220),也称为富含锚蛋白重复的膜跨越蛋白(ARMS),是一种跨膜支架蛋白。不受管制的Kidins220已被观察到用于各种恶性肿瘤,包括黑色素瘤、胶质瘤、神经母细胞瘤、前列腺癌、胰腺癌和卵巢癌。材料和方法:在目前的研究中,Kidins220在转录物和蛋白水平上表达。建立了Kidins220敲低细胞模型,以确定其在细胞周期、增殖和侵袭等细胞功能中的作用。通过蛋白阵列和TCGA胃癌队列分析细胞信号传导。结果:与邻近正常组织相比,胃肿瘤中Kidins220转录物水平显著升高。与早期肿瘤(TNMI和TNMII)相比,晚期肿瘤(TNMIII和TNMIV)表现出更高的Kidins220蛋白水平。胃癌中Kidins220的表达增加与较差的总生存期相关。Kidins220的缺失促进了胃癌细胞的侵袭和粘附,并与上皮间质转化(EMT)和基质金属蛋白酶(MMP)信号传导有关。在G2/M期,敲低Kidins220促进了胃癌细胞的增殖,增加了胃癌细胞的数量。结论:我们的研究发现,Kidins220在胃癌中表达增加,与疾病进展和预后不良有关。然而,Kidins220通过调节EMT、MMP和细胞周期对增殖、侵袭和粘附有抑制作用。
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Kinase D-interacting Substrate of 220 kDa Is Overexpressed in Gastric Cancer and Associated With Local Invasion.

Background/aim: Kinase D-interacting substrate of 220 kDa (Kidins220), also known as ankyrin repeat-rich membrane spanning protein (ARMS), is a transmembrane scaffold protein. Deregulated Kidins220 has been observed in various malignancies including melanoma, glioma, neuroblastoma, prostate cancer, pancreatic cancer, and ovarian cancer.

Materials and methods: In the current study, Kidins220 expression was determined at transcript and protein levels. A Kidins220 knockdown cell model was established to identify its role in cellular functions including cell cycle, proliferation, and invasion. Cell signalling was analysed by protein array and the TCGA gastric cancer cohort.

Results: Kidins220 transcript levels were significantly increased in gastric tumours, compared with adjacent normal tissues. More advanced tumours (TNMIII and TNMIV) exhibited higher protein levels of Kidins220 compared with early-stage tumours (TNMI and TNMII). Increased expression of Kidins220 in gastric cancer was associated with poorer overall survival. Loss of Kidins220 promoted cell invasion and adhesion of gastric cancer and correlated to epithelial-mesenchymal transition (EMT) and matrix metalloproteinase (MMP) signalling. Knockdown of Kidins220 promoted proliferation of gastric cancer cells with an increased population at the G2/M phase.

Conclusion: Our study identified increased expression of Kidins220 in gastric cancer, which is associated with disease progression and poor prognosis. However, Kidins220 presented an inhibitory effect on the proliferation, invasion, and adhesion through a regulation of EMT, MMP and cell cycle.

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来源期刊
Cancer Genomics & Proteomics
Cancer Genomics & Proteomics ONCOLOGY-GENETICS & HEREDITY
CiteScore
5.00
自引率
8.00%
发文量
51
期刊介绍: Cancer Genomics & Proteomics (CGP) is an international peer-reviewed journal designed to publish rapidly high quality articles and reviews on the application of genomic and proteomic technology to basic, experimental and clinical cancer research. In this site you may find information concerning the editorial board, editorial policy, issue contents, subscriptions, submission of manuscripts and advertising. The first issue of CGP circulated in January 2004. Cancer Genomics & Proteomics is a journal of the International Institute of Anticancer Research. From January 2013 CGP is converted to an online-only open access journal. Cancer Genomics & Proteomics supports (a) the aims and the research projects of the INTERNATIONAL INSTITUTE OF ANTICANCER RESEARCH and (b) the organization of the INTERNATIONAL CONFERENCES OF ANTICANCER RESEARCH.
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