S100A16与DEPDC1协同通过PI3K/Akt/mTOR通路促进肾母细胞瘤的进展和血管生成。

IF 0.7 4区 医学 Q4 PATHOLOGY
Geng Geng, Yongtao Xu, Qingfang Li, Qinghao Li, Lili Yuan, Mengyao Dong, Ming Ming
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引用次数: 0

摘要

S100钙结合蛋白A16 (S100A16)先前被报道在肿瘤细胞中发挥作用。然而,S100A16在肾母细胞瘤细胞中的作用尚不清楚。RT-q PCR和western blotting检测S100A16和DEPDC1的表达。细胞转染后过表达DEPDC1或干扰S100A16。采用CCK8评价细胞活力。采用Tunel法、Transwell法和创面愈合法分别评价WiT49细胞的凋亡水平和增殖、侵袭、迁移能力。通过成管实验估计血管生成情况。采用免疫共沉淀法(CO-IP)检测S100A16与DEPDC1的靶向结合。western blot检测PI3K/Akt/mTOR通路相关蛋白的含量。S100A16和DEPDC1在肾母细胞瘤细胞系中的表达水平显著升高。S100A16缺失抑制肾母细胞瘤细胞的增殖、侵袭、迁移和血管生成能力,促进细胞凋亡水平。此外,S100A16可以结合DEPDC1, DEPDC1过表达部分逆转了S100A16干扰对肾母细胞瘤细胞的抑制作用。DEPDC1过表达也部分抵消了S100A16干扰对PI3K/Akt/mTOR通路相关蛋白的抑制作用。S100A16与DEPDC1协同作用,通过PI3K/Akt/mTOR通路促进肾母细胞瘤细胞的进展和血管生成。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
S100A16 cooperates with DEPDC1 to promote the progression and angiogenesis of nephroblastoma through PI3K/Akt/mTOR pathway.

S100 calcium-binding protein A16 (S100A16) has previously been reported to play a role in tumor cells. Nevertheless, the role that S100A16 played in nephroblastoma cells remains obscure. The expression of S100A16 and DEPDC1 were detected via RT-q PCR and western blotting. Cell transfection was performed to overexpress DEPDC1 or interfere S100A16. CCK8 was applied for the assessment of cell viability. The apoptotic level and the capabilities of WiT49 cells to proliferate, invade and migrated were appraised utilizing Tunel, colony formation Transwell, and wound healing, separately. The angiogenesis was estimated through tube formation assay. Co-immunoprecipitation (CO-IP) was performed to examine the targeted binding of S100A16 to DEPDC1. The contents of PI3K/Akt/mTOR pathway-related proteins were resolved by virtue of western blot. S100A16 and DEPDC1 expression levels were significantly increased in nephroblastoma cell lines. S100A16 deletion suppressed nephroblastoma cell proliferative, invasive, migrative and angiogenetic capabilities but facilitated the apoptotic level. Moreover, S100A16 could bind DEPDC1, DEPDC1 overexpression partially reversed the inhibitory effect of S100A16 interference on nephroblastoma cell. DEPDC1 overexpression also partially counteracted the suppressive impacts of S100A16 interference on PI3K/Akt/mTOR pathway-related proteins. S100A16 synergistic with DEPDC1 promotes the progression and angiogenesis of nephroblastoma cell through the PI3K/Akt/mTOR pathway.

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来源期刊
CiteScore
1.00
自引率
0.00%
发文量
21
审稿时长
>12 weeks
期刊介绍: Polish Journal of Pathology is an official magazine of the Polish Association of Pathologists and the Polish Branch of the International Academy of Pathology. For the last 18 years of its presence on the market it has published more than 360 original papers and scientific reports, often quoted in reviewed foreign magazines. A new extended Scientific Board of the quarterly magazine comprises people with recognised achievements in pathomorphology and biology, including molecular biology and cytogenetics, as well as clinical oncology. Polish scientists who are working abroad and are international authorities have also been invited. Apart from presenting scientific reports, the magazine will also play a didactic and training role.
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