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KIF4A在体外和体内促进肾透明细胞癌(ccRCC)的增殖。

KIF4A Promotes Clear Cell Renal Cell Carcinoma (ccRCC) Proliferation in vitro and in vivo.

作者信息

Yang Guang-Hua, Ren Zhi-Xing, Yang Xiong, Zhang Yan-Gang

机构信息

Department of Urology, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Taiyuan City, Shanxi Province 030032, People's Republic of China.

Education and Research Center, Taiyuan Radio and Television University, Taiyuan City, Shanxi Province 030024, People's Republic of China.

出版信息

Onco Targets Ther. 2020 Mar 31;13:2667-2676. doi: 10.2147/OTT.S240734. eCollection 2020.

DOI:10.2147/OTT.S240734
PMID:32280241
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7127824/
Abstract

PURPOSE

To evaluate the expression in human clear cell renal cell carcinoma (ccRCC) tissues and explore the effects of kinesin family member 4A (KIF4A) on ccRCC progression.

METHODS

GEPIA was used to evaluate the mRNA levels of KIF4A in human ccRCC tissues from TCGA database, and Immunohistochemistry (IHC) assays were performed to assess its expression in human ccRCC tissues collected in our hospital. The clinical-pathological analysis was performed to explore the correlation with KIF4A expression. The effects of KIF4A on ccRCC cell proliferation were detected through colony formation and MTT assays. Finally, the effects of KIF4A on tumor growth were measured using a mice model.

RESULTS

Bioinformation results showed the expression of KIF4A mRNA was upregulated in ccRCC tissues and high expression of KIF4A was related with poor prognosis in ccRCC patients. We also found a high expression of KIF4A in human ccRCC tissues collected in our hospital. We also found its expression level was correlated with clinical characteristics, including T stage (P=0.035*) and lymphatic metastasis (P=0.028*). We further confirmed that knockdown of KIF4A suppressed cell proliferation in HTB-47 and CRL-1932 cells. Furthermore, KIF4A contributes to tumor growth of ccRCC cells in mice.

CONCLUSION

We found the abnormal high expression of KIF4A in human ccRCC tissues and demonstrated that KIF4A could serve as a tumor induction gene.

摘要

目的

评估驱动蛋白家族成员4A(KIF4A)在人肾透明细胞癌(ccRCC)组织中的表达,并探讨其对ccRCC进展的影响。

方法

利用GEPIA评估来自TCGA数据库的人ccRCC组织中KIF4A的mRNA水平,并进行免疫组织化学(IHC)分析以评估其在我院收集的人ccRCC组织中的表达。进行临床病理分析以探讨与KIF4A表达的相关性。通过集落形成和MTT试验检测KIF4A对ccRCC细胞增殖的影响。最后,使用小鼠模型测量KIF4A对肿瘤生长的影响。

结果

生物信息学结果显示,ccRCC组织中KIF4A mRNA表达上调,KIF4A高表达与ccRCC患者预后不良相关。我们还发现我院收集的人ccRCC组织中KIF4A高表达。我们还发现其表达水平与临床特征相关,包括T分期(P=0.035*)和淋巴转移(P=0.028*)。我们进一步证实,敲低KIF4A可抑制HTB-47和CRL-1932细胞的增殖。此外,KIF4A促进ccRCC细胞在小鼠体内的肿瘤生长。

结论

我们发现人ccRCC组织中KIF4A异常高表达,并证明KIF4A可作为肿瘤诱导基因。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6647/7127824/cd710287a7f3/OTT-13-2667-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6647/7127824/30685a330a2c/OTT-13-2667-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6647/7127824/0147ffd86b1c/OTT-13-2667-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6647/7127824/3e843108a550/OTT-13-2667-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6647/7127824/8f0cf501edce/OTT-13-2667-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6647/7127824/cd710287a7f3/OTT-13-2667-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6647/7127824/30685a330a2c/OTT-13-2667-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6647/7127824/0147ffd86b1c/OTT-13-2667-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6647/7127824/3e843108a550/OTT-13-2667-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6647/7127824/8f0cf501edce/OTT-13-2667-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6647/7127824/cd710287a7f3/OTT-13-2667-g0005.jpg

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Impaired DNA double-strand breaks repair by kinesin family member 4A inhibition renders human H1299 non-small-cell lung cancer cells sensitive to cisplatin.抑制驱动蛋白家族成员 4A 可损害 DNA 双链断裂修复,从而使人类 H1299 非小细胞肺癌细胞对顺铂敏感。
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