中国科学院机构知识库网格
Chinese Academy of Sciences Institutional Repositories Grid
GeneChip expression profiling identified OLFML2A as a potential therapeutic target in TNBC cells

文献类型:期刊论文

作者Gao, Xiufei2; Yang, Zimei1; Xu, Chuchu1; Yu, Qinghong1; Wang, Mengqian1; Song, Jiaqing1; Wu, Chunyu3; Chen, Mingcang4,5
刊名ANNALS OF TRANSLATIONAL MEDICINE
出版日期2022-03-14
页码23
ISSN号2305-5839
关键词Olfactomedin-like-2A (OLFML2A) triple-negative breast cancer (TNBC) GeneChip ingenuity pathway analysis (IPA) therapeutic target
DOI10.21037/atm-22-757
通讯作者Wu, Chunyu(xiaoyu9.05@163.com) ; Chen, Mingcang(baidulyac@126.com)
英文摘要Background: An elevated level of olfactomedin-like-2A (OLFML2A) is unfavorable for female breast cancer patients. Patients with a high mRNA level of OLFML2A receive a poor prognosis. Therefore, we speculate that inhibiting the expression of this gene may be beneficial to breast cancer patients. We previously found that silencing the OLFML2A gene by using mRNA interference significantly inhibited proliferation and migration in triple-negative breast cancer (TNBC) cells. Methods: Cell activity and proliferation were determined by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and Celigo analyses. Cell migration and invasion were determined by wound-healing and transwell invasion assays. The mechanism of the inhibition of a small hairpin RNA that targets OLFML2A (shOLFML2A) was determined by using a GeneChip array, real-time quantitative PCR (RT-qPCR), and western blot analysis. Results: Gene silencing by shOLFML2A induces apoptosis by promoting S phase arrest in TNBC cells. In addition, shOLFML2A decreased the progression of epithelial-mesenchymal transition (EMT). Additionally, microarray analysis showed that shOLFML2A significantly upregulated 428 genes and downregulated 712 genes. These significantly changed genes regulated DNA synthesis, chromosome alignment, microtubules and the cytoskeleton, cell movement, the cell cycle, cell necrosis, and apoptosis because they promoted G2/M DNA damage checkpoint regulation and p53 signaling, and because they inhibited integrin, hepatocyte growth factor (HGF), nerve growth Factor (NGF), and other tumor-promoting signaling pathways. Conclusions: shOLFML2A reduces cell proliferation, migration, and invasion and promotes cell apoptosis. Therefore, the results of the present study suggest that OLFML2A is a potential therapeutic target for TNBC.
WOS关键词BREAST-CANCER CELLS ; DOMAIN-CONTAINING PROTEINS ; FUNCTIONAL GENOMICS ; MESSENGER-RNAS ; IDENTIFICATION ; METASTASIS ; GENES ; PROLIFERATION ; MICRORNAS ; ADHESION
资助项目National Natural Science Foundation of China[82074438] ; Natural Science Foundation of Zhejiang Province[LY18H270006] ; Zhejiang Province Traditional Chinese Medicine Scientific Research Foundation[2016ZQ015]
WOS研究方向Oncology ; Research & Experimental Medicine
语种英语
出版者AME PUBL CO
WOS记录号WOS:000774719200001
源URL[http://119.78.100.183/handle/2S10ELR8/299914]  
专题中国科学院上海药物研究所
通讯作者Wu, Chunyu; Chen, Mingcang
作者单位1.Zhejiang Chinese Med Univ, Hangzhou, Peoples R China
2.Zhejiang Chinese Med Univ, Affiliated Hosp 1, Dept Breast, Zhejiang Prov Hosp Tradit Chinese Med, Hangzhou, Peoples R China
3.Shanghai Univ Tradit Chinese Med, Longhua Hosp, Dept Breast Surg Integrated Tradit & Western Med, Shanghai, Peoples R China
4.Zhejiang Univ Technol, Coll Biotechnol & Bioengn, Hangzhou, Peoples R China
5.Chinese Acad Sci, Shanghai Inst Mat Med, 501 Haike Rd, Shanghai 201203, Peoples R China
推荐引用方式
GB/T 7714
Gao, Xiufei,Yang, Zimei,Xu, Chuchu,et al. GeneChip expression profiling identified OLFML2A as a potential therapeutic target in TNBC cells[J]. ANNALS OF TRANSLATIONAL MEDICINE,2022:23.
APA Gao, Xiufei.,Yang, Zimei.,Xu, Chuchu.,Yu, Qinghong.,Wang, Mengqian.,...&Chen, Mingcang.(2022).GeneChip expression profiling identified OLFML2A as a potential therapeutic target in TNBC cells.ANNALS OF TRANSLATIONAL MEDICINE,23.
MLA Gao, Xiufei,et al."GeneChip expression profiling identified OLFML2A as a potential therapeutic target in TNBC cells".ANNALS OF TRANSLATIONAL MEDICINE (2022):23.

入库方式: OAI收割

来源:上海药物研究所

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