{"title":"FAM129A Aggravates the Malignant Progression of Breast Cancer with the Synergistical Interaction with CXCL14","authors":"Yijie Yuan, Yuxin Zhou, Shuixin Yan, Jiadi Li, Weizhu Wu","doi":"10.1166/jbn.2023.3696","DOIUrl":null,"url":null,"abstract":"To detect differential levels of FAM129A and CXCL14 in breast cancer samples, and to explore their influences on breast cancer proliferation. Differential levels of FAM129A and CXCL14 in breast cancer samples were examined by qRT-PCR. The correlation between FAM129A level and clinic pathological factors in breast cancer patients was analyzed. The regulatory effects of FAM129A and CXCL14 on proliferative potential in highly invasive breast cancer cell lines MCF-7 and SKBR-3 were assessed by CCK-8 and EdU assay. The interaction between FAM129A and CXCL14 was explored by bioinformatics analysis and Dual-Luciferase reporter assay. FAM129A was upregulated in breast cancer samples, and it was positively correlated to TNM staging in breast cancer patients. Knockdown of FAM129A markedly attenuated in vitro proliferative ability in breast cancer. CXCL14 was lowly expressed in breast cancer tissues and cell lines, which was able to inhibit breast cancer proliferation. FAM129A could bind CXCL14 and negatively regulate its level in breast cancer samples. Rescue experiments demonstrated that knockdown of CXCL14 could abolish the inhibited proliferative ability in breast cancer cells with FAM129A knockdown. FAM129A is upregulated in breast cancer samples with highly invasive potential, and it is linked to TNM staging. It aggravates the malignant proliferation of breast cancer cells by targeting and downregulating CXCL14.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"55 1","pages":""},"PeriodicalIF":2.9000,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of biomedical nanotechnology","FirstCategoryId":"5","ListUrlMain":"https://doi.org/10.1166/jbn.2023.3696","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 0
Abstract
To detect differential levels of FAM129A and CXCL14 in breast cancer samples, and to explore their influences on breast cancer proliferation. Differential levels of FAM129A and CXCL14 in breast cancer samples were examined by qRT-PCR. The correlation between FAM129A level and clinic pathological factors in breast cancer patients was analyzed. The regulatory effects of FAM129A and CXCL14 on proliferative potential in highly invasive breast cancer cell lines MCF-7 and SKBR-3 were assessed by CCK-8 and EdU assay. The interaction between FAM129A and CXCL14 was explored by bioinformatics analysis and Dual-Luciferase reporter assay. FAM129A was upregulated in breast cancer samples, and it was positively correlated to TNM staging in breast cancer patients. Knockdown of FAM129A markedly attenuated in vitro proliferative ability in breast cancer. CXCL14 was lowly expressed in breast cancer tissues and cell lines, which was able to inhibit breast cancer proliferation. FAM129A could bind CXCL14 and negatively regulate its level in breast cancer samples. Rescue experiments demonstrated that knockdown of CXCL14 could abolish the inhibited proliferative ability in breast cancer cells with FAM129A knockdown. FAM129A is upregulated in breast cancer samples with highly invasive potential, and it is linked to TNM staging. It aggravates the malignant proliferation of breast cancer cells by targeting and downregulating CXCL14.