FAM129A Aggravates the Malignant Progression of Breast Cancer with the Synergistical Interaction with CXCL14

IF 2.9 4区 医学 Q1 Medicine Journal of biomedical nanotechnology Pub Date : 2023-11-01 DOI:10.1166/jbn.2023.3696
Yijie Yuan, Yuxin Zhou, Shuixin Yan, Jiadi Li, Weizhu Wu
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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.
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FAM129A 与 CXCL14 的协同作用加剧了乳腺癌的恶性进展
检测乳腺癌样本中 FAM129A 和 CXCL14 的不同水平,并探讨它们对乳腺癌增殖的影响。通过 qRT-PCR 检测乳腺癌样本中 FAM129A 和 CXCL14 的差异水平。分析了FAM129A水平与乳腺癌患者临床病理因素的相关性。通过CCK-8和EdU检测法评估了FAM129A和CXCL14对高侵袭性乳腺癌细胞株MCF-7和SKBR-3增殖潜力的调控作用。生物信息学分析和双荧光素酶报告实验探讨了 FAM129A 和 CXCL14 之间的相互作用。FAM129A在乳腺癌样本中上调,并且与乳腺癌患者的TNM分期呈正相关。敲除 FAM129A 能显著降低乳腺癌的体外增殖能力。CXCL14在乳腺癌组织和细胞系中低表达,能抑制乳腺癌的增殖。FAM129A 能与 CXCL14 结合并负向调节其在乳腺癌样本中的水平。拯救实验表明,敲除 CXCL14 可以消除 FAM129A 敲除后对乳腺癌细胞增殖能力的抑制。FAM129A在具有高度侵袭性的乳腺癌样本中上调,并且与TNM分期有关。它通过靶向和下调 CXCL14 来加重乳腺癌细胞的恶性增殖。
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来源期刊
CiteScore
4.30
自引率
17.20%
发文量
145
审稿时长
2.3 months
期刊介绍: Information not localized
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