Article Summary
郭绍文,谢轶群,鄂裘恺,钟锦婵,常聪聪,林 昀.N-豆蔻酰化转移酶在乳腺癌组织中的表达及作用研究[J].现代生物医学进展英文版,2022,(20):3828-3833.
N-豆蔻酰化转移酶在乳腺癌组织中的表达及作用研究
Galactophore Department The Clinical and Biological Role of N-mytistoyltransferase in Breast Cancer
Received:April 22, 2022  Revised:May 18, 2022
DOI:10.13241/j.cnki.pmb.2022.20.006
中文关键词: 乳腺癌  N-豆蔻酰化转移酶  增殖  转移
英文关键词: Breast cancer  N-myristoyltransferase  Proliferation  Migration
基金项目:上海市卫生健康委员会科研项目(2020040464)
Author NameAffiliationE-mail
郭绍文 上海交通大学医学院附属第九人民医院黄浦分院病理科 上海 200011 guo_19730@sina.com 
谢轶群 上海交通大学医学院附属第九人民医院黄浦分院乳腺科 上海 200011  
鄂裘恺 上海交通大学医学院附属第九人民医院黄浦分院病理科 上海 200011  
钟锦婵 上海交通大学医学院附属第九人民医院黄浦分院病理科 上海 200011  
常聪聪 上海交通大学医学院附属第九人民医院黄浦分院病理科 上海 200011  
林 昀 同济大学附属东方医院肿瘤科 上海200120  
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中文摘要:
      摘要 目的:研究N-豆蔻酰化转移酶1(NMT1)和2(NMT2)在乳腺癌组织中的表达及对乳腺癌细胞生物学作用。方法:ELISA检测NMT1和NMT2在40例乳腺癌组织中含量,免疫组化证实其表达。小RNA干扰技术敲减乳腺癌细胞MCF-7及BT-474中NMT1和NMT2表达水平。CCK-8及Transwell小室穿膜试验检测NMT1和NMT2敲减前后细胞增殖及转移能力变化。结果:NMT1及NMT2在发生淋巴结转移、III/IV期患者的乳腺癌组织中表达显著升高(P<0.01)。利用CCK-8检测发现NMT1或NMT2敲减48h后乳腺癌细胞BT-474、MCF-7增殖活性较对照组细胞显著减弱(P<0.0001)。Transwell小室穿膜试验检测发现,NMT1或NMT2敲减组细胞较对照组细胞,穿膜细胞数显著减低(P<0.01)。结论:NMT1及NMT2在乳腺癌的发生、发展过程中起到关键作用,敲减NMT1及NMT2可削弱乳腺癌细胞增殖和转移能力。靶向抑制NMT1及NMT2有望成为干预乳腺癌的重要分子靶点。
英文摘要:
      ABSTRACT Objective: To study the expression of N-myristoyltransferase 1 (NMT1) and 2 (NMT2) in breast cancer tissues and their biological effects on breast cancer cells. Methods: The expression of NMT1 and NMT2 in 40 breast cancer tissues were detected by ELISA, and their expressions were confirmed by immunohistochemistry. Small RNA interference technology knocked down the expression levels of NMT1 and NMT2 in breast cancer cells MCF-7 and BT-474. CCK-8 and Transwell chamber transmembrane assays were used to detect the changes of cell proliferation and metastasis before and after NMT1 and NMT2 knockdown. Results: The expressions of NMT1 and NMT2 in breast cancer tissues of patients with lymph node metastasis and stage III/IV were significantly increased (P<0.01). Using CCK-8 detection, it was found that the proliferation activity of breast cancer cells BT-474 and MCF-7 after NMT1 or NMT2 knockdown for 48 h was significantly lower than that of control cells (P<0.0001). Transwell chamber penetration test showed that the number of transmembrane cells in the NMT1 or NMT2 knockdown group was significantly lower than that in the control group (P<0.01). Conclusion: NMT1 and NMT2 play a key role in the occurrence and development of breast cancer. Knockdown of NMT1 and NMT2 can weaken the proliferation and metastasis of Breast cancer cancer cells. Targeted inhibition of NMT1 and NMT2 is expected to become an important molecular target for intervention in breast cancer.
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