Punicalagin inhibits the viability, migration, invasion, and EMT by regulating GOLPH3 in breast cancer cells
Punicalagin inhibits the viability, migration, invasion, and EMT by regulating GOLPH3 in breast cancer cells
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DOI：
10.1080/10799893.2020.1719152
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发表时间：
2020-02-06
影响因子：
2.8
通讯作者：
Lou, Lihua
中科院分区：
文献类型：
--
作者：
Pan, Lei;Duan, Yin;Lou, Lihua
乳腺癌（BC）是世界上最常见的恶性肿瘤之一。Punicalagin （PN）是一种多酚，据报道具有肿瘤抑制作用。本研究旨在探讨PN对BC细胞过程的影响及其分子机制。通过CCK-8、创面愈合和Transwell实验检测不同剂量PN对MCF-7和MDA-MB-231细胞活力、迁移和侵袭能力的影响。将高尔基磷酸化蛋白3 （GOLPH3）转染到PN处理和未处理的细胞中，采用实时荧光定量聚合酶链反应（qRT-PCR）和Western blot检测GPLPH3的表达水平，Western blot检测上皮-间质转化（EMT）相关蛋白基质金属蛋白酶-2 （MMP-2）、基质金属蛋白酶-9 （MMP-9）、E-Cadherin、N-Cadherin的表达。高剂量PN处理（50 μ M或更高）显著抑制MCF-7和MDA-MB-231细胞的活力、迁移和侵袭，而过表达GOLPH3促进细胞活力、迁移和侵袭，并部分逆转PN处理对BC细胞的影响。PN抑制了GOLPH3、MMP-2、MMP-9和N-Cadherin的表达，促进了E-Cadherin的表达，而过表达GOLPH3部分逆转了上述作用。由此可见，PN通过调控GOLPH3抑制BC细胞活力和转移，为BC的治疗提供了可能的治疗方向。
Breast cancer (BC) is one of the most common malignancies worldwide. Punicalagin (PN), which is a type of polyphenol, has been reported to act as a tumor suppressor. This study aimed to investigate the effects of PN on cellular process in BC and its molecular mechanism. The effects of various doses of PN on cell viability, migration, and invasion capacities of MCF-7 and MDA-MB-231 cells were detected by CCK-8, wound-healing, and Transwell assays. Golgi phosphoprotein 3 (GOLPH3) was then transfected into the cells with or without PN treatment, and GPLPH3 expression level was examined by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot, and expressions of epithelial-mesenchymal transition (EMT)-related protein matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9), E-Cadherin, and N-Cadherin were measured by Western blot. High dose of PN treatment (50 mu M or higher) significantly inhibited viability, migration, and invasion of MCF-7 and MDA-MB-231 cells, while overexpressed GOLPH3 promoted cell viability, migration, and invasion, and partially reversed the effects of PN treatment on the BC cells. PN inhibited the expressions of GOLPH3, MMP-2, MMP-9, and N-Cadherin, and promoted E-Cadherin expression, while overexpression of GOLPH3 partly reversed above effects attributing to PN. Thus, PN suppresses cell viability and metastasis via regulating GOLPH3 in BC, which provides a possible therapeutic direction to the treatment of BC.