Effect of a hot water extract of Chlorella vulgaris on proliferation of IEC-6
Effect of a hot water extract of Chlorella vulgaris on proliferation of IEC-6
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DOI：
10.3892/ijmm.2012.899
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发表时间：
2012-05-01
影响因子：
5.4
通讯作者：
Nam, Taek-Jeong
中科院分区：
文献类型：
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作者：
Song, Seo-Hyeon;Kim, In-Hye;Nam, Taek-Jeong
小球藻是一种单细胞微藻，具有多种生物效应；然而，它们对正常细胞增殖信号通路的影响尚未被研究。研究了小球藻（Chlorella vulgaris， CVE）热水提取物对大鼠肠上皮细胞（IEC-6）增殖及相关信号通路的影响。CV E增加胰岛素样生长因子- 1受体（IGF-IR）的表达以及局灶黏附激酶（FAK）和Src的磷酸化。此外，CV E诱导丝裂原活化蛋白激酶（MAPK）和磷脂酰肌醇3-激酶(PI3K)/Akt通路的激活。我们发现细胞外信号相关激酶（ERK）和Akt磷酸化增加，P13K调控亚基p85表达增加。CVE还通过增加核β -连环蛋白、细胞周期蛋白D1的表达来影响典型的Wnt通路。FAK的tyr397介导了许多其他信号蛋白与Src同源性2 （SH2）结构域的相互作用，包括PI3K、PLC-gamma、She。Grb7， Src和Nck2。由于CV E诱导FA K活化，FA K可能影响Wnt通路。FAK抑制剂的加入降低了细胞核β -catenin、cyclin D1和c-myc的表达，增加了细胞质β -catenin的表达。我们得出结论，CVE通过MAPK、PI3K/Akt和典型Wnt通路刺激IEC-6细胞的增殖，并影响典型Wnt通路。
Chlorella vulgaris, a unicellular microalgae, exerts various biological effects; however their effect on proliferation signaling pathways in normal cells has not been studied. We investigated the effect of hot water extracts of Chlorella vulgaris (CVE) on cell proliferation and related signaling pathways in rat intestinal epithelial cells (IEC-6). CV E increased the expression of insulin-like growth factor-I receptor (IGF-IR) and the phosphorylation of focal adhesion kinase (FAK) and Src. In addition, CV E induced activation of the mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI3K)/Akt pathways. We Trifled the increased phosphorylation of extracellular-signal-related kinase (ERK) and Akt and the increased expression of the P13K regulatory subunit p85. CVE also influenced the canonical Wnt pathway through increased expression of the nuclear beta-catenin, cyclin D1. Tyr-397 of FAK mediates interactions with Src homology 2 (SH2) domains in a number of other signaling proteins, including PI3K, PLC-gamma, She. Grb7, Src and Nck2. Because CV E induced FA K activation, FA K may affect the Wnt pathway. Addition of a FAK inhibitor decreased the expression of nuclear beta-catenin, cyclin D1 and c-myc, and increased the expression of cytosolic beta-catenin. We conclude that CVE stimulated proliferation of IEC-6 cells via the MAPK, PI3K/Akt and canonical Wnt pathways, and that this affected the canonical Wnt pathway.