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首页> 外文期刊>Biological chemistry >GD3 synthase overexpression enhances proliferation and migration of MDA-MB-231 breast cancer cells.
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GD3 synthase overexpression enhances proliferation and migration of MDA-MB-231 breast cancer cells.

机译:GD3合酶的过表达增强了MDA-MB-231乳腺癌细胞的增殖和迁移。

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摘要

The disialoganglioside G(D3) is an oncofetal marker of a variety of human tumors including melanoma and neuroblastoma, playing a key role in tumor progression. G(D3) and 9-O-acetyl-G(D3) are overexpressed in approximately 50% of invasive ductal breast carcinoma, but no relationship has been established between disialoganglioside expression and breast cancer progression. In order to determine the effect of G(D3) expression on breast cancer development, we analyzed the biosynthesis of gangliosides in several breast epithelial cell lines including MDA-MB-231, MCF-7, BT-20, T47-D, and MCF10A, by immunocytochemistry, flow cytometry, and real-time PCR. Our results show that, in comparison to tumors, cultured breast cancer cells express a limited pattern of gangliosides. Disialogangliosides were not detected in any cell line and G(M3) was only observed at the cell surface of MDA-MB-231 cells. To evaluate the influence of G(D3) in breast cancer cell behavior, we established and characterized MDA-MB-231 cells overexpressing G(D3) synthase. We show that G(D3) synthase expressing cells accumulate G(D3), G(D2), and G(T3) at the cell surface. Moreover, G(D3) synthase overexpression bypasses the need of serum for cell growth and increases cell migration. This suggests that G(D3) synthase overexpression may contribute to increasing the malignant properties of breast cancer cells.
机译:双唾液酸神经节苷脂G(D3)是包括黑色素瘤和神经母细胞瘤在内的多种人类肿瘤的癌胚标志物,在肿瘤进展中起关键作用。 G(D3)和9-O-乙酰基-G(D3)在约50%的浸润性导管癌中过表达,但在反唾液酸神经节苷脂表达与乳腺癌进展之间未建立联系。为了确定G(D3)表达对乳腺癌发展的影响,我们分析了几种乳腺上皮细胞系(包括MDA-MB-231,MCF-7,BT-20,T47-D和MCF10A)中神经节苷脂的生物合成。 ,免疫细胞化学,流式细胞仪和实时PCR。我们的结果表明,与肿瘤相比,培养的乳腺癌细胞表达神经节苷脂的模式有限。在任何细胞系中均未检出双唾液酸神经节苷脂,仅在MDA-MB-231细胞的细胞表面观察到G(M3)。为了评估G(D3)对乳腺癌细胞行为的影响,我们建立并表征了过表达G(D3)合酶的MDA-MB-231细胞。我们显示,G(D3)合酶表达细胞在细胞表面积累G(D3),G(D2)和G(T3)。此外,G(D3)合酶过表达绕开了细胞生长所需的血清,并增加了细胞迁移。这表明G(D3)合酶的过表达可能有助于增加乳腺癌细胞的恶性特性。

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