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首页> 美国卫生研究院文献>Acta Biochimica et Biophysica Sinica >Galectin-1 knockdown in carcinoma-associated fibroblasts inhibits migration and invasion of human MDA-MB-231 breast cancer cells by modulating MMP-9 expression
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Galectin-1 knockdown in carcinoma-associated fibroblasts inhibits migration and invasion of human MDA-MB-231 breast cancer cells by modulating MMP-9 expression

机译：癌相关成纤维细胞中的Galectin-1基因敲低通过调节MMP-9表达来抑制人MDA-MB-231乳腺癌细胞的迁移和侵袭

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Carcinoma-associated fibroblasts (CAFs) play central roles in facilitating tumor progression and metastasis in breast cancer. Galectin-1 (Gal-1), a marker of CAFs, was previously reported to be associated with tumorigenesis and metastasis of various types of tumors. The aim of this study is to investigate the role of Gal-1 in CAF-mediated breast cancer metastasis and its underlying molecular mechanisms. Our results showed that CAFs isolated from human breast tumor tissues expressed higher level of Gal-1 compared with paired normal fibroblasts, and the conditioned medium (CM) of CAFs significantly induced the migration and invasion of human MDA-MB-231 breast cancer cells. Knockdown of Gal-1 in CAFs dramatically inhibited CAF-CM-induced cell migration and invasion, probably by inhibiting the expression of matrix metalloprotein 9 (MMP-9). Our findings demonstrate that Gal-1-regulated CAFs activation promotes breast cancer cell metastasis by upregulating MMP-9 expression, which indicated that Gal-1 in CAFs might be a potential novel target for breast cancer therapy.
机译：癌相关成纤维细胞（CAF）在促进乳腺癌的肿瘤进展和转移中起着核心作用。据报道，CAFs的标记物Galectin-1（Gal-1）与各种类型的肿瘤的发生和转移有关。这项研究的目的是调查在CAF介导的乳腺癌转移中Gal-1的作用及其潜在的分子机制。我们的结果表明，与配对的正常成纤维细胞相比，从人乳腺肿瘤组织中分离出的CAF表达更高的Gal-1水平，并且CAF的条件培养基（CM）显着诱导了人MDA-MB-231乳腺癌细胞的迁移和侵袭。敲除CAF中的Gal-1可能会抑制基质金属蛋白9（MMP-9）的表达，从而显着抑制CAF-CM诱导的细胞迁移和侵袭。我们的发现表明，Gal-1调节的CAF激活通过上调MMP-9表达来促进乳腺癌细胞转移，这表明CAFs中的Gal-1可能是乳腺癌治疗的潜在新靶标。

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