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Leptin utilizes Jun N-terminal kinases to stimulate the invasion of MCF-7 breast cancer cells

机译:瘦素利用Jun N端激酶刺激MCF-7乳腺癌细胞的侵袭

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摘要

In breast tumors, high levels of leptin have been associated with increased incidence of breast cancer metastasis. Breast cancer metastasis is directly associated with breast cancer cell invasion. However, whether leptin could augment breast cancer cell invasion is not known. Here we showed that leptin increased the invasiveness and the matrix metallo-proteinase-2 (MMP-2) activity of the MCF-7 breast cancer cell line. Leptin stimulated the phosphorylation of extracellular signals regulated kinases, signal transducers and activators of transcription 3 and Jun N-terminal kinases (JNK); however, only inhibition of JNK decreased leptin-mediated activation of MMP-2. Furthermore, inhibition of JNK suppressed leptin-mediated breast cancer cell invasion. Here we report the novel findings that leptin increased invasion of breast cancer cells by activating JNK, resulting in increased MMP-2 activity.
机译:在乳腺肿瘤中,高水平的瘦素与乳腺癌转移的发生率增加有关。乳腺癌转移与乳腺癌细胞侵袭直接相关。但是,瘦素是否可以增加乳腺癌细胞的侵袭性尚不清楚。在这里,我们表明瘦素增加了MCF-7乳腺癌细胞系的侵袭性和基质金属蛋白酶2(MMP-2)活性。瘦蛋白刺激细胞外信号调节激酶,信号转导子和转录激活因子3和Jun N端激酶(JNK)的磷酸化;但是,只有抑制JNK才能降低瘦素介导的MMP-2激活。此外,JNK的抑制抑制了瘦素介导的乳腺癌细胞的侵袭。在这里我们报告了新发现,瘦素通过激活JNK增加了MMP-2活性,从而增加了对乳腺癌细胞的侵袭。

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