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首页> 外文期刊>Cellular Physiology and Biochemistry >Osteopontin Knockdown Inhibits αv,β3 Integrin-Induced Cell Migration and Invasion and Promotes Apoptosis of Breast Cancer Cells by Inducing Autophagy and Inactivating the PI3K/Akt/mTOR Pathway
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Osteopontin Knockdown Inhibits αv,β3 Integrin-Induced Cell Migration and Invasion and Promotes Apoptosis of Breast Cancer Cells by Inducing Autophagy and Inactivating the PI3K/Akt/mTOR Pathway

机译：骨桥蛋白的抑制通过诱导自噬和灭活PI3K / Akt / mTOR途径抑制αv，β3整合素诱导的细胞迁移和侵袭并促进乳腺癌细胞凋亡。

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biBackground /i/bOsteopontin (OPN) is associated with tumor formation, progression and metastasis, and increased OPN levels have been associated with poor survival in breast cancer. We investigated the mechanisms responsible for OPN activity, and the relationships between OPN expression and clinical parameters in breast cancer. biMethods /i/bOPN mRNA and protein levels were compared in malignant and benign breast tumors by polymerase chain reaction (PCR) and immunohistochemistry, respectively, and levels in breast cancer cells were determined by PCR and western blotting. The effects of lentiviral-mediated knockdown of OPN on OPN and αsubv/sub,βsub3/sub integrin expression, cell invasion and migration, autophagy and apoptosis were analyzed in MDA-MB-231 cells. biResults /i/bOPN expression increased with aggressiveness of breast cancer phenotype. OPN knockdown inhibited αsubv/sub,βsub3/sub integrin expression in MDA-MB-231 cells, with subsequent inhibition of cell migration and invasion. Knockdown also inhibited the PI3K/Akt/mTOR pathway, promoted expression of the autophagy-related gene products LC3 and Beclin 1, and increased apoptosis. OPN expression was positively associated with tumor grade and lymph node metastasis. biConclusion /i/bThese results suggest that knockdown of OPN may inhibit breast cancer metastasis by regulating αsubv/sub,βsub3/sub integrin expression and inducing autophagy and subsequent inhibition of PI3K/Akt/mTOR signaling, thus providing further insights into the complex mechanisms regulating tumor growth and metastasis.
机译：背景 骨桥蛋白（OPN）与肿瘤的形成，进展和转移有关，OPN水平升高与乳腺癌的不良存活率有关。我们调查了负责OPN活性的机制，以及乳腺癌中OPN表达与临床参数之间的关系。 方法 通过聚合酶链反应（PCR）和免疫组织化学分别比较恶性和良性乳腺肿瘤中OPN mRNA和蛋白的水平，并通过PCR测定乳腺癌细胞中的蛋白水平和蛋白质印迹。慢病毒介导的敲除OPN对MDA-MB-231中OPN和α v ，β 3 整联蛋白表达，细胞侵袭和迁移，自噬和凋亡的影响细胞。 结果 OPN表达随着乳腺癌表型的侵袭性而增加。 OPN抑制可抑制MDA-MB-231细胞中α v ，β 3 整合素的表达，并随后抑制细胞迁移和侵袭。敲低还抑制了PI3K / Akt / mTOR途径，促进了自噬相关基因产物LC3和Beclin 1的表达，并增加了细胞凋亡。 OPN表达与肿瘤分级和淋巴结转移呈正相关。 结论 这些结果表明，敲低OPN可能通过调节α v ，β 3 整合素的表达来抑制乳腺癌的转移并诱导自噬并随后抑制PI3K / Akt / mTOR信号传导，从而为调节肿瘤生长和转移的复杂机制提供了进一步的见识。

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