Abstract
Breast cancer, a most common malignancy among women with high lethality. Polypeptide-N-acetyl-galactosaminlytransferase 7 (GALNT7) contributes to carcino-genesis and development of breast cancer. Activation of signal transducer and activator of transcription 3 (STAT3) is vital in the initiation and development of cancers. In this work, GALNT7 was upregulated in breast cancer cells, and promoted cell proliferation. GALNT7 knockdown suppressed proliferation of breast cancer cells. GALNT7 overexpression upregulated B-cell lymphoma protein 2 (BCL2) expression and suppressed the expression levels of Bcl-2-associated X protein (BAX), cleaved caspase 3, LC3-II/LC3-I ratio and Atg5, which was dramatically suppressed by knockdown of GALNT7 in breast cancer cells. GALNT7 overexpression favored the phosphorylation of STAT3, which was significantly prevented by knockdown of GALNT7 in breast cancer cells. Inactivation of STAT3 by Stattic increased the expressions levels of LC3-II/LC3-I ratio and Atg5, which was prevented by GALNT7 overexpression in breast cancer cells. Knockdown of GALNT7 promoted cell apoptosis and autophagy of breast cancer cells via inactivation of STAT3.
Subject
Obstetrics and Gynecology,Oncology
Cited by
3 articles.
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