Abstract:
BACKGROUND INFORMATION:Previous studies have revealed that leptin may be involved in epithelial-mesenchymal transition (EMT), a crucial initiator of cancer progression to facilitate metastatic cascade, increase tumor recurrence, and ultimately cause poor prognosis. However, the underlying mechanism remains unclear. The aim of our present study was to investigate the effect of leptin on EMT of breast cancer cells and the underlying mechanism. RESULTS:Our data demonstrated that leptin significantly increased the phosphorylation of STAT3, Akt, and ERK1/2, elevated the expression of IL-8, and induced breast cancer cells to undergo EMT. The effect of leptin on IL-8 could visibly abolished by the inhibitor of PI3K LY294002. In addition, leptin-induced EMT of breast cancer cells was blocked by anti-IL-8 antibodies. Examination of the expression of ObR, leptin, IL-8 and EMT-related biomarkers in patient specimens demonstrated that malignant breast carcinoma with lymph node metastases (LNM), which represents poor prognosis, expressed higher levels of ObR, leptin, IL-8 than other types of breast cancer, and displayed more obvious EMT transversion. In vivo xenograft experiment revealed that leptin signally promoted tumor growth and metastasis and increased the expressions of IL-8 and EMT-related biomarkers. CONCLUSIONS:Our results support that leptin-induced EMT in breast cancer cells requires IL-8 activation via the PI3K/Akt signal pathway.
journal_name
Cancer Biol Therjournal_title
Cancer biology & therapyauthors
Wang L,Tang C,Cao H,Li K,Pang X,Zhong L,Dang W,Tang H,Huang Y,Wei L,Su M,Chen Tdoi
10.1080/15384047.2015.1056409subject
Has Abstractpub_date
2015-01-01 00:00:00pages
1220-30issue
8eissn
1538-4047issn
1555-8576journal_volume
16pub_type
杂志文章abstract::In the immune system, activation of naïve T (Tn) cells into effector T cells (Teff) involves a metabolic switch to glycolysis to promote rapid proliferation and differentiation. In the October issue of The Journal of Clinical Investigation, Sukumar et al. have demonstrated that in CD8(+) memory T (Tems) cells glycolyt...
journal_title:Cancer biology & therapy
pub_type: 评论,杂志文章
doi:10.4161/cbt.28160
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journal_title:Cancer biology & therapy
pub_type: 杂志文章,评审
doi:10.4161/cbt.4.10.2195
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journal_title:Cancer biology & therapy
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journal_title:Cancer biology & therapy
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doi:10.4161/cbt.6.9.4539
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journal_title:Cancer biology & therapy
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journal_title:Cancer biology & therapy
pub_type: 杂志文章,评审
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journal_title:Cancer biology & therapy
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journal_title:Cancer biology & therapy
pub_type: 杂志文章,评审
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journal_title:Cancer biology & therapy
pub_type: 杂志文章,评审
doi:10.4161/cbt.7.9.6992
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journal_title:Cancer biology & therapy
pub_type: 杂志文章
doi:10.4161/cbt.12.3.15949
更新日期:2011-08-01 00:00:00
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journal_title:Cancer biology & therapy
pub_type: 杂志文章,多中心研究
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更新日期:2013-04-01 00:00:00
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pub_type: 杂志文章
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journal_title:Cancer biology & therapy
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更新日期:2006-11-01 00:00:00
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journal_title:Cancer biology & therapy
pub_type: 杂志文章
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更新日期:2018-05-04 00:00:00
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journal_title:Cancer biology & therapy
pub_type: 杂志文章
doi:10.4161/cbt.20840
更新日期:2012-08-01 00:00:00
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journal_title:Cancer biology & therapy
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journal_title:Cancer biology & therapy
pub_type: 杂志文章
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更新日期:2014-10-01 00:00:00
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