کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10815239 | 1058462 | 2014 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Lysyl oxidase-like 2 (LOXL2) controls tumor-associated cell proliferation through the interaction with MARCKSL1
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کلمات کلیدی
ECMCDKmTORFAK4E-binding protein 1PKCo-nitrophenyl β-D-galactopyranoside4E-BP1LOXL2ONPGSmall interfering RNA - RNA تداخل کوچکsiRNA - siRNAProtein–protein interaction - تعامل پروتئین-پروتئینEMT - تکنسین فوریتهای پزشکیExtracellular matrix - ماتریکس خارج سلولیmammalian target of rapamycin - هدف پستانداران رپامایسینProtein kinase C - پروتئین کیناز سیcyclin-dependent kinases - کیناز وابسته به سیکلینfocal adhesion kinase - کیناز چسبندگی کانونیEpithelial–mesenchymal transition - گذار اپیتلیال-مزانشیمی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Lysyl oxidase-like 2 (LOXL2) is a member of the lysyl oxidase gene family that contributes to the invasiveness and metastasis in tumor progression. However, the role of LOXL2 in cellular signaling is incompletely understood. In this study, we investigated a possible mechanism of LOXL2 function in tumor metastases in vitro, using a human breast carcinoma cell line. Myristoylated alanine-rich C kinase substrate-like 1 (MARCKSL1), a modulator in the regulation of cellular homeostasis, was identified as a LOXL2 interacting protein. We examined the binding domains that are required for the interaction between LOXL2 and MARCKSL1. The scavenger-receptor domain of LOXL2 was shown to interact with the N-terminal domain of MARCKSL1. Luciferase activity was noticeably reduced by the transfection of MARCKSL1 in a dose-dependent manner. In addition, over-expression of LOXL2 activates cell growth by inhibiting MARCKSL1-induced apoptosis. The effect of LOXL2 on cell cycle and apoptosis-related components was also confirmed through the silencing of LOXL2 expression. LOXL2 activates the FAK/Akt/mTOR signaling pathways, and MARCKSL1 suppresses LOXL2-induced oncogenesis. These insights supply evidence that LOXL2 promotes cell proliferation and inhibits apoptotic cell death. Taken together, our results indicate an underlying mechanism for an increase of LOXL2-related activity in breast tumor cells.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cellular Signalling - Volume 26, Issue 9, September 2014, Pages 1765-1773
Journal: Cellular Signalling - Volume 26, Issue 9, September 2014, Pages 1765-1773
نویسندگان
Boh-Ram Kim, Seung Myung Dong, Seung Hee Seo, Ji-Hae Lee, Jae Myun Lee, Seung-Hoon Lee, Seung Bae Rho,