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Metformin represses cancer cells via alternate pathways in N-cadherin expressing vs. N-cadherin deficient cells.

Metformin has emerged as a potential anticancer agent. Here, we demonstrate that metformin plays an anti-tumor role via repressing N-cadherin, independent of AMPK, in wild-type N-cadherin cancer cells. Ectopic-expression of N-cadherin develops metformin-resistant cancer cells, while suppression of N... Full description

Journal Title: OncoTarget 2015, Vol.6(30)
Main Author: Ge, Rongbin
Other Authors: Wang, Zongwei , Wu, Shulin , Zhuo, Yangjia , Otsetov, Aleksandar G , Cai, Chao , Zhong, Weide , Wu, Chin-Lee , Olumi, Aria F
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: ISSN: 1949-2553 ; ISSN: 1949-2553 ; PMID: 26359363 ; DOI: 10.18632/oncotarget.5023
Link: http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-128209
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recordid: swepuboai:DiVA.org:umu-128209
title: Metformin represses cancer cells via alternate pathways in N-cadherin expressing vs. N-cadherin deficient cells.
format: Article
creator:
  • Ge, Rongbin
  • Wang, Zongwei
  • Wu, Shulin
  • Zhuo, Yangjia
  • Otsetov, Aleksandar G
  • Cai, Chao
  • Zhong, Weide
  • Wu, Chin-Lee
  • Olumi, Aria F
subjects:
  • Research Paper
  • Prostate Cancer
  • Metformin
  • Twist
  • N-Cadherin
ispartof: OncoTarget, 2015, Vol.6(30)
description: Metformin has emerged as a potential anticancer agent. Here, we demonstrate that metformin plays an anti-tumor role via repressing N-cadherin, independent of AMPK, in wild-type N-cadherin cancer cells. Ectopic-expression of N-cadherin develops metformin-resistant cancer cells, while suppression of N-cadherin sensitizes cancer to metformin. Manipulation of AMPK expression does not alter sensitivity of cancer to metformin. We show that NF-kappaB is a downstream molecule of N-cadherin and metformin regulates NF-kappaB signaling via suppressing N-cadherin. Moreover, we also suggest that TWIST1 is an upstream molecule of N-cadherin/NF-kappaB signaling and manipulation of TWIST1 expression changes the sensitivity of cancer cells to metformin. In contrast to the cells that express N-cadherin, in N-cadherin deficient cells, metformin plays an anti-tumor role via activation of AMPK. Ectopic expression of N-cadherin makes cancer more resistant to metformin. Therefore, we suggest that metformin's...
language: eng
source:
identifier: ISSN: 1949-2553 ; ISSN: 1949-2553 ; PMID: 26359363 ; DOI: 10.18632/oncotarget.5023
fulltext: fulltext
issn:
  • 1949-2553
  • 19492553
url: Link


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titleMetformin represses cancer cells via alternate pathways in N-cadherin expressing vs. N-cadherin deficient cells.
creatorGe, Rongbin ; Wang, Zongwei ; Wu, Shulin ; Zhuo, Yangjia ; Otsetov, Aleksandar G ; Cai, Chao ; Zhong, Weide ; Wu, Chin-Lee ; Olumi, Aria F
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descriptionMetformin has emerged as a potential anticancer agent. Here, we demonstrate that metformin plays an anti-tumor role via repressing N-cadherin, independent of AMPK, in wild-type N-cadherin cancer cells. Ectopic-expression of N-cadherin develops metformin-resistant cancer cells, while suppression of N-cadherin sensitizes cancer to metformin. Manipulation of AMPK expression does not alter sensitivity of cancer to metformin. We show that NF-kappaB is a downstream molecule of N-cadherin and metformin regulates NF-kappaB signaling via suppressing N-cadherin. Moreover, we also suggest that TWIST1 is an upstream molecule of N-cadherin/NF-kappaB signaling and manipulation of TWIST1 expression changes the sensitivity of cancer cells to metformin. In contrast to the cells that express N-cadherin, in N-cadherin deficient cells, metformin plays an anti-tumor role via activation of AMPK. Ectopic expression of N-cadherin makes cancer more resistant to metformin. Therefore, we suggest that metformin's...
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titleMetformin represses cancer cells via alternate pathways in N-cadherin expressing vs. N-cadherin deficient cells.
descriptionMetformin has emerged as a potential anticancer agent. Here, we demonstrate that metformin plays an anti-tumor role via repressing N-cadherin, independent of AMPK, in wild-type N-cadherin cancer cells. Ectopic-expression of N-cadherin develops metformin-resistant cancer cells, while suppression of N-cadherin sensitizes cancer to metformin. Manipulation of AMPK expression does not alter sensitivity of cancer to metformin. We show that NF-kappaB is a downstream molecule of N-cadherin and metformin regulates NF-kappaB signaling via suppressing N-cadherin. Moreover, we also suggest that TWIST1 is an upstream molecule of N-cadherin/NF-kappaB signaling and manipulation of TWIST1 expression changes the sensitivity of cancer cells to metformin. In contrast to the cells that express N-cadherin, in N-cadherin deficient cells, metformin plays an anti-tumor role via activation of AMPK. Ectopic expression of N-cadherin makes cancer more resistant to metformin. Therefore, we suggest that metformin's...
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titleMetformin represses cancer cells via alternate pathways in N-cadherin expressing vs. N-cadherin deficient cells.
authorGe, Rongbin ; Wang, Zongwei ; Wu, Shulin ; Zhuo, Yangjia ; Otsetov, Aleksandar G ; Cai, Chao ; Zhong, Weide ; Wu, Chin-Lee ; Olumi, Aria F
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abstractMetformin has emerged as a potential anticancer agent. Here, we demonstrate that metformin plays an anti-tumor role via repressing N-cadherin, independent of AMPK, in wild-type N-cadherin cancer cells. Ectopic-expression of N-cadherin develops metformin-resistant cancer cells, while suppression of N-cadherin sensitizes cancer to metformin. Manipulation of AMPK expression does not alter sensitivity of cancer to metformin. We show that NF-kappaB is a downstream molecule of N-cadherin and metformin regulates NF-kappaB signaling via suppressing N-cadherin. Moreover, we also suggest that TWIST1 is an upstream molecule of N-cadherin/NF-kappaB signaling and manipulation of TWIST1 expression changes the sensitivity of cancer cells to metformin. In contrast to the cells that express N-cadherin, in N-cadherin deficient cells, metformin plays an anti-tumor role via activation of AMPK. Ectopic expression of N-cadherin makes cancer more resistant to metformin. Therefore, we suggest that metformin's...
doi10.18632/oncotarget.5023
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