Inactivation of ATF‐2 enhances epithelial‐mesenchymal transition and gemcitabine sensitivity in human pancreatic cancer cells-Reference-Cited by-同舟云学术

Inactivation of ATF‐2 enhances epithelial‐mesenchymal transition and gemcitabine sensitivity in human pancreatic cancer cells

Published:2018-10-26 Issue:3 Volume:120 Page:4463-4471
ISSN:0730-2312
Container-title:Journal of Cellular Biochemistry
language:en
Short-container-title:J Cell Biochem

Author:

Wu Xingda¹,Liu Zhe¹,Guo Kejia¹,Ma Gang¹,Song Shaowei¹^ORCID

Affiliation:

1. Department of General Surgery The First Hospital of China Medical University Shenyang China

Publisher

Wiley

Subject

Cell Biology,Molecular Biology,Biochemistry

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1002/jcb.27734

Reference39 articles.

1. The Activation of c-Jun NH2-terminal Kinase (JNK) by DNA-damaging Agents Serves to Promote Drug Resistance via Activating Transcription Factor 2 (ATF2)-dependent Enhanced DNA Repair

2. High glucose upregulates arginase 1 and decreases nitric oxide production through ATF‐2 and c‐Jun transcription factors;Shatanawi A;Life Sci J,2014

3. ATF2 contributes to cisplatin resistance in non-small cell lung cancer and celastrol induces cisplatin resensitization through inhibition of JNK/ATF2 pathway

4. Angiotensin II limits NO production by upregulating arginase through a p38 MAPK–ATF-2 pathway

5. Autocrine IL-8 and VEGF mediate epithelial–mesenchymal transition and invasiveness via p38/JNK-ATF-2 signalling in A549 lung cancer cells

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2. Overexpression of Activating Transcription Factor-2 (ATF-2) Activates Wnt/Ca2+ Signaling Pathways and Promotes Proliferation and Invasion in Non-Small-Cell Lung Cancer;Disease Markers;2022-06-02

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