3/12/2024 10:04:17 AM | Browse: 134 | Download: 468
Publication Name | World Journal of Gastrointestinal Oncology |
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Manuscript ID | 89399 |
Country | China |
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ISSN | 1948-5204 (online) |
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Open Access | This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/Licenses/by-nc/4.0/ |
Copyright | © The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved. |
Article Reprints | For details, please visit: http://www.wjgnet.com/bpg/gerinfo/247 |
Permissions | For details, please visit: http://www.wjgnet.com/bpg/gerinfo/207 |
Publisher | Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA |
Website | http://www.wjgnet.com |
Category | Gastroenterology & Hepatology | ||||||||||
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Manuscript Type | Basic Study | ||||||||||
Article Title | CALD1 facilitates gastric cancer epithelial-mesenchymal transition progression by modulating the PI3K-Akt pathway | ||||||||||
Manuscript Source | Unsolicited Manuscript | ||||||||||
All Author List | Wen-Qian Ma, Ming-Chang Miao, Ping-An Ding, Bi-Bo Tan, Wen-Bo Liu, Shuo Guo, Li-Mian Er, Zhi-Dong Zhang and Qun Zhao | ||||||||||
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Corresponding Author | Qun Zhao, MD, PhD, Chief Doctor, Professor, The Third Department of Surgery, The Fourth Hospital of Hebei Medical University, No. 12 Jiankang Road, Changan District, Shijiazhuang 050011, Hebei Province, China. zhaoqun@hebmu.edu.cn | ||||||||||
Key Words | Gastric tumor; CALD1; Epithelial-mesenchymal transition; Gene disruption; Invasion; Migration; Bioinformatics | ||||||||||
Core Tip | In this study, the relationship between CALD1 and gastric cancer (GC) and the possible network regulatory mechanisms of CALD1 were explored and validated by bioinformatics. We conducted functional analysis and verification through tissue and cell experiments, delving into its pathways and mechanisms, it was showed that CALD1 may participate in the proliferation, invasion, and migration and epithelial-mesenchymal transition (EMT)-related gene and protein expression of GC cells. Our study propounds that CALD1, through PI3K-Akt signaling pathway activation, may regulate the EMT process in GC cells, thereby presenting a potentially novel target for GC treatment. | ||||||||||
Publish Date | 2024-03-12 10:04 | ||||||||||
Citation | Ma WQ, Miao MC, Ding PA, Tan BB, Liu WB, Guo S, Er LM, Zhang ZD, Zhao Q. CALD1 facilitates gastric cancer epithelial-mesenchymal transition progression by modulating the PI3K-Akt pathway. World J Gastrointest Oncol 2024; 16(3): 1029-1045 | ||||||||||
URL | https://www.wjgnet.com/1948-5204/full/v16/i3/1029.htm | ||||||||||
DOI | https://dx.doi.org/10.4251/wjgo.v16.i3.1029 |
Full Article (PDF) | WJGO-16-1029-with-cover.pdf |
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Full Article (Word) | WJGO-16-1029.docx |
Manuscript File | 89399_Auto_Edited-YJP_WangTQ.docx |
Answering Reviewers | 89399-Answering reviewers.pdf |
Audio Core Tip | 89399-Audio core tip.m4a |
Biostatistics Review Certificate | 89399-Biostatistics statement.pdf |
Conflict-of-Interest Disclosure Form | 89399-Conflict-of-interest statement.pdf |
Copyright License Agreement | 89399-Copyright license agreement.pdf |
Approved Grant Application Form(s) or Funding Agency Copy of any Approval Document(s) | 89399-Grant application form(s).pdf |
Institutional Review Board Approval Form or Document | 89399-Institutional review board statement.pdf |
Non-Native Speakers of English Editing Certificate | 89399-Language certificate.pdf |
Peer-review Report | 89399-Peer-review(s).pdf |
Scientific Misconduct Check | 89399-Bing-Gong ZM-2.png |
Scientific Misconduct Check | 89399-CrossCheck.png |
Scientific Editor Work List | 89399-Scientific editor work list.pdf |
CrossCheck Report | 89399-CrossCheck report.pdf |