Miao YD, Wang JT, Tang XL, Mi DH. Microarray analysis to explore the effect of CXCL12 isoforms in a pancreatic pre-tumor cell model. World J Gastroenterol 2021; 27(47): 8194-8198 [PMID: 35068863 DOI: 10.3748/wjg.v27.i47.8194]
Corresponding Author of This Article
Yan-Dong Miao, MD, Doctor, The First Clinical Medical College, Lanzhou University, No. 1 Donggang West Road, Chengguan District, Lanzhou 730000, Gansu Province, China. miaoyd19@lzu.edu.cn
Research Domain of This Article
Medicine, Research & Experimental
Article-Type of This Article
Letter to the Editor
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (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/
World J Gastroenterol. Dec 21, 2021; 27(47): 8194-8198 Published online Dec 21, 2021. doi: 10.3748/wjg.v27.i47.8194
Microarray analysis to explore the effect of CXCL12 isoforms in a pancreatic pre-tumor cell model
Yan-Dong Miao, Jiang-Tao Wang, Xiao-Long Tang, Deng-Hai Mi
Yan-Dong Miao, Jiang-Tao Wang, Xiao-Long Tang, Deng-Hai Mi, The First Clinical Medical College, Lanzhou University, Lanzhou 730000, Gansu Province, China
Deng-Hai Mi, Dean's office, Gansu Academy of Traditional Chinese Medicine, Lanzhou 730000, Gansu Province, China
Author contributions: Mi DH and Miao YD designed the research; Miao YD wrote this comment; Wang JT and Tang XL made academic advice; Mi DH reviewed this manuscript; all authors approved the final manuscript.
Conflict-of-interest statement: No conflict of interest associated with any of the senior authors or other coauthors contributed their efforts in this manuscript.
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: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Yan-Dong Miao, MD, Doctor, The First Clinical Medical College, Lanzhou University, No. 1 Donggang West Road, Chengguan District, Lanzhou 730000, Gansu Province, China. miaoyd19@lzu.edu.cn
Received: June 22, 2021 Peer-review started: June 22, 2021 First decision: July 4, 2021 Revised: July 6, 2021 Accepted: December 2, 2021 Article in press: December 2, 2021 Published online: December 21, 2021
Abstract
CXCL12 expression was significantly lower in tumor samples than in corresponding normal samples. CXCL12 expression was significantly positively related to the infiltration levels of T cells, dendritic cells (DCs), immature DCs, cytotoxic cells, Tfh cells, mast cells, B cells, Th1 cells, natural killer (NK) cells, pDCs, neutrophils, and T helper cells (Spearman correlation coefficient > 0.5, P < 0.001) and negatively correlated with the infiltration level of NK CD56bright cells. In addition, pancreatic hTERT-HPNE cells treated with three diverse CXCL12 isoforms exhibited changes mainly in the regulation of the epithelial-mesenchymal transition activation pathway.
Core Tip: CXCL12 expression was significantly lower in tumor samples than in normal samples. CXCL12 expression was significantly positively associated with the infiltration levels of 12 immune cells, especially T cells, which may encourage further exploration of the effect of CXCL12 in pancreatic ductal adenocarcinoma immunotherapy. In addition, treating pancreatic hTERT-HPNE cells with three diverse CXCL12 isoforms mainly affected the regulation of the epithelial-mesenchymal transition activation pathway.
