Wang J, Tan Y, Jia QY, Tang FQ. Transcriptional factor III A promotes colorectal cancer progression by upregulating cystatin A. World J Gastrointest Oncol 2022; 14(10): 1918-1932 [PMID: 36310710 DOI: 10.4251/wjgo.v14.i10.1918]
Corresponding Author of This Article
Fa-Qin Tang, MD, PhD, Doctor, Professor, Hunan Key Laboratory of Oncotarget Gene, Hunan Cancer Hospital & The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, No. 283 Tongzipo Road, Changsha 410013, Hunan Province, China. tangfq@hnca.org.cn
Research Domain of This Article
Oncology
Article-Type of This Article
Basic Study
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Wang J, Tan Y, Jia QY, Tang FQ. Transcriptional factor III A promotes colorectal cancer progression by upregulating cystatin A. World J Gastrointest Oncol 2022; 14(10): 1918-1932 [PMID: 36310710 DOI: 10.4251/wjgo.v14.i10.1918]
World J Gastrointest Oncol. Oct 15, 2022; 14(10): 1918-1932 Published online Oct 15, 2022. doi: 10.4251/wjgo.v14.i10.1918
Transcriptional factor III A promotes colorectal cancer progression by upregulating cystatin A
Fa-Qin Tang, Qun-Ying Jia, Yuan Tan, Jing Wang
Jing Wang, Yuan Tan, Qun-Ying Jia, Fa-Qin Tang, Hunan Key Laboratory of Oncotarget Gene, Hunan Cancer Hospital & The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha 410013, Hunan Province, China
Author contributions: Tang FQ designed and coordinated the study; Wang J, Tan Y, and Jia QY performed the experiments, and acquired and analyzed data; Wang J and Tang FQ wrote the manuscript; and all authors approved the final version of the article.
Supported bythe National Natural Science Foundation of China, No. 81872226; Changsha Science and Technology Project, No. 2019TP1046; and the Research Projects of Hunan Health Commission, No. B2019084.
Institutional review board statement: The study was reviewed and approved by the Hunan Cancer Hospital Institutional Review Board (Approval No. KYJJ-2020-004).
Institutional animal care and use committee statement: All procedures involving animals were reviewed and approved by the Institutional Animal Care and Use Committee of the Hunan Cancer Hospital (No. 2020-118).
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Data sharing statement: No additional data are available.
ARRIVE guidelines statement: The authors have read the ARRIVE Guidelines, and the manuscript was prepared and revised according to the ARRIVE Guidelines.
Corresponding author: Fa-Qin Tang, MD, PhD, Doctor, Professor, Hunan Key Laboratory of Oncotarget Gene, Hunan Cancer Hospital & The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, No. 283 Tongzipo Road, Changsha 410013, Hunan Province, China. tangfq@hnca.org.cn
Received: May 7, 2022 Peer-review started: May 7, 2022 First decision: July 13, 2022 Revised: July 23, 2022 Accepted: September 8, 2022 Article in press: September 8, 2022 Published online: October 15, 2022 Processing time: 160 Days and 9.1 Hours
ARTICLE HIGHLIGHTS
Research background
Advanced colorectal cancer (CRC) generally has poor outcomes and high mortality rates. Clarifying the molecular mechanisms underlying CRC progression is necessary to develop new diagnostic and therapeutic strategies to improve CRC outcome and decrease mortality.
Research motivation
Transcriptional factor III A (GTF3A), an RNA polymerase III transcriptional factor, is a critical driver of tumorgenesis and aggravates CRC cell growth. The mechanism of GTF3A participating in CRC is not clear.
Research objectives
To confirm whether GTF3A aggravates CRC progression and investigate molecular mechanisms underlying CRC progression.
Research methods
Immunohistochemistry was used to detect GTF3A expression in CRC tissues. Short hairpin GTF3As and CSTAs were designed and packaged into the virus to block the expression of Gtf3a and Csta genes. RNA sequencing and data analysis was used to screen the target genes of GTF3A. Fluorescence in situ hybridization assay was used to detect the interaction of GTF3A with Csta, and luciferase activity assay was used to evaluate the expression of Gtf3a and Csta genes.
Research results
GTF3A was highly expressed in CRC tissues and metastatic tissues, and its expression was associated with CRC prognosis. Knockdown of the Gtf3a gene impaired CRC cell proliferation, invasion, and motility in vitro and in vivo. GTF3A increased Csta transcription, and increased CSTA upregulated epithelial-mesenchymal transition (EMT) markers.
Research conclusions
GTF3A increases CSTA expression by binding to the Csta promoter, and increased CSTA levels promote CRC progression by regulating EMT. Inhibition of GTF3A prevents CRC progression.
Research perspectives
GTF3A may be a potential novel therapeutic target and biomarker for CRC.
