Evidence map›Paper›PMID 34919666›Full record

ArticleCarcinogenesis2022

TBX1 functions as a putative oncogene of breast cancer through promoting cell cycle progression.

Shuya Huang, Xiang Shu, Jie Ping, Jie Wu, Jifeng Wang, Chris Shidal, Xingyi Guo, Joshua A Bauer, Jirong Long, Xiao-Ou Shu and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Carcinogenesis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 46% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 2 countries.

Shuya HuangDepartment of Medicine, Division of Epidemiology, Vanderbilt Epidemiology Center, Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
Xiang ShuDepartment of Medicine, Division of Epidemiology, Vanderbilt Epidemiology Center, Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
Jie PingDepartment of Medicine, Division of Epidemiology, Vanderbilt Epidemiology Center, Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
Jie WuDepartment of Medicine, Division of Epidemiology, Vanderbilt Epidemiology Center, Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
Jifeng WangDepartment of Medicine, Division of Epidemiology, Vanderbilt Epidemiology Center, Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
Chris ShidalDepartment of Medicine, Division of Epidemiology, Vanderbilt Epidemiology Center, Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
Xingyi GuoDepartment of Medicine, Division of Epidemiology, Vanderbilt Epidemiology Center, Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
Joshua A BauerDepartment of Biochemistry, Vanderbilt Institute of Chemical Biology, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.
Jirong LongDepartment of Medicine, Division of Epidemiology, Vanderbilt Epidemiology Center, Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
Xiao-Ou ShuDepartment of Medicine, Division of Epidemiology, Vanderbilt Epidemiology Center, Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
Wei ZhengDepartment of Medicine, Division of Epidemiology, Vanderbilt Epidemiology Center, Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, TN 37232, USA.ORCID 0000-0003-1226-070X
Qiuyin CaiDepartment of Medicine, Division of Epidemiology, Vanderbilt Epidemiology Center, Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, TN 37232, USA.ORCID 0000-0002-9384-5648
Vanderbilt University Medical Center · USMemorial Sloan Kettering Cancer Center · USSecond Hospital of Shandong University · CNVanderbilt University · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Hongbiao Carl Lekaye · 1985 to 2026
$347.4M
Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI STACIE B DUSETZINA · 1995 to 2026
$172.8M
Vanderbilt Institute for Clinical and Translational Research (VICTR) -Identifying correlates of functional immunity in SARS-CoV-2 convalescent plasmaUL1TR002243 · NCATS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Paul A. Harris, Wesley H Self · 2017 to 2026
$130.7M
Integrating genomic and transcriptomic data to identify breast cancer susceptibility genesR01CA235553 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI LONG, JIRONG, ZHENG, WEI · 2019 to 2024
$3.3M
Cancer Pharmacologist and HTS ScientistR50CA211206 · NCI · VANDERBILT UNIVERSITY · PI Joshua A. Bauer · 2016 to 2026
$1.8M
Uncovering Roles of Metabolites in Colorectal Cancer EtiologyR00CA230205 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI SHU, XIANG · 2020 to 2022
$888k
Uncovering roles of metabolites in colorectal cancer etiologyK99CA230205 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI SHU, XIANG · 2019 to 2020
$194k
NCATS NIH HHS UL1 TR002243NCI NIH HHS K99 CA230205NCI NIH HHS P30 CA008748NCI NIH HHS P30 CA068485NCI NIH HHS R00 CA230205NCI NIH HHS R01 CA235553NCI NIH HHS R50 CA211206
6 · The paper itself

Abstract

We have previously identified a genetic variant, rs34331122 in the 22q11.21 locus, as being associated with breast cancer risk in a genome-wide association study. This novel variant is located in the intronic region of the T-box transcription factor 1 (TBX1) gene. Cis-expression quantitative trait loci analysis showed that expression of TBX1 was regulated by the rs34331122 variant. In the current study, we investigated biological functions and potential molecular mechanisms of TBX1 in breast cancer. We found that TBX1 expression was significantly higher in breast cancer tumor tissues than adjacent normal breast tissues and increased with tumor stage (P < 0.05). We further knocked-down TBX1 gene expression in three breast cancer cell lines, MDA-MB-231, MCF-7 and T47D, using small interfering RNAs and examined consequential changes on cell oncogenicity and gene expression. TBX1 knock-down significantly inhibited breast cancer cell proliferation, colony formation, migration and invasion. RNA sequencing and flow cytometry analysis revealed that TBX1 knock-down in breast cancer cells induced cell cycle arrest in the G1 phase through disrupting expression of genes involved in the cell cycle pathway. Furthermore, survival analysis using the online Kaplan-Meier Plotter suggested that higher TBX1 expression was associated with worse outcomes in breast cancer patients, especially for estrogen receptor-positive breast cancer, with HRs (95% CIs) for overall survival (OS) and distant metastasis free survival (DMFS) of 1.5 (1.05-2.15) and 1.55 (1.10-2.18), respectively. In conclusion, our results suggest that the TBX1 gene may act as a putative oncogene of breast cancer through regulating expressions of cell cycle-related genes.

Indexed as

Breast NeoplasmsCell CycleCell Line, TumorCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMCF-7 CellsOncogenesRNA, Small InterferingT-Box Domain ProteinsRNA, Small InterferingT-Box Domain ProteinsTBX1 protein, human

Identifiers

PMID34919666
PMCPMC8832409
OpenAlexW4200516574

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.