Evidence map›Paper›PMID 38200280›Full record

ArticleFunctional & integrative genomics2024

ETV7 promotes colorectal cancer progression through upregulation of IFIT3.

Bao Chai, Yanjun Li, Yarong Guo, Zhuowei Zhang, Kai Jia, Xinhao Chai, Yuhong Suo

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Functional & integrative genomics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

5 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
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  4. Review
  5. Review
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

7 authors at 4 institutions in 1 country.

Bao Chai *Department of Gastroenterology, Shanxi Academy of Medical Science, Shanxi Bethune Hospital, Taiyuan, China.
Yanjun Li *Department of Surgery, Shanxi Academy of Medical Science, Shanxi Bethune Hospital, Taiyuan, China.
Yarong GuoDepartment of Oncology, The First Affiliated Hospital of Shanxi Medical University, 85 South Jiefang Road, TaiyuanTaiyuan, 030001, Shanxi Province, China. gyr5258@126.com.
Zhuowei ZhangMedical Imaging Department, Shanxi Medical University, Taiyuan, China.
Kai JiaDepartment of Surgery, The First Affiliated Hospital of Shanxi Medical University, Taiyuan, China.
Xinhao ChaiDepartment of Oncology, The First Affiliated Hospital of Shanxi Medical University, 85 South Jiefang Road, TaiyuanTaiyuan, 030001, Shanxi Province, China.
Yuhong SuoLiver Cancer Center, Tianjin Medical University Cancer Institute and Hospital, Taiyuan, China.
Shanxi Medical University · CNShanxi Academy of Medical Sciences · CNFirst Hospital of Shanxi Medical University · CNTianjin Medical University Cancer Institute and Hospital · CN

Funding

Natural Science Foundation of Shanxi Province 201901D111413Scientific and Technological Activities of Overseas Students of Shanxi Province 20210004The 70th batch of general projects of China Postdoctoral Foundation 2021M702051The central government guides local science and technology development fund projects YDZJSX2021A041
6 · The paper itself

Abstract

Members of the E26 transformation-specific (ETS) variant transcription factor family act as either tumor suppressors or oncogenic factors in numerous types of cancer. ETS variant transcription factor 7 (ETV7) participates in the development of malignant tumors, whereas its involvement in colorectal cancer (CRC) is less clear. In this study, The Cancer Genome Atlas (TCGA) and immunochemistry staining were applied to check the clinical relevance of ETV7 and interferon-induced protein with tetratricopeptide repeats 3 (IFIT3) in CRC patients. Overexpression and knockdown of ETV7 and IFIT3 were conducted by transfecting the cells with pCDNA3.1 plasmids and siRNAs, respectively. Western blotting was used to detect the protein expression of ETV7 in CRC cells. Cell Counting Kit-8, cell colony formation, and Transwell assays, as well as flow cytometry, were used to evaluate the proliferation, migration, cell cycle, and apoptosis of CRC cells. Furthermore, western blotting, RT-qPCR, and luciferase assay were used to explore the regulation of ETV7 on IFIT3. Rescue assay was used to investigate the significance of ETV7/IFIT3 axis on CRC progression. We found that ETV7 was upregulated in CRC tissues and cells. Overexpression of ETV7 stimulated the proliferation, migration, and cell cycle amplification, and reduced the apoptosis of CRC cells. Downregulation of ETV7 exerted the opposite effect on CRC cell progression. Moreover, we demonstrated that ETV7 stimulated the transcription activity, the mRNA and protein expression of IFIT3 in CRC cells. There was a positive correlation between ETV7 and IFIT3 in CRC patients. IFIT3 knockdown reversed the promotive effect exerted by overexpression of ETV7 on the amplification and migration of CRC cells. By contrast, overexpression of IFIT3 blocked the inhibitory effect of ETV7-targeting siRNA. In summary, ETV7 induces progression of CRC by activating the transcriptional expression of IFIT3. The EVT7/IFIT3 axis may be a novel target for CRC therapy.

Indexed as

ApoptosisColorectal NeoplasmsDown-RegulationHumansIntracellular Signaling Peptides and ProteinsProto-Oncogene Proteins c-etsUp-RegulationETV7 protein, humanIFIT3 protein, humanIntracellular Signaling Peptides and ProteinsProto-Oncogene Proteins c-etsCancer progressionColorectal cancerETV7IFIT3

Identifiers

PMID38200280
PMCPMC10781848
OpenAlexW4390691886

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.