Evidence map›Paper›PMID 38476309›Full record

ArticleOncoTargets and therapy2024

TSC22D2 Regulates ACOT8 to Delay the Malignant Progression of Colorectal Cancer.

Nana Zhou, Chaoqin Guo, Jingyang Du, Xu Zhang, Qiuran Xu, Xiaoliang Zheng, Linglan Tu

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
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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

7 authors at 2 institutions in 1 country.

Nana Zhou *School of Basic Medical Sciences and Forensic Medicine, Hangzhou Medical College, Hangzhou, 310053, People's Republic of China.
Chaoqin Guo *School of Basic Medical Sciences and Forensic Medicine, Hangzhou Medical College, Hangzhou, 310053, People's Republic of China.
Jingyang DuSchool of Basic Medical Sciences and Forensic Medicine, Hangzhou Medical College, Hangzhou, 310053, People's Republic of China.
Xu ZhangSchool of Basic Medical Sciences and Forensic Medicine, Hangzhou Medical College, Hangzhou, 310053, People's Republic of China.
Qiuran XuThe Key Laboratory of Tumor Molecular Diagnosis and Individualized Medicine of Zhejiang Province, Zhejiang Provincial People's Hospital, Affiliated People's Hospital, Hangzhou Medical College, Hangzhou, 310014, People's Republic of China.ORCID 0000-0003-2171-9279
Xiaoliang ZhengSchool of Laboratory Medicine and Bioengineering, Hangzhou Medical College, Hangzhou, 310053, People's Republic of China.ORCID 0000-0002-7955-7455
Linglan TuSchool of Laboratory Medicine and Bioengineering, Hangzhou Medical College, Hangzhou, 310053, People's Republic of China.
Hangzhou Medical College · CNZhejiang Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Purpose: Colorectal cancer (CRC) is one of the cancers with high incidence and mortality rates worldwide. In China, there are approximately 400,000 new CRC cases each year, seriously endangering people's life and health. Transforming growth factor β-stimulated clone 22 domain family, member 2 (TSC22D2) is widely expression in cancers, but the role of TSC22D2 in CRC are still unknown. Methods: Real‑time quantitative PCR (qRT-PCR) and Western blot were applied to determine the TSC22D2 levels. CCK-8, colony formation and transwell assays were used to determine the proliferation and metastasis abilities of CRC cells in vitro. In vivo metastatic potential was assessed using a subcutaneously injected mouse model and. Western-blot and immunoprecipitation experiments were used to study the mechanism of TSC22D2‑mediated metastasis. Results: We found TSC22D2 was deregulated in CRC tissues and cells and implied poor prognosis. Overexpression TSC22D2 significantly promoted CRC cells proliferation and tumorigenicity both in vitro and vivo, whereas knockdown TSC22D2 resulted in the opposite effects. Importantly using a co-immunoprecipitation (co-IP) assay combined with mass spectrometry analysis to identify TSC22D2-interacting acyl-coenzyme A thioesterases 8 (ACOT8), TSC22D2 maintained stability of ACOT8. Overexpression of TCC22D2 in CRC cells can promote the expression of ACOT8 and inhibit the proliferation and metastasis of CRC cells through EMT mechanism, highlighting the possibility of TSC22D2 as a potential target in CRC development. Conclusion: In summary, the present study revealed the inhibitory effect of TSC22D2 on the proliferation of colorectal cancer cells, suggesting that TSC22D2 may be an important tumor suppressor and a potential therapeutic target during colorectal carcinogenesis.

Indexed as

ACOT8colorectal cancerEMTTSC22D2

Identifiers

PMID38476309
PMCPMC10929132
OpenAlexW4392378059

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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 OpenQuestion graph.