Evidence map›Paper›PMID 32020212›Full record

ArticleOncology reports2020

TGM3 functions as a tumor suppressor by repressing epithelial‑to‑mesenchymal transition and the PI3K/AKT signaling pathway in colorectal cancer.

Yifei Feng, Dongjian Ji, Yuanjian Huang, Bing Ji, Yue Zhang, Jie Li, Wen Peng, Chuan Zhang, Dongsheng Zhang, Yueming Sun and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

20 citing papers in PubMed, 32 citations in OpenAlex.

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  15. Clinical significance of CD34Frontiers of medicine · 2021
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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

11 authors at 2 institutions in 1 country.

Yifei Feng *Department of Colorectal Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Dongjian Ji *Department of Colorectal Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Yuanjian Huang *Department of Colorectal Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Bing JiDepartment of General Surgery, Yancheng City No. 1 People's Hospital, Yancheng, Jiangsu 224005, P.R. China.
Yue ZhangDepartment of Colorectal Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Jie LiDepartment of General Surgery, Yancheng City No. 1 People's Hospital, Yancheng, Jiangsu 224005, P.R. China.
Wen PengDepartment of Colorectal Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Chuan ZhangDepartment of Colorectal Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Dongsheng ZhangDepartment of Colorectal Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Yueming SunDepartment of Colorectal Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Ziwei XuDepartment of Colorectal Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Nanjing Medical University · CNJiangsu Province Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The dysregulation of transcription factors contributes to the unlimited proliferation of cancer cells. Transglutaminase 3 (TGM3) has been demonstrated to play a crucial role in physiology and pathology. However, the potential role of TGM3 in colorectal cancer (CRC) remains unknown. In the present study, reverse transcription‑quantitative PCR and immunohistochemistry were utilized to analyze the expression of TGM3 in CRC and adjacent normal tissues. LoVo and HCT116 cell lines were then selected to further investigate the function of TGM3 in the proliferation, invasion and metastasis of CRC both in vitro and in vivo. Finally, western blotting was performed to investigate the molecular mechanisms underlying the effects of TGM3 in CRC. The expression level of TGM3 was significantly downregulated in CRC tissues, and was associated with tumor invasion, metastasis and patient prognosis. Following TGM3 inhibition and overexpression in CRC cells, it was revealed that TGM3 suppressed cell proliferation, potentially via the promotion of apoptosis and cell cycle regulation. Furthermore, TGM3 also inhibited invasion and metastasis. Finally, it was observed that TGM3 inhibited epithelial‑to‑mesenchymal transition and activated phosphorylated AKT serine/threonine kinase in CRC cells. The results from the present study revealed that TGM3 is a tumor suppressor in the progression of CRC, and may be used as a novel target for CRC treatment.

Indexed as

AgedApoptosisBiomarkers, TumorCell ProliferationColorectal NeoplasmsEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHCT116 CellsHumansMaleMiddle AgedNeoplasm InvasivenessNeoplasm MetastasisPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktBiomarkers, TumorPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTGM3 protein, humanTransglutaminasesTumor Suppressor Proteinscolorectal cancerepithelial-mesenchymal transitionPI3K-AKT pathwayTGM3

Identifiers

PMID32020212
PMCPMC7041123
OpenAlexW3002753540

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.