Evidence map›Paper›PMID 29343267›Full record

ArticleJournal of translational medicine2018

TIPE2 suppresses progression and tumorigenesis of esophageal carcinoma via inhibition of the Wnt/β-catenin pathway.

Linan Zhu, Xudong Zhang, Xiaorui Fu, Zhaoming Li, Zhenchang Sun, Jingjing Wu, Xinhua Wang, Feng Wang, Xiangke Li, Songtao Niu and 6 more

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Journal of translational medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 16% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
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  5. A Novel Prognostic Factor TIPE2 in Bladder Cancer.Pathology oncology research : POR · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 1 institution in 1 country.

Linan ZhuDepartment of Oncology, The First Affiliated Hospital of Zhengzhou University, Νo. 1 Jianshe East Road, Zhengzhou, 450052, Henan, People's Republic of China.
Xudong ZhangDepartment of Oncology, The First Affiliated Hospital of Zhengzhou University, Νo. 1 Jianshe East Road, Zhengzhou, 450052, Henan, People's Republic of China.
Xiaorui FuDepartment of Oncology, The First Affiliated Hospital of Zhengzhou University, Νo. 1 Jianshe East Road, Zhengzhou, 450052, Henan, People's Republic of China.
Zhaoming LiDepartment of Oncology, The First Affiliated Hospital of Zhengzhou University, Νo. 1 Jianshe East Road, Zhengzhou, 450052, Henan, People's Republic of China.
Zhenchang SunDepartment of Oncology, The First Affiliated Hospital of Zhengzhou University, Νo. 1 Jianshe East Road, Zhengzhou, 450052, Henan, People's Republic of China.
Jingjing WuDepartment of Oncology, The First Affiliated Hospital of Zhengzhou University, Νo. 1 Jianshe East Road, Zhengzhou, 450052, Henan, People's Republic of China.
Xinhua WangDepartment of Oncology, The First Affiliated Hospital of Zhengzhou University, Νo. 1 Jianshe East Road, Zhengzhou, 450052, Henan, People's Republic of China.
Feng WangDepartment of Oncology, The First Affiliated Hospital of Zhengzhou University, Νo. 1 Jianshe East Road, Zhengzhou, 450052, Henan, People's Republic of China.
Xiangke LiDepartment of Oncology, The First Affiliated Hospital of Zhengzhou University, Νo. 1 Jianshe East Road, Zhengzhou, 450052, Henan, People's Republic of China.
Songtao NiuDepartment of Oncology, The First Affiliated Hospital of Zhengzhou University, Νo. 1 Jianshe East Road, Zhengzhou, 450052, Henan, People's Republic of China.
Mengjie DingDepartment of Oncology, The First Affiliated Hospital of Zhengzhou University, Νo. 1 Jianshe East Road, Zhengzhou, 450052, Henan, People's Republic of China.
Zhenzhen YangDepartment of Oncology, The First Affiliated Hospital of Zhengzhou University, Νo. 1 Jianshe East Road, Zhengzhou, 450052, Henan, People's Republic of China.
Wanqiu YangDepartment of Oncology, The First Affiliated Hospital of Zhengzhou University, Νo. 1 Jianshe East Road, Zhengzhou, 450052, Henan, People's Republic of China.
Meifeng YinDepartment of Oncology, The First Affiliated Hospital of Zhengzhou University, Νo. 1 Jianshe East Road, Zhengzhou, 450052, Henan, People's Republic of China.
Lei ZhangDepartment of Oncology, The First Affiliated Hospital of Zhengzhou University, Νo. 1 Jianshe East Road, Zhengzhou, 450052, Henan, People's Republic of China.
Mingzhi ZhangDepartment of Oncology, The First Affiliated Hospital of Zhengzhou University, Νo. 1 Jianshe East Road, Zhengzhou, 450052, Henan, People's Republic of China. mingzhi_zhang1@126.com.ORCID 0000-0003-3581-551X
First Affiliated Hospital of Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEsophageal carcinoma is the eighth prevalent malignancy and ranks the sixth in carcinoma-related death worldwide. Tumor necrosis factor-α-induced protein-8 like-2 (TIPE2) has been identified as a tumor suppressor in multiple carcinomas. However, its roles and molecular mechanisms underlying esophageal carcinoma progression are still undefined till now.

methodsRT-qPCR assay was employed to detect the expression of TIPE2 mRNA. TIPE2 protein expression was measured by using western blot assay. Ad-V and Ad-TIPE2 adenoviruses were constructed to overexpress TIPE2. The effects of TIPE2 overexpression on cell proliferation, invasion and apoptosis were assessed by MTT and Edu incorporation assays, transwell invasion assay and flow cytometry analysis, respectively. The effect of TIPE2 overexpression on xenograft tumor growth was determined by measuring tumor volume and weight, together with immunohistochemistry assay. The effect of TIPE2 overexpression on the Wnt/β-catenin signaling pathway was evaluated by detecting the protein levels of β-catenin, c-Myc and cyclinD1 in EC9076 cells and xenograft tumors of esophageal carcinoma.

resultsTIPE2 expression was downregulated in esophageal carcinoma tissues and cells. Adenovirus-mediated TIPE2 overexpression suppressed cell proliferation and invasion, and induced apoptosis in esophageal carcinoma cells. Enforced expression of TIPE2 inhibited tumor growth in vivo, as evidenced by the reduced tumor volume, tumor weight and proliferating cell nuclear antigen expression. Overexpression of TIPE2 inhibited the Wnt/β-catenin signaling pathway in esophageal carcinoma in vitro and in vivo.

conclusionsThese results suggest that TIPE2 suppressed progression and tumorigenesis of esophageal carcinoma via inhibition of the Wnt/β-catenin pathway.

Indexed as

Disease ProgressionWnt Signaling PathwayAgedAnimalsApoptosisCarcinogenesisCell Line, TumorCell ProliferationDown-RegulationEsophageal NeoplasmsFemaleGene Expression Regulation, NeoplasticHumansIntracellular Signaling Peptides and ProteinsMaleMice, Inbred BALB CIntracellular Signaling Peptides and ProteinsTNFAIP8L2 protein, humanEsophageal carcinomaProliferationTIPE2TumorigenesisWnt/β-catenin pathway

Identifiers

PMID29343267
PMCPMC5773041
OpenAlexW2791195074

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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.