Evidence map›Paper›PMID 33935281›Full record

ArticleCell death & disease2021

ITIH5, a p53-responsive gene, inhibits the growth and metastasis of melanoma cells by downregulating the transcriptional activity of KLF4.

Jia Liu, Feng Cao, Xiaojie Li, Li Zhang, Zhengrong Liu, Xiaodong Li, Jingrong Lin, Chuanchun Han

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

19 citing papers in PubMed, 42 citations in OpenAlex.

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  19. p53 signaling in cancer progression and therapy.Cancer cell international · 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

8 authors at 3 institutions in 1 country.

Jia Liu *Department of Gynecology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Shenyang, China.
Feng Cao *Institute of Cancer Stem Cell & Department of Dermatology, The First Affiliated Hospital of Dalian Medical University, Dalian, 116044, China.
Xiaojie Li *College of Stomatology, Dalian Medical University, Dalian, 116044, China.
Li Zhang *Laboratory of Pathogenic Biology, College of Basic Medical Science of Dalian Medical University, Dalian, 116044, China.
Zhengrong LiuDepartment of Gastrointestinal Surgery, People's Hospital of China Medical University, People's Hospital of Liaoning Province, Shenyang, China.
Xiaodong LiInstitute of Cancer Stem Cell & Department of Dermatology, The First Affiliated Hospital of Dalian Medical University, Dalian, 116044, China. xd_li201212@dmu.edu.cn.
Jingrong LinInstitute of Cancer Stem Cell & Department of Dermatology, The First Affiliated Hospital of Dalian Medical University, Dalian, 116044, China. amy4963@163.com.
Chuanchun HanDepartment of Gynecology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Shenyang, China. hanchuanchun@163.com.ORCID 0000-0001-5680-3564
Dalian Medical University · CNLiaoning Cancer Hospital & Institute · CNLiaoning Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ITIH5, a member of the inter-α-trypsin inhibitory (ITI) gene family, acts as a putative tumour-suppressor gene in many cancers. However, its role and the regulatory mechanism in melanoma are still unclear. Here, we found that the expression of ITIH5 was decreased in melanoma tissues compared with normal skin tissues. Decreased expression of ITIH5 was correlated with clinicopathological features and predicted poor prognosis in patients with melanoma. Forced expression of ITIH5 significantly inhibited melanoma cell proliferation and metastasis in vitro and ex vivo while knockdown of ITIH5 expression enhanced the malignant behaviour of melanoma cells. In further mechanistic studies, we showed that p53 can directly bind to the promoter of ITIH5 and thus promotes transcription of ITIH5 in melanoma cells. Additionally, we found that ITIH5 interacted with Krüppel-like factor 4 (KLF4) and inhibited its transcriptional activity. Collectively, our data not only identified a tumour-suppressive role of ITIH5 in melanoma but also revealed that upregulation of ITIH5 by p53 suppressed melanoma cell growth and migration likely by downmodulating the transcriptional activity of KLF4.

Indexed as

AnimalsCell Line, TumorDown-RegulationHeterograftsHumansKruppel-Like Factor 4Kruppel-Like Transcription FactorsMaleMelanomaMiceMice, NudeNeoplasm MetastasisProteinase Inhibitory Proteins, SecretoryTumor Suppressor Protein p53ITIH5 protein, humanKLF4 protein, humanKlf4 protein, mouseKruppel-Like Factor 4Kruppel-Like Transcription FactorsProteinase Inhibitory Proteins, SecretoryTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID33935281
PMCPMC8089095
OpenAlexW3157566382

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.