Evidence map›Paper›PMID 38254118›Full record

ArticleCell communication and signaling : CCS2024

A positive feedback between PDIA3P1 and OCT4 promotes the cancer stem cell properties of esophageal squamous cell carcinoma.

Tao Huang, Qi You, Dengjun Huang, Yan Zhang, Zhijie He, Xuguang Shen, Fei Li, Qiang Shen, Ifeanyi Christian Onyebuchi, Chengwei Wu and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.7field-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

15 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
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  7. Translational cancer research · 2025
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  12. Research on Correlations of lncRNA ST7-AS1 with Progression and Therapeutic Targets of Esophageal Cancer.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2024
    Article
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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

12 authors at 2 institutions in 1 country.

Tao Huang *Department of Thoracic Surgery, The First Affiliated Hospital of Wannan Medical College (Yijishan Hospital of Wannan Medical College), Wuhu, 241001, China.
Qi You *Department of Thoracic Surgery, The First Affiliated Hospital of Wannan Medical College (Yijishan Hospital of Wannan Medical College), Wuhu, 241001, China.
Dengjun HuangDepartment of Thoracic Surgery, The First Affiliated Hospital of Wannan Medical College (Yijishan Hospital of Wannan Medical College), Wuhu, 241001, China.
Yan ZhangDepartment of Thoracic Surgery, The First Affiliated Hospital of Wannan Medical College (Yijishan Hospital of Wannan Medical College), Wuhu, 241001, China.
Zhijie HeDepartment of Thoracic Surgery, The First Affiliated Hospital of Wannan Medical College (Yijishan Hospital of Wannan Medical College), Wuhu, 241001, China.
Xuguang ShenDepartment of Thoracic Surgery, The First Affiliated Hospital of Wannan Medical College (Yijishan Hospital of Wannan Medical College), Wuhu, 241001, China.
Fei LiDepartment of Thoracic Surgery, The First Affiliated Hospital of Wannan Medical College (Yijishan Hospital of Wannan Medical College), Wuhu, 241001, China.
Qiang ShenDepartment of Thoracic Surgery, The First Affiliated Hospital of Wannan Medical College (Yijishan Hospital of Wannan Medical College), Wuhu, 241001, China.
Ifeanyi Christian OnyebuchiDepartment of Thoracic Surgery, The First Affiliated Hospital of Wannan Medical College (Yijishan Hospital of Wannan Medical College), Wuhu, 241001, China.
Chengwei WuDepartment of Gastrointestinal Surgery, The First Affiliated Hospital of Wannan Medical College (Yijishan Hospital of Wannan Medical College), Wuhu, 241001, China.
Feng LiuDepartment of Thoracic Surgery, Lishui Branch, Zhongda Hospital Affiliated to Southeast University, Nanjing, 211200, China. wyliufengwy@163.com.
Shaojin ZhuDepartment of Thoracic Surgery, The First Affiliated Hospital of Wannan Medical College (Yijishan Hospital of Wannan Medical College), Wuhu, 241001, China. 20111177@wnmc.edu.cn.ORCID 0000-0002-0633-3987
Wannan Medical College · CNZhongda Hospital Southeast University · CN

Funding

Natural Science Foundation of Anhui Education Department 2023AH040264Nature and Science Fund of Key Cultivate Program from Wannan Medical College WK2018ZF06Science Fund for Key Program of Three Creative Research Z1810Talent Scientific Research Start-Up Foundation of Yijishan Hospital YR201806
6 · The paper itself

Abstract

backgroundIncreasing evidence has indicated that long non-coding RNAs (lncRNAs) have been proven to regulate esophageal cancer progression. The lncRNA protein disulfide isomerase family A member 3 pseudogene 1 (PDIA3P1) has been shown to promote cancer stem cell properties; however, its mechanism of action remains unclear. In this study, we investigated the regulation of esophageal cancer stem cell properties by the interaction of PDIA3P1 with proteins.

methodsThe GEPIA2 and Gene Expression Omnibus databases were used to analyze gene expression. PDIA3P1 expression in human esophageal squamous cell carcinoma (ESCC) tissues and cell lines was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Loss-of-function experiments were performed to determine the effects of PDIA3P1 on ESCC cell proliferation, migration, and invasion. The sphere formation assay, number of side population cells, and CD271 + /CD44 + cells were detected by flow cytometry to identify the cancer stem cell properties. RNA immunoprecipitation (RIP), RNA pull-down, co-immunoprecipitation (co-IP), dual luciferase reporter, and cleavage under targets and tagmentation (CUT&Tag) assays were performed to elucidate the underlying molecular mechanisms.

resultsPDIA3P1 expression was upregulated in ESCC cell lines and tissues. Functionally, higher PDIA3P1 expression promoted cell proliferation, invasion, and metastasis and inhibited apoptosis in esophageal cancer. Importantly, PDIA3P1 promoted cancer stem cell properties in ESCC. Mechanistically, PDIA3P1 interacted with and stabilized octamer-binding transcription factor 4 (OCT4) by eliminating its ubiquitination by the ubiquitinating enzyme WW domain-containing protein 2 (WWP2). Moreover, as a transcription factor, OCT4 bound to the PDIA3P1 promoter and promoted its transcription.

conclusionsOur research revealed a novel mechanism by which a positive feedback loop exists between PDIA3P1 and OCT4. It also demonstrated that the PDIA3P1-WWP2-OCT4 loop is beneficial for promoting the cancer stem cell properties of ESCC. Owing to this regulatory relationship, the PDIA3P1-WWP2-OCT4-positive feedback loop might be used in the diagnosis and prognosis, as well as in the development of novel therapeutics for esophageal cancer.

Indexed as

Esophageal NeoplasmsEsophageal Squamous Cell CarcinomaNeoplastic Stem CellsOctamer Transcription Factor-3RNA, Long NoncodingHumansNerve Tissue ProteinsReceptors, Nerve Growth FactorRNAUbiquitin-Protein LigasesNerve Tissue ProteinsNGFR protein, humanOctamer Transcription Factor-3POU5F1 protein, humanReceptors, Nerve Growth FactorRNARNA, Long NoncodingUbiquitin-Protein LigasesWWP2 protein, humanCancer stem cellEsophageal squamous cell carcinomaOCT4PDIA3P1UbiquitinationWWP2

Identifiers

PMID38254118
PMCPMC10801955
OpenAlexW4391105806

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LicenceCC BY
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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.