Evidence map›Paper›PMID 28534513›Full record

ArticleOncogene2017

Protein disulfide isomerase a4 acts as a novel regulator of cancer growth through the procaspase pathway.

T-F Kuo, T-Y Chen, S-T Jiang, K-W Chen, Y-M Chiang, Y-J Hsu, Y-J Liu, H-M Chen, K K Yokoyama, K-C Tsai and 5 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

32 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Biomarkers of tumor invasiveness in proteomics (Review).International journal of oncology · 2020
    Pooled it
  2. Review
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  8. Spatial protein redistribution: wandering but not lost.Cellular and molecular life sciences : CMLS · 2025
    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

15 authors.

T-F KuoAgricultural Biotechnology Research Center, Academia Sinica, Taipei, Taiwan.
T-Y ChenAgricultural Biotechnology Research Center, Academia Sinica, Taipei, Taiwan.
S-T JiangNational Laboratory Animal Center, National Applied Research Laboratories, Taipei, Taiwan.
K-W ChenAgricultural Biotechnology Research Center, Academia Sinica, Taipei, Taiwan.
Y-M ChiangAgricultural Biotechnology Research Center, Academia Sinica, Taipei, Taiwan.
Y-J HsuAgricultural Biotechnology Research Center, Academia Sinica, Taipei, Taiwan.
Y-J LiuAgricultural Biotechnology Research Center, Academia Sinica, Taipei, Taiwan.
H-M ChenAgricultural Biotechnology Research Center, Academia Sinica, Taipei, Taiwan.
K K YokoyamaGraduate Institute of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
K-C TsaiNational Research Institute of Chinese Medicine, Ministry of Health and Welfare, Taipei, Taiwan.
H-H YehDrug Discovery and Development Center, Chia Nan University of Pharmacy and Science, Tainan, Taiwan.
Y-R ChenAgricultural Biotechnology Research Center, Academia Sinica, Taipei, Taiwan.
M-T YangAgricultural Biotechnology Research Center, Academia Sinica, Taipei, Taiwan.
C-Y YangAgricultural Biotechnology Research Center, Academia Sinica, Taipei, Taiwan.
W-C YangAgricultural Biotechnology Research Center, Academia Sinica, Taipei, Taiwan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Protein disulfide isomerase a4 (PDIA4) is implicated in the growth and death of tumor cells; however, its molecular mechanism and therapeutic potential in cancer are unclear. Here, we found that PDIA4 expression was upregulated in a variety of tumor cell lines and human lung adenocarcinoma tissues. Knockdown and overexpression of PDIA4 in tumor cells showed that PDIA4 facilitated cell growth via the reduction of caspases 3 and 7 activity. Consistently, Lewis lung carcinoma cells overexpressing PDIA4 grew faster than did parental cells in tumor-bearing mice, as shown by a reduced survival rate, increased tumor size and metastasis, and decreased cell death and caspases 3 and 7 activity. PDIA4 knockdown resulted in opposite outcomes. Moreover, results obtained in mice with spontaneous hepatoma indicated that PDIA4 deficiency significantly reduced hepatic tumorigenesis and cyst formation and increased mouse survival, tumor death, and caspases 3 and 7 activity. Mechanistic studies illustrated that PDIA4 negatively regulated tumor cell death by inhibiting degradation and activation of procaspases 3 and 7 via their mutual interaction in a CGHC-dependent manner. Finally, we found that 1,2-dihydroxytrideca-5,7,9,11-tetrayne, a PDIA4 inhibitor, reduced tumor development via enhancement of caspase-mediated cell death in TSA tumor-bearing mice. These findings characterize PDIA4 as a negative regulator of cancer cell apoptosis and suggest that PDIA4 is a potential therapeutic target for cancer.

Indexed as

AnimalsCaspasesCell Line, TumorEnzyme PrecursorsFemaleHEK293 CellsHep G2 CellsHumansJurkat CellsMaleMCF-7 CellsMelanoma, ExperimentalMiceMice, Inbred BALB CMice, Inbred C57BLProtein Disulfide-IsomerasesCaspasesEnzyme PrecursorsPDIA4 protein, humanPdia4 protein, mouseProtein Disulfide-Isomerases

Identifiers

PMID28534513

What OpenQuestion holds

Textmetadata
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.