Evidence map›Paper›PMID 32319631›Full record

ArticleMolecular medicine reports2020

TNF‑α‑mediated epithelial‑to‑mesenchymal transition regulates expression of immune checkpoint molecules in hepatocellular carcinoma.

Ritu Shrestha, Kim R Bridle, Darrell H G Crawford, Aparna Jayachandran

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.7field-weighted citation impact, top 14% 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

24 citing papers in PubMed, 28 citations in OpenAlex.

  1. RBMX2 linkseLife · 2025
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  14. CD73 and PD-L1 as Potential Therapeutic Targets in Gallbladder Cancer.International journal of molecular sciences · 2022
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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

4 authors at 2 institutions in 1 country.

Ritu ShresthaUniversity of Queensland, Faculty of Medicine, Greenslopes Private Hospital, Brisbane, QLD 4120, Australia.
Kim R BridleUniversity of Queensland, Faculty of Medicine, Greenslopes Private Hospital, Brisbane, QLD 4120, Australia.
Darrell H G CrawfordUniversity of Queensland, Faculty of Medicine, Greenslopes Private Hospital, Brisbane, QLD 4120, Australia.
Aparna JayachandranUniversity of Queensland, Faculty of Medicine, Greenslopes Private Hospital, Brisbane, QLD 4120, Australia.
Greenslopes Private Hospital · AUUniversity of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is the fastest growing cause of cancer‑related deaths globally. Epithelial‑to‑mesenchymal transition (EMT) is a cellular process that confers HCC tumor cells with the ability to evade the immune system. Immune escape in most tumors, including HCC, is controlled by immune checkpoint molecules. The aim of the present study was to investigate the association between EMT and immune checkpoint in HCC, and identify novel therapeutic targets for HCC. An in vitro model of reversible EMT was utilized based on cytokine tumor necrosis factor (TNF)‑α treatment of HCC cell lines Hep3B and PLC/PRF/5. Hep3B and PLC/PRF/5 cells were treated with TNF‑α, and the EMT status and the expression of immune checkpoint molecules was assessed by reverse transcription‑quantitative PCR, western blotting and immunofluorescence. To confirm an association between EMT and immune modulators, cells were exposed to culture medium with TNF‑α for 3 days to induce EMT, following which a reversal assay was performed. The expression of immune modulators and mesenchymal‑to‑epithelial transition (MET) status was investigated upon reversal of EMT. Furthermore, SurvExpress, a web‑based platform was utilized to analyze survival and recurrence in a dataset of patients with HCC. TNF‑α treatment for 3 days induced EMT in Hep3B and PLC/PRF/5 cells, as demonstrated by the downregulation of epithelial markers along with upregulation in mesenchymal markers. An EMT reversal assay was able to induce MET by increasing epithelial markers and decreasing mesenchymal markers. TNF‑α‑induced EMT led to the upregulation of immune modulators, including programmed death receptor ligand (PD‑L)1, PD‑L2, CD73 and B7‑H3. In contrast, reversal of EMT suppressed the expression of PD‑L1, PD‑L2, CD73 and B7‑H3. In addition, high expression of TNF‑α and PD‑L1 in 422 patients with HCC was associated with poor overall survival. The coordinate expression of TNF‑α with PD‑L2 in this patient cohort was associated with increased HCC recurrence. In conclusion, the present study demonstrated a close association between immune modulator expression and EMT induction/reversal driven by TNF‑α.

Indexed as

Epithelial-Mesenchymal TransitionCarcinoma, HepatocellularCell Line, TumorGene Expression Regulation, NeoplasticHumansImmune Checkpoint ProteinsKaplan-Meier EstimateLiver NeoplasmsTumor Necrosis Factor-alphaImmune Checkpoint ProteinsTumor Necrosis Factor-alphaepithelial-to-mesenchymal transitionhepatocellular carcinomaimmune checkpoint moleculesmesenchymal-to-epithelial transitionprogrammed death ligand-1tumor necrosis factor-α

Identifiers

PMID32319631
PMCPMC7057769
OpenAlexW3007681243

What OpenQuestion holds

Textmetadata
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.