Evidence map›Paper›PMID 32509204›Full record

ReviewAmerican journal of translational research2020

Dedifferentiation of hepatocellular carcinoma: molecular mechanisms and therapeutic implications.

Jiashuo Chao, Senlin Zhao, Hongcheng Sun

Open access · greenAbstract readReview
In one paragraph

Review in American journal of translational research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

29 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
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  5. Review
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  11. A Novel Transgenic Mouse Model ImplicatesInternational journal of molecular sciences · 2023
    Article
  12. Article
  13. HCV Core protein represses DKK3 expression via epigenetic silencing and activates the Wnt/β-catenin signaling pathway during the progression of HCC.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    Article
  14. Article
  15. Review
  16. Article
  17. Notch-Sox9 Axis Mediates Hepatocyte Dedifferentiation inInternational journal of molecular sciences · 2022
    Article
  18. Article
  19. Article
  20. Article
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

3 authors at 2 institutions in 1 country.

Jiashuo ChaoDepartment of General Surgery, Shanghai General Hospital, Shanghai Jiaotong University School of Medicine Shanghai 200080, China.
Senlin ZhaoDepartment of Colorectal Surgery, Fudan University Shanghai Cancer Center Shanghai 200032, China.
Hongcheng SunDepartment of General Surgery, Shanghai General Hospital, Shanghai Jiaotong University School of Medicine Shanghai 200080, China.
Shanghai First People's Hospital · CNFudan University Shanghai Cancer Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is a common cancer with high morbidity and mortality. Poorer differentiation status indicates worse prognosis of HCC patients. Regain of better differentiation status may improve the prognosis. Differentiation therapy for HCC is based on the fact that agents may reverse the dedifferentiation process from hepatocytes to HCC cells and thus improve tumor differentiation status. Reversal of progenitor-like property and restoration of hepatic characteristics are main objectives of HCC differentiation therapy. Comprehending the mechanisms of HCC dedifferentiation provides ideas for drug design. Diverse dysregulated molecules and signalings cooperatively cause HCC dedifferentiation. Dysregulation of liver enriched transcription factors, especially hepatocyte nuclear factor 4α, was a critical determinant of HCC dedifferentiation. Aberrant pivotal signaling molecules such as transforming factor-β, β-catenin and Yes-associated protein caused disordered signalings, which promoted HCC dedifferentiation. Loss of epithelial morphology during epithelial-mesenchymal transition (EMT) concurred with HCC dedifferentiation. Some EMT-related molecules exerted double-sided role in concurrently inducing EMT and HCC dedifferentiation. Besides, microRNAs (e.g. miR-122 and miR-148a) as well as some impressive proteins (i.e. KLF4, gankyrin and CHD1L) functioned in manipulating HCC differentiation status. Restoring normal expression levels of these molecules could induce HCC differentiation and inhibited malignant tumor behaviors. Based on the knowledge above, some agents have been found effective in lab, but need more data to support their reliability. Additionally, peretinoin as a potential drug is in progress of several phase III clinical trials. It's promising that differentiation therapy for HCC may be a part of options in future HCC treatment.

Indexed as

dedifferentiationdifferentiation therapyepithelial-mesenchymal transitionHepatocellular carcinomaliver cancer stem cellmolecular mechanism

Identifiers

PMID32509204
PMCPMC7269980
OpenAlexW3033956554

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.