Evidence map›Paper›PMID 30687637›Full record

ArticleFrontiers in oncology2018

PDCD4 Knockdown Induces Senescence in Hepatoma Cells by Up-Regulating the p21 Expression.

Jing Guo, Iwata Ozaki, Jinghe Xia, Takuya Kuwashiro, Motoyasu Kojima, Hirokazu Takahashi, Kenji Ashida, Keizo Anzai, Sachiko Matsuhashi

Open access · goldAbstract read
In one paragraph

Article in Frontiers in oncology, 2018. 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
1.3field-weighted citation impact, top 18% 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, 26 citations in OpenAlex.

  1. Review
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  6. Review
  7. The Impact of Pdcd4, a Translation Inhibitor, on Drug Resistance.Pharmaceuticals (Basel, Switzerland) · 2024
    Review
  8. Article
  9. Article
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  12. Article
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  14. Article
  15. Control Mechanisms of the Tumor Suppressor PDCD4: Expression and Functions.International journal of molecular sciences · 2019
    Review
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

9 authors at 1 institution in 1 country.

Jing GuoDivision of Hepatology, Diabetology and Endocrinology, Department of Internal Medicine, Saga Medical School, Saga University, Saga, Japan.
Iwata OzakiDivision of Hepatology, Diabetology and Endocrinology, Department of Internal Medicine, Saga Medical School, Saga University, Saga, Japan.
Jinghe XiaDivision of Hepatology, Diabetology and Endocrinology, Department of Internal Medicine, Saga Medical School, Saga University, Saga, Japan.
Takuya KuwashiroDivision of Hepatology, Diabetology and Endocrinology, Department of Internal Medicine, Saga Medical School, Saga University, Saga, Japan.
Motoyasu KojimaDivision of Hepatology, Diabetology and Endocrinology, Department of Internal Medicine, Saga Medical School, Saga University, Saga, Japan.
Hirokazu TakahashiDivision of Hepatology, Diabetology and Endocrinology, Department of Internal Medicine, Saga Medical School, Saga University, Saga, Japan.
Kenji AshidaDivision of Hepatology, Diabetology and Endocrinology, Department of Internal Medicine, Saga Medical School, Saga University, Saga, Japan.
Keizo AnzaiDivision of Hepatology, Diabetology and Endocrinology, Department of Internal Medicine, Saga Medical School, Saga University, Saga, Japan.
Sachiko MatsuhashiDivision of Hepatology, Diabetology and Endocrinology, Department of Internal Medicine, Saga Medical School, Saga University, Saga, Japan.
Saga University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

While the over-expression of tumor suppressor programmed cell death 4 (PDCD4) induces apoptosis, it was recently shown that PDCD4 knockdown also induced apoptosis. In this study, we examined the cell cycle regulators whose activation is affected by PDCD4 knockdown to investigate the contribution of PDCD4 to cell cycle regulation in three types of hepatoma cells: HepG2, Huh7 (mutant p53 and p16-deficient), and Hep3B (p53- and Rb-deficient). PDCD4 knockdown suppressed cell growth in all three cell lines by inhibiting Rb phosphorylation via down-regulating the expression of Rb itself and CDKs, which phosphorylate Rb, and up-regulating the expression of the CDK inhibitor p21 through a p53-independent pathway. We also found that apoptosis was induced in a p53-dependent manner in PDCD4 knockdown HepG2 cells (p53+), although the mechanism of cell death in PDCD4 knockdown Hep3B cells (p53-) was different. Furthermore, PDCD4 knockdown induced cellular senescence characterized by β-galactosidase staining, and p21 knockdown rescued the senescence and cell death as well as the inhibition of Rb phosphorylation induced by PDCD4 knockdown. Thus, PDCD4 is an important cell cycle regulator of hepatoma cells and may be a promising therapeutic target for the treatment of hepatocellular carcinoma.

Indexed as

apoptosishepatoma cellsp21PDCD4senescence

Identifiers

PMID30687637
PMCPMC6334536
OpenAlexW2768317570

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.