Evidence map›Paper›PMID 36672157›Full record

ArticleCells2023

Polydatin Inhibits Hepatocellular Carcinoma Cell Proliferation and Sensitizes Doxorubicin and Cisplatin through Targeting Cell Mitotic Machinery.

Umar Farooq, Hao Wang, Jingru Hu, Guangyue Li, Shah Jehan, Jinming Shi, Dangdang Li, Guangchao Sui

Open access · goldAbstract read
In one paragraph

Article in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
3.9field-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

11 citing papers in PubMed, 17 citations in OpenAlex.

  1. Polydatin: A natural compound with multifaceted anticancer properties.Journal of traditional and complementary medicine · 2025
    Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. 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

8 authors at 2 institutions in 1 country.

Umar FarooqCollege of Life Sciences, Northeast Forestry University, 26 Hexing Road, Harbin 150040, China.
Hao WangCollege of Life Sciences, Northeast Forestry University, 26 Hexing Road, Harbin 150040, China.
Jingru HuKey Laboratory of Cell Proliferation and Differentiation of the Ministry of Education and State Key Laboratory of Membrane Biology, College of Life Sciences, Peking University, Beijing 100871, China.
Guangyue LiCollege of Life Sciences, Northeast Forestry University, 26 Hexing Road, Harbin 150040, China.
Shah JehanCollege of Life Sciences, Northeast Forestry University, 26 Hexing Road, Harbin 150040, China.
Jinming ShiCollege of Life Sciences, Northeast Forestry University, 26 Hexing Road, Harbin 150040, China.
Dangdang LiCollege of Life Sciences, Northeast Forestry University, 26 Hexing Road, Harbin 150040, China.
Guangchao SuiCollege of Life Sciences, Northeast Forestry University, 26 Hexing Road, Harbin 150040, China.ORCID 0000-0002-8164-5585
Northeast Forestry University · CNPeking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Polydatin (PD) is a natural compound with anticancer activities, but the underlying mechanisms remain largely unclear. To understand how PD inhibited hepatocellular carcinoma (HCC), we studied PD treatments in HCC HepG2 and SK-HEP1 cells, and normal liver HL-7702 cells. PD selectively blocked the proliferation of HCC cells but showed low toxicity in normal cells, while the effects of doxorubicin (DOX) and cisplatin (DDP) on HCC and normal liver cells were opposite. In the cotreatment studies, PD synergistically improved the inhibitory activities of DOX and DDP in HCC cells but alleviated their toxicity in HL-7702 cells. Furthermore, RNA-seq studies of PD-treated HepG2 cells revealed multiple altered signaling pathways. We identified 1679 Differentially Expressed Genes (DEGs) with over a 2.0-fold change in response to PD treatment. Integrative analyses using the DEGs in PD-treated HepG2 cells and DEGs in a TCGA dataset of HCC patients revealed five PD-repressed DEGs regulating mitotic spindle midzone formation. The expression of these genes showed significantly positive correlation with poor clinical outcomes of HCC patients, suggesting that mitotic machinery was likely a primary target of PD. Our findings improve the understanding of PD's anticancer mechanisms and provide insights into developing effective clinical approaches in HCC therapies.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsCell Line, TumorCell ProliferationCisplatinDoxorubicinGlucosidesHumansStilbenesCisplatinDoxorubicinGlucosidespolydatinStilbenesanticancer activitycell mitosisdifferential gene expressionhepatocellular carcinomapolydatinsynergism

Identifiers

PMID36672157
PMCPMC9856937
OpenAlexW4313500208

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.