Evidence map›Paper›PMID 25596082›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2015

Induction of S phase arrest and apoptosis by ethyl acetate extract from Tetrastigma hemsleyanum in human hepatoma HepG2 cells.

Xin Peng, Ding-ding Zhuang, Qiao-sheng Guo

Abstract read
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In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. In Vitro Cytotoxic Activity of Clinacanthus nutans Leaf Extracts Against HeLa CellsAsian Pacific journal of cancer prevention : APJCP · 2019
    Article
  7. RadixOncoTargets and therapy · 2018
    Article
  8. Ethylacetate extract fromCancer management and research · 2018
    Article
  9. Isoquercitrin, ingredients inCell adhesion & migration · 2018
    Article
  10. Article
  11. Review
  12. Ethylacetate extract from Tetrastigma hemsleyanum induces apoptosis via the mitochondrial caspase-dependent intrinsic pathway in HepG2 cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    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.

Xin PengInstitute and Department of Chinese Medicinal Materials, Nanjing Agricultural University, Nanjing, Jiangsu, People's Republic of China, 210095, px4142@163.com.
Ding-ding Zhuang
Qiao-sheng Guo
Nanjing Agricultural University · CNUniversity of Nottingham Ningbo China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tetrastigma hemsleyanum, a rare and endangered medicinal plant, has attracted much attention due to antitumor and immunomodulatory activities. In this study, the effect and mechanism of ethyl acetate extract from T. hemsleyanum (EET) on cell cycle and apoptosis in human hepatoma HepG2 cells were investigated. Twenty-five to 200 μg/mL of EET were found to have the antiproliferation effect toward HepG2 cells determined by MTT assay. The morphology of EET-treated HepG2 cells showed evidence of apoptosis that included blebbing and chromatin condensation, nucleic fragmentation, and so on. The DNA laddering assay confirmed that DNA fragmentation had occurred during late apoptosis. The cell-cycle analysis indicated that EET was able to induce S phase arrest and typical subdiploid peak in a dose- and time-dependent manner. The apoptosis rate of 200 μg/mL treatment for 24 h was 42.24 ± 4.90%. The protein expression of Bax and P53 was increased after treatment, while that of Bcl2 was significantly decreased in a dose-dependent manner, which suggested that a high Bax/Bcl2 ratio and an upregulated P53 might contribute to the pro-apoptotic activity of EET via the mitochondria-dependent pathway. The protein expression of cyclin-dependent kinase 1 (CDK1) was decreased in EET-treated HepG2 cells, suggesting that EET evoked S phase arrest possibly through the downregulation of cyclin A-CDK1 complex. In conclusion, the cytotoxicity on HepG2 cells induced by EET is a result of both cell-cycle arrest and apoptosis. Thus, it may have therapeutic potential for the treatment of liver cancer.

Indexed as

ApoptosisCarcinoma, HepatocellularCell ProliferationHep G2 CellsHumansLiver NeoplasmsMitochondriaPlant ExtractsS PhaseVitaceaePlant Extracts

Identifiers

PMID25596082
OpenAlexW2066370816

What OpenQuestion holds

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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.