Evidence map›Paper›PMID 27654866›Full record

ArticleBMC cancer2016

Bicyclol induces cell cycle arrest and autophagy in HepG2 human hepatocellular carcinoma cells through the PI3K/AKT and Ras/Raf/MEK/ERK pathways.

Yu Wang, Hao Nie, Xin Zhao, Yong Qin, Xingguo Gong

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

25 citing papers in PubMed, 68 citations in OpenAlex.

  1. The Interplay between Autophagy and Mitochondria in Cancer.International journal of molecular sciences · 2024
    Review
  2. An overview of pyridazin-3(2Future medicinal chemistry · 2024
    Review
  3. Article
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  5. Molecules (Basel, Switzerland) · 2023
    Review
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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

5 authors at 1 institution in 1 country.

Yu WangInstitute of Biochemistry, College of Life Sciences, Zijingang campus, Zhejiang University, Room 345, Hangzhou, 310058, Zhejiang, China.
Hao NieInstitute of Biochemistry, College of Life Sciences, Zijingang campus, Zhejiang University, Room 345, Hangzhou, 310058, Zhejiang, China.
Xin ZhaoInstitute of Biochemistry, College of Life Sciences, Zijingang campus, Zhejiang University, Room 345, Hangzhou, 310058, Zhejiang, China.
Yong QinInstitute of Biochemistry, College of Life Sciences, Zijingang campus, Zhejiang University, Room 345, Hangzhou, 310058, Zhejiang, China. happy_ququ@126.com.
Xingguo GongInstitute of Biochemistry, College of Life Sciences, Zijingang campus, Zhejiang University, Room 345, Hangzhou, 310058, Zhejiang, China. gongxg@zju.edu.cn.
Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBicyclol, a novel synthetic antihepatitis drug, is widely known to protect against liver injury. However, few reports have focused on the possible effect of bicyclol on anti-proliferation and autophagy induction in cancer cells, particularly hepatocellular carcinoma cells.

methodsIn this study, we investigated the antitumor efficacy of Bicyclol in HepG2 cells and the mechanism of cell growth inhibition. Cell proliferation was analyzed by MTT assay, and the cell cycle and apoptosis were assessed by flow cytometry. And we transfected the cells with the GFP-RFP-LC3 vector to detect the autophagy flux in the cells. Mechanisms of bicyclol-induced cell growth inhibition were probed by western blot analysis.

resultsBicyclol effectively inhibited HepG2 cell proliferation in a dose- and time-dependent manner. In addition, we found that bicyclol inhibited cell cycle progression at G1 phase and induced autophagy in HepG2 cells, which implied that the significant decrease in cell proliferation was mainly induced by autophagy and inhibition of cell proliferation. Furthermore, western blot showed that bicyclol inhibited phosphorylation of Akt and ERK, down-regulated the expressions of cyclin D1, cyclin E2, CDK2, CDK4, p-Rb and p-mTOR. Moreover, AKT or ERK knockdown by siRNA enhanced bicyclol-induced autophagy and inhibition of cell proliferation.

conclusionThese results suggest that bicyclol has potent anti-proliferative activity against malignant human hepatoma cells via modulation of the PI3K/AKT pathway and the Ras/Raf/MEK/ERK pathway, and indicate that bicyclol is a potential liver cancer drug worthy of further research and development.

Indexed as

AKTAutophagyBicyclolCell cycleERKHepG2

Identifiers

PMID27654866
PMCPMC5031284
OpenAlexW2522460275

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.