Evidence map›Paper›PMID 32677672›Full record

ArticleBioscience reports2020

Erianin suppresses hepatocellular carcinoma cells through down-regulation of PI3K/AKT, p38 and ERK MAPK signaling pathways.

Liang Yang, Yue Hu, Guanbao Zhou, Qi Chen, Zhenshun Song

Open access · goldAbstract read
In one paragraph

Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
4.2field-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

19 citing papers in PubMed, 43 citations in OpenAlex.

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  7. Exploration of the Mechanism of Action ofJournal of hepatocellular carcinoma · 2025
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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 2 institutions in 1 country.

Liang YangDepartment of General Surgery, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, China.
Yue HuDepartment of Hepatobiliary Surgery, Ningbo First Hospital, Zhejiang Province 315010, China.
Guanbao ZhouDepartment of Hepatobiliary Surgery, Ningbo First Hospital, Zhejiang Province 315010, China.
Qi ChenDepartment of Hepatobiliary Surgery, Ningbo First Hospital, Zhejiang Province 315010, China.
Zhenshun SongDepartment of General Surgery, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, China.
Ningbo First Hospital · CNTongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHepatocellular carcinoma (HCC) is the dominant pathological type of primary liver cancer and no effective methods are available for its treatment. Erianin is a natural product extracted from Dendrobium, which possesses multiple pharmacological activities, including antioxidative and antitumor activity.

objectiveTo evaluate the anti-HCC activities of erianin and explore its underlying mechanism.

methodsMTT assay and Crystal Violet staining assay were used to select the non-toxic concentrations for the subsequent experiments. The colony formation assay and PCNA fluorescent staining were used to investigate the antiproliferative effects of erianin on human SMMC-7721 and HepG2 cells. Wound healing and transwell test were used to analyze cell migration and invasion. Caspase3 and Tunel staining were used to detect apoptosis. Western blot was used to examine the expression levels of proteins associated with invasion and key proteins in the phosphatidylinositol-3-kinase/protein kinase B (PI3K/Akt), p38 and ERK mitogen-activated protein kinase (MAPK) signaling pathways.

resultsErianin inhibited HCC cell proliferation in a dose-dependent manner. Decreased migration rate and invaded cells were observed with erianin supplement. The expression of invasion-associated proteins in the erianin group was also down-regulated. Besides, more apoptotic cells were observed after erianin treatment. For the molecular mechanism, erianin inhibited the phosphorylation of Akt, ERK and P38 in the PI3K/Akt and ERK/P38 pathway.

conclusionWe demonstrated, for the first time, that erianin inhibited the proliferation, migration, invasion and induced the apoptosis of HCC through PI3K/Akt, p38 and ERK MAPK signaling pathway, indicating that erianin is a promising agent for the HCC treatment.

Indexed as

ApoptosisBibenzylsCarcinoma, HepatocellularCell ProliferationDown-RegulationDrug Screening Assays, AntitumorGene Expression Regulation, NeoplasticHep G2 CellsHumansLiver NeoplasmsMAP Kinase Signaling SystemNeoplasm InvasivenessPhenolPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAKT1 protein, humanBibenzylsErianinPhenolPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akterianinhepatocellular carcinomap38 and ERK MAPKPI3K/Akt

Identifiers

PMID32677672
PMCPMC7385585
OpenAlexW3043427509

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.