Evidence map›Paper›PMID 34837922›Full record

ArticleAsian Pacific journal of cancer prevention : APJCP2021

Suppression of Cholangiocarcinoma Cell Growth and Proliferation by Atractylodes lancea (Thunb) DC. through ERK-Signaling Cascade.

Pongsakorn Martviset, Luxsana Panrit, Pathanin Chantree, Phunuch Muhamad, Kesara Na-Bangchang

Open access · goldAbstract read
In one paragraph

Article in Asian Pacific journal of cancer prevention : APJCP, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

7 citing papers in PubMed, 8 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Ethyl Acetate Extract ofPreventive nutrition and food science · 2023
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  5. Article
  6. Article
  7. Molecular Cloning and Characterization of aPathogens (Basel, Switzerland) · 2022
    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

5 authors at 1 institution in 1 country.

Pongsakorn MartvisetDivision of Parasitology, Department of Preclinical Science, Faculty of Medicine, Thammasat University, Pathumthani, Thailand.ORCID 0000-0003-4168-5950
Luxsana PanritCenter of Excellence in Molecular Biology and Pharmacology of Malaria and Cholangiocarcinoma, Thammasat University, Pathumthani, Thailand.
Pathanin ChantreeDivision of Anatomy, Department of Preclinical Science, Faculty of Medicine, Thammasat University, Pathumthani, Thailand.ORCID 0000-0003-4974-9584
Phunuch MuhamadCenter of Excellence in Molecular Biology and Pharmacology of Malaria and Cholangiocarcinoma, Thammasat University, Pathumthani, Thailand.
Kesara Na-BangchangCenter of Excellence in Molecular Biology and Pharmacology of Malaria and Cholangiocarcinoma, Thammasat University, Pathumthani, Thailand.ORCID 0000-0001-6389-0897
Thammasat University · TH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThe study aimed to investigate the inhibitory effects of AL on the ERK signaling molecules (ERK, p-ERK, cyclin D, and eIF4B) and the growth and proliferation of CCA cells. MATERIALS AND

methodsThe viability of the three CCA cell lines CL-6, HuCCT1, and HuH28 was determined using MTT assay. The effect of Ras/ERK inhibitors on protein expression in the presence of AL extract was investigated. The protein extracted from each CCA cell following exposure to AL and/or Ras/ERK inhibitors were separated on 12.5% SDS-PAGE. The analysis of mRNA expression following 48 and 72 hours of AL exposure in comparison with 0 hours (non-exposed cells) was performed by using RT-PCR.

resultsThe potency of cytotoxic activity of AL (by MTT assay) was about three times higher than the standard drug 5-fluorouracil. The IC50 (concentration that inhibits cell growth by 50%) of AL for the CL-6, HuCCT-1 and HuH28 cell lines were 29.77±6.64, 35.45±4.96, and 35.32±6.69 µg/mL (mean+SD), respectively. The cells were exposed to AL extract at the IC50 for 0, 12, 24, 48, and 72 hours in the absence and presence of Ras/ERK inhibitors (salirasib and XMD8-92). Protein expression was determined by Western blot analysis. The results suggested the lack of significant inhibitory effect of AL on ERK at 48 and 72 hours of exposure in all CCA cell types. On the other hand, a significant inhibitory effect was observed with p-ERK expression in all CCA cell types. Cyclin D was significantly down-regulated at 72 hours of exposure in all cell types with different potencies. The expression of eIF4B was markedly inhibited in HuCCT-1 but slightly inhibited in CL-6 and HuH28 cells. Real-time PCR analysis revealed significant down-regulation of ERK following 72 hours of AL exposure in the HuCCT1 and HuH28, but not CL-6 cell.

conclusionThe ERK signaling cascade and downstream molecules are potential targets of action of AL in CCA.

Indexed as

AtractylodesAntineoplastic AgentsBile Duct NeoplasmsCell Growth ProcessesCell Line, TumorCell ProliferationCholangiocarcinomaDown-RegulationFluorouracilHumansMAP Kinase Signaling SystemPlant ExtractsProtein Kinase InhibitorsSignal TransductionAntineoplastic AgentsFluorouracilPlant ExtractsProtein Kinase InhibitorsAnticancerBile duct cancerextracellular signal-regulated kinase

Identifiers

PMID34837922
PMCPMC9068173
OpenAlexW3215689442

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.