Evidence map›Paper›PMID 32986368›Full record

ArticleAsian Pacific journal of cancer prevention : APJCP2020

Anti-Proliferative Effects of Compound A and Its Effect in Combination with Cisplatin in Cholangiocarcinoma Cells.

Mutita Junking, Thidarath Rattanaburee, Aussara Panya, Irina Budunova, Guy Haegeman, Pa-Thai Yenchitsomanus

Open access · goldAbstract read
In one paragraph

Article in Asian Pacific journal of cancer prevention : APJCP, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

0 citing papers in PubMed, 3 citations in OpenAlex.

No citing paper in PubMed yet.

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

6 authors at 3 institutions in 2 countries.

Mutita JunkingDivision of Molecular Medicine, Research Department, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand.ORCID 0000-0002-8347-3000
Thidarath RattanabureeDivision of Molecular Medicine, Research Department, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand.
Aussara PanyaDepartment of Biology, Faculty of Science, Chiang Mai University, Chiang Mai, Thailand.
Irina BudunovaDepartment of Dermatology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
Guy HaegemanLaboratory of Eukaryotic Gene Expression and Signal Transduction (LEGEST), Department of Physiology, Faculty of Sciences, Ghent University, Ghent, Belgium.
Pa-Thai YenchitsomanusDivision of Molecular Medicine, Research Department, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand.
Siriraj Hospital · THChiang Mai University · THNorthwestern University · US

Funding

REDD1 dissociates the therapeutic and adverse effects of glucocorticoids in skinR01AI125366 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI BUDUNOVA, IRINA · 2017 to 2021
$2.4M
NIAID NIH HHS R01 AI125366
6 · The paper itself

Abstract

backgroundCholangiocarcinoma (CCA) is a fatal cancer with high resistance to anticancer drugs.  The development of new drugs or compounds to be used alone or in combination with currently available chemotherapeutic agents to improve the treatment of CCA is needed. Compound A (CpdA), which is a small plant-derived glucocorticoid receptor modulator, strongly inhibited the growth and survival of several cancers.  However, the effect of CpdA on cholangiocarcinoma has not been elucidated. The aim of this study was to investigate the effect of CpdA on CCA.

methodsCytotoxicity of CpdA was tested in primary cells including peripheral blood mononuclear cells (PBMCs), fibroblasts, and human umbilical vein endothelial cells (HUVECs), as well as on CCA cell lines (KKU-100, KKU-055, and KKU-213) was examined. Cell cycle distribution and IL-6 expression was assessed by flow cytometry and real-time polymerase chain reaction, respectively.  The effect of combination CpdA and cisplatin was evaluated by cell viability assay.

resultsCpdA significantly inhibited cell cycle at G1 phase in CCA cell lines, and reduced IL-6 mRNA expression.  However, combination CpdA and cisplatin did not enhance the inhibitory effect. TGFβR-II expression was increased in CCA cells after the combination treatment.

conclusionsThese results indicate the potential of CpdA for CCA treatment. However, combination treatment with CpdA and cisplatin increased CCA cell survival. The molecular mechanism is likely attributable to promotes cell survival via the TGFβR-II signaling pathway. The combination of CpdA with other anticancer drugs for CCA treatment should be further examined.

Indexed as

AcetatesAnti-Inflammatory Agents, Non-SteroidalAntineoplastic AgentsApoptosisBile Duct NeoplasmsCell CycleCell ProliferationCholangiocarcinomaCisplatinDrug Therapy, CombinationHumansLeukocytes, MononuclearTumor Cells, CulturedTyramine2-(4-acetoxyphenyl)-2-chloro-N-methylethylamineAcetatesAnti-Inflammatory Agents, Non-SteroidalAntineoplastic AgentsCisplatinTyramineBile duct cancercholangiocarcinomaCompound AGlucocorticoidInterleukin-6

Identifiers

PMID32986368
PMCPMC7779449
OpenAlexW3091342456

What OpenQuestion holds

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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.