Evidence map›Paper›PMID 31729681›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2020

CD147 augmented monocarboxylate transporter-1/4 expression through modulation of the Akt-FoxO3-NF-κB pathway promotes cholangiocarcinoma migration and invasion.

Paweena Dana, Saowaluk Saisomboon, Ryusho Kariya, Seiji Okada, Sumalee Obchoei, Kanlayanee Sawanyawisuth, Chaisiri Wongkham, Chawalit Pairojkul, Sopit Wongkham, Kulthida Vaeteewoottacharn

Abstract read
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.7field-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

17 citing papers in PubMed, 25 citations in OpenAlex.

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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

10 authors at 3 institutions in 2 countries.

Paweena DanaDepartment of Biochemistry, Faculty of Medicine, Khon Kaen University, Khon Kaen, 40005, Thailand.
Saowaluk SaisomboonDepartment of Biochemistry, Faculty of Medicine, Khon Kaen University, Khon Kaen, 40005, Thailand.
Ryusho KariyaDivision of Hematopoiesis, Joint Research Center for Human Retrovirus Infection and Graduate School of Medical Sciences, Kumamoto University, Kumamoto, 860-0811, Japan.
Seiji OkadaDivision of Hematopoiesis, Joint Research Center for Human Retrovirus Infection and Graduate School of Medical Sciences, Kumamoto University, Kumamoto, 860-0811, Japan.
Sumalee ObchoeiDepartment of Biochemistry, Faculty of Science, Prince of Songkla University, Songkhla, 90110, Thailand.
Kanlayanee SawanyawisuthDepartment of Biochemistry, Faculty of Medicine, Khon Kaen University, Khon Kaen, 40005, Thailand.
Chaisiri WongkhamDepartment of Biochemistry, Faculty of Medicine, Khon Kaen University, Khon Kaen, 40005, Thailand.
Chawalit PairojkulCholangiocarcinoma Research Institute, Khon Kaen University, Khon Kaen, 40002, Thailand.
Sopit WongkhamDepartment of Biochemistry, Faculty of Medicine, Khon Kaen University, Khon Kaen, 40005, Thailand.
Kulthida VaeteewoottacharnDepartment of Biochemistry, Faculty of Medicine, Khon Kaen University, Khon Kaen, 40005, Thailand. kulthidava@kku.ac.th.ORCID http://orcid.org/0000-0001-6557-9680
Khon Kaen University · THKumamoto University · JPPrince of Songkla University · TH

Funding

Khon Kaen University KKU61003502Thailand Research Fund DBG5980004Thailand Research Fund RTA5780012
6 · The paper itself

Abstract

purposeCholangiocarcinoma (CCA) is an aggressive type of cancer. The major obstacles for treatment are its late presentation and the occurrence metastases. Targeting the metastatic process may serve as a treatment option. CD147 is a membrane protein that promotes CCA metastasis. High lactate levels in CCA are predicted to result from lactate dehydrogenase A expression and sensitivity to monocarboxylate transporter (MCT) inhibitors. An involvement of CD147 in MCT maturation has been reported, but the exact role of MCT in CCA is not clear. Here, we aimed to assess the mechanism of CD147-promoted CCA progression through MCT regulation.

methodsThe expression levels of CD147 and MCT-1/4 in human CCA tissues were determined by immunohistochemistry. Two CD147 knockout (CD147 KO) CCA cell (KKU-213) clones were established using the CRISPR/Cas9 system. Cell migration and invasion were determined using a Boyden chamber assay. Temporal protein levels were modified by siRNA, specific inhibitors and/or activators. The expression of target proteins was determined using Western blot analyses.

resultsCD147 and MCT-1/4 were found to be overexpressed in CCA tissues compared to normal bile duct tissues. In addition, we found that CD147 knockdown significantly alleviated CCA cell migration and invasion, concomitant with decreased pAkt, pFoxO3, pNF-κB (pp65) and MCT-1/4 levels. Conversely, we found that FoxO3 knockdown led to recovered migration/invasion abilities and increased pp65 and MCT-1/4 expression levels. The involvement of Akt in the regulation of MCT-1/4 expression through CD147 was established by inhibition and activation of Akt phosphorylation.

conclusionOur data indicate that CD147 promotes the malignant progression of CCA cells by activating the Akt-FoxO3-NF-κB-MCT-1/4 axis. As such, CD147 may serve as a possible target for advanced CCA treatment.

Indexed as

BasiginBile Duct NeoplasmsBlotting, WesternCell Line, TumorCell MovementCholangiocarcinomaForkhead Box Protein O3Gene Expression Regulation, NeoplasticHumansMonocarboxylic Acid TransportersNeoplasm InvasivenessNF-kappa BProteinsProto-Oncogene Proteins c-aktRNA InterferenceSignal TransductionBasiginForkhead Box Protein O3Monocarboxylic Acid TransportersNF-kappa BProteinsProto-Oncogene Proteins c-aktAktCD147CholangiocarcinomaFoxO3MCTNF-κB

Identifiers

PMID31729681
PMCPMC12990748
OpenAlexW2986252592

What OpenQuestion holds

Textmetadata
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.