Evidence map›Paper›PMID 38114514›Full record

ArticleScientific reports2023

Upregulated LAMA3 modulates proliferation, adhesion, migration and epithelial‑to‑mesenchymal transition of cholangiocarcinoma cells.

Kittiya Islam, Brinda Balasubramanian, Simran Venkatraman, Parichut Thummarati, Janpen Tunganuntarat, Nut Phueakphud, Phongthon Kanjanasirirat, Tanawadee Khumpanied, Pornparn Kongpracha, Yingpinyapat Kittirat and 6 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
4.8field-weighted citation impact, top 4% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Pooled it
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  8. HEYL-mediated activation of LAMA3 influences radiotherapy response in esophageal cancer.Esophagus : official journal of the Japan Esophageal Society · 2025
    Article
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  10. PPY-Induced iCAFs Cultivate an Immunosuppressive Microenvironment in Pancreatic Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 4 institutions in 1 country.

Kittiya IslamDepartment of Biochemistry, Faculty of Science, Mahidol University, Bangkok, 10400, Thailand.ORCID http://orcid.org/0000-0001-9266-4434
Brinda BalasubramanianDepartment of Biochemistry, Faculty of Science, Mahidol University, Bangkok, 10400, Thailand.ORCID http://orcid.org/0000-0003-4808-9748
Simran VenkatramanGraduate Program in Molecular Medicine, Faculty of Science, Mahidol University, Bangkok, 10400, Thailand.ORCID http://orcid.org/0000-0002-2037-0952
Parichut ThummaratiDepartment of Clinical Chemistry, Faculty of Allied Health Sciences, Chulalongkorn University, Bangkok, 10330, Thailand.ORCID http://orcid.org/0000-0002-0308-0769
Janpen TunganuntaratDepartment of Biochemistry, Faculty of Science, Mahidol University, Bangkok, 10400, Thailand.ORCID http://orcid.org/0000-0002-0447-2246
Nut PhueakphudDepartment of Biochemistry, Faculty of Science, Mahidol University, Bangkok, 10400, Thailand.
Phongthon KanjanasiriratExcellent Center for Drug Discovery (ECDD), Faculty of Science, Mahidol University, Bangkok, 10400, Thailand.ORCID http://orcid.org/0000-0002-1046-7152
Tanawadee KhumpaniedExcellent Center for Drug Discovery (ECDD), Faculty of Science, Mahidol University, Bangkok, 10400, Thailand.
Pornparn KongprachaDepartment of Biochemistry, Faculty of Science, Mahidol University, Bangkok, 10400, Thailand.ORCID http://orcid.org/0000-0003-1759-213X
Yingpinyapat KittiratDepartment of Biochemistry, Faculty of Medicine, Khon Kaen University, Khon Kaen, 40002, Thailand.
Rutaiwan TohtongDepartment of Biochemistry, Faculty of Science, Mahidol University, Bangkok, 10400, Thailand.ORCID http://orcid.org/0000-0003-3670-1004
Tavan JanvilisriDepartment of Biochemistry, Faculty of Science, Mahidol University, Bangkok, 10400, Thailand.ORCID http://orcid.org/0000-0002-6376-5575
Patompon WongtrakoongateDepartment of Biochemistry, Faculty of Science, Mahidol University, Bangkok, 10400, Thailand.ORCID http://orcid.org/0000-0001-6070-1843
Suparerk BorwornpinyoExcellent Center for Drug Discovery (ECDD), Faculty of Science, Mahidol University, Bangkok, 10400, Thailand.ORCID http://orcid.org/0000-0001-6211-3615
Nisana NamwatDepartment of Biochemistry, Faculty of Medicine, Khon Kaen University, Khon Kaen, 40002, Thailand.ORCID http://orcid.org/0000-0002-6743-5047
Tuangporn SuthiphongchaiDepartment of Biochemistry, Faculty of Science, Mahidol University, Bangkok, 10400, Thailand. tuangporn.sut@mahidol.ac.th.ORCID http://orcid.org/0000-0002-0124-7780
Mahidol University · THChulalongkorn University · THKhon Kaen University · THMinistry of Public Health · TH

Funding

Basic Research Funding: Fiscal year 2021, Mahidol University BRF2-NDFR21/2564
6 · The paper itself

Abstract

A poor outcome for cholangiocarcinoma (CCA) patients is still a clinical challenge. CCA is typically recognized by the desmoplastic nature, which accounts for its malignancy. Among various extracellular matrix proteins, laminin is the most potent inducer for CCA migration. Herein, we accessed the expression profiles of laminin gene family and explored the significance of the key laminin subunit on CCA aggressiveness. Of all 11 laminin genes, LAMA3, LAMA5, LAMB3 and LAMC2 were concordantly upregulated based on the analysis of multiple public transcriptomic datasets and also overexpressed in Thai CCA cell lines and patient tissues in which LAMA3A upregulated in the highest frequency (97%) of the cases. Differential expression genes (DEGs) analysis of low and high laminin signature groups revealed LAMA3 as the sole common DEG in all investigated datasets. Restratifying CCA samples according to LAMA3 expression indicated the association of LAMA3 in the focal adhesion pathway. Silencing LAMA3 revealed that it plays important roles in CCA cell proliferation, adhesion, migration and epithelial-to-mesenchymal transition. Taken together, this research signifies the roles of dysregulated ECM homeostasis in CCA malignancy and highlights, for the first time, the potential usage of LAMA3 as the diagnostic biomarker and the therapeutic target to tackle the CCA stromal.

Indexed as

Bile Duct NeoplasmsCholangiocarcinomaBile Ducts, IntrahepaticCell Adhesion MoleculesCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansLamininCell Adhesion MoleculesLaminin

Identifiers

PMID38114514
PMCPMC10730521
OpenAlexW4389952197

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.