Evidence map›Paper›PMID 37026527›Full record

ArticleCancer science2023

Establishment and characterization of a novel cancer stem-like cell of cholangiocarcinoma.

Orasa Panawan, Atit Silsirivanit, Chih-Hsiang Chang, Siyaporn Putthisen, Piyanard Boonnate, Taro Yokota, Yuki Nishisyama-Ikeda, Marutpong Detarya, Kanlayanee Sawanyawisuth, Worasak Kaewkong and 10 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. 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

20 authors at 4 institutions in 2 countries.

Orasa PanawanDepartment of Tumor Genetics and Biology, Graduate School of Medical Sciences, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Atit SilsirivanitDepartment of Tumor Genetics and Biology, Graduate School of Medical Sciences, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.ORCID https://orcid.org/0000-0002-5777-3843
Chih-Hsiang ChangDepartment of Tumor Genetics and Biology, Graduate School of Medical Sciences, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Siyaporn PutthisenDepartment of Biochemistry, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand.
Piyanard BoonnateDivision of Hematopoiesis, Joint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto, Japan.
Taro YokotaDepartment of Tumor Genetics and Biology, Graduate School of Medical Sciences, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Yuki Nishisyama-IkedaDepartment of Tumor Genetics and Biology, Graduate School of Medical Sciences, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Marutpong DetaryaDepartment of Tumor Genetics and Biology, Graduate School of Medical Sciences, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Kanlayanee SawanyawisuthDepartment of Biochemistry, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand.
Worasak KaewkongDepartment of Biochemistry, Faculty of Medical Sciences, Naresuan University, Phitsanulok, Thailand.
Kanha MuisukDepartment of Forensic Medicine, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand.
Sukanya LuangDepartment of Biochemistry, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand.
Kulthida VaeteewoottacharnDepartment of Biochemistry, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand.
Ryusho KariyaDivision of Hematopoiesis, Joint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto, Japan.
Hiromu YanoDepartment of Cell Pathology, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Yoshihiro KomoharaDepartment of Cell Pathology, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.ORCID https://orcid.org/0000-0001-9723-0846
Kunimasa OhtaDepartment of Stem Cell Biology, Faculty of Arts and Science, Kyushu University, Fukuoka, Japan.
Seiji OkadaDivision of Hematopoiesis, Joint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto, Japan.
Sopit WongkhamDepartment of Biochemistry, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand.
Norie ArakiDepartment of Tumor Genetics and Biology, Graduate School of Medical Sciences, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.ORCID https://orcid.org/0000-0001-9987-6229
Khon Kaen University · THKumamoto University · JPKyushu University · JPNaresuan University · TH

Funding

Japan Society for the Promotion of Science JP14F099Japan Society for the Promotion of Science JP17K07199Japan Society for the Promotion of Science JP19H03772Japan Society for the Promotion of Science JP22F22111Japan Society for the Promotion of Science JP22H03187Khon Kaen University IN63219National Research Council of Thailand N42A650238
6 · The paper itself

Abstract

Cholangiocarcinoma (CCA) is an aggressive malignant tumor of bile duct epithelia. Recent evidence suggests the impact of cancer stem cells (CSC) on the therapeutic resistance of CCA; however, the knowledge of CSC in CCA is limited due to the lack of a CSC model. In this study, we successfully established a stable sphere-forming CCA stem-like cell, KKU-055-CSC, from the original CCA cell line, KKU-055. The KKU-055-CSC exhibits CSC characteristics, including: (1) the ability to grow stably and withstand continuous passage for a long period of culture in the stem cell medium, (2) high expression of stem cell markers, (3) low responsiveness to standard chemotherapy drugs, (4) multilineage differentiation, and (5) faster and constant expansive tumor formation in xenograft mouse models. To identify the CCA-CSC-associated pathway, we have undertaken a global proteomics and functional cluster/network analysis. Proteomics identified the 5925 proteins in total, and the significantly upregulated proteins in CSC compared with FCS-induced differentiated CSC and its parental cells were extracted. Network analysis revealed that high mobility group A1 (HMGA1) and Aurora A signaling through the signal transducer and activator of transcription 3 pathways were enriched in KKU-055-CSC. Knockdown of HMGA1 in KKU-055-CSC suppressed the expression of stem cell markers, induced the differentiation followed by cell proliferation, and enhanced sensitivity to chemotherapy drugs including Aurora A inhibitors. In silico analysis indicated that the expression of HMGA1 was correlated with Aurora A expressions and poor survival of CCA patients. In conclusion, we have established a unique CCA stem-like cell model and identified the HMGA1-Aurora A signaling as an important pathway for CSC-CCA.

Indexed as

Bile Duct NeoplasmsCholangiocarcinomaAnimalsBile Ducts, IntrahepaticCell Line, TumorCell ProliferationHMGA1a ProteinHumansMiceNeoplastic Stem CellsHMGA1a Proteinbile ductcancer stem cellcholangiocarcinomaHMGA1liver

Identifiers

PMID37026527
PMCPMC10394157
OpenAlexW4362691826

What OpenQuestion holds

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LicenceCC BY-NC
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.