Evidence map›Paper›PMID 34129628›Full record

ArticlePloS one2021

Autophagy activity in cholangiocarcinoma is associated with anatomical localization of the tumor.

Gábor Lendvai, Tímea Szekerczés, Ildikó Illyés, Milán Csengeri, Krisztina Schlachter, Erzsébet Szabó, Gábor Lotz, András Kiss, Katalin Borka, Zsuzsa Schaff

Open access · goldAbstract readComparative Study
In one paragraph

Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Hydroxychloroquine Induces Apoptosis in CholangiocarcinomaFrontiers in molecular biosciences · 2021
    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

10 authors at 2 institutions in 1 country.

Gábor Lendvai2nd Department of Pathology, Semmelweis University, Budapest, Hungary.ORCID 0000-0002-0931-380X
Tímea Szekerczés2nd Department of Pathology, Semmelweis University, Budapest, Hungary.ORCID 0000-0002-7373-8730
Ildikó Illyés2nd Department of Pathology, Semmelweis University, Budapest, Hungary.
Milán Csengeri2nd Department of Pathology, Semmelweis University, Budapest, Hungary.
Krisztina SchlachterDepartment of Surgical and Molecular Pathology, Center of Tumor Pathology, National Institute of Oncology, Budpest, Hungary.
Erzsébet Szabó2nd Department of Pathology, Semmelweis University, Budapest, Hungary.
Gábor Lotz2nd Department of Pathology, Semmelweis University, Budapest, Hungary.
András Kiss2nd Department of Pathology, Semmelweis University, Budapest, Hungary.ORCID 0000-0002-7453-3163
Katalin Borka2nd Department of Pathology, Semmelweis University, Budapest, Hungary.
Zsuzsa Schaff2nd Department of Pathology, Semmelweis University, Budapest, Hungary.
Semmelweis University · HUNational Institute of Oncology · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The presence of autophagy has been indicated in cholangiocarcinoma (CC), which disease has poor prognosis and limited treatment options. Recently, CC has been classified by anatomical localization as intrahepatic (iCC), perihilar (pCC) and distal (dCC), showing different clinical and molecular characteristics. Thus, our aim was to compare autophagy activity in CC samples resected from different anatomical locations. Further, we investigated whether autophagy could be modulated in cell lines originated from iCC and extrahepatic CC (eCC) following the treatments with autophagy inhibitory and inducing agents. Tissue microarrays were prepared from 70 CC (28 iCC, 19 pCC and 23 dCC), 31 adjacent non-tumorous and 9 hepatocellular carcinoma (HCC) samples. Autophagy markers LC3, p62 and Beclin1 as well as proliferation marker Ki-67 were monitored by immunohistochemistry and were associated with patients' survival. Modulation of autophagy was investigated in cell lines originated from iCC (HuH-28), eCC (TFK-1) and HCC (HepG2) by treating the cells with chloroquine (CQ) for inhibition and with Rapamycin, 5-Fluorouracil (5-FU) and Sorafenib for induction of autophagy. Our results indicated an inhibited autophagy in iCC and pCC tumor tissues, whereas active autophagy seemed to occur in dCC, especially in samples displaying low Ki-67 index. Additionally, low level of Beclin1 and high level of Ki-67 were associated with poor overall survival in dCC, suggesting the prognostic role of these proteins in dCC. Beside a baseline autophagy detected in each cell line, Rapamycin and 5-FU induced autophagy in iCC and HepG2 cell lines, Sorafenib in iCC cells. A chemotherapy agent in combination with CQ decreased IC50 effectively in the cell lines where basal and/or induced autophagy were present. In conclusion, we revealed differences in the autophagy activities of CC tissues and cell lines originated from different anatomical locations, which might influence patients' treatment. Our results also suggest a prognostic role of Beclin1 and Ki-67 in dCC.

Indexed as

AdultAgedAged, 80 and overAntineoplastic AgentsAutophagyBeclin-1Bile Duct NeoplasmsBile Ducts, IntrahepaticCell Line, TumorCholangiocarcinomaFemaleGene Expression Regulation, NeoplasticHep G2 CellsHumansKi-67 AntigenKlatskin TumorAntineoplastic AgentsBeclin-1BECN1 protein, humanKi-67 AntigenMKI67 protein, human

Identifiers

PMID34129628
PMCPMC8205141
OpenAlexW3172253406

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.