Evidence map›Paper›PMID 39239747›Full record

ArticleMolecular medicine reports2024

Knockdown of cullin 3 inhibits progressive phenotypes and increases chemosensitivity in cholangiocarcinoma cells.

Kandawasri Pratummanee, Kankamol Kerdkumthong, Sittiruk Roytrakul, Phonprapavee Tantimetta, Phanthipha Runsaeng, Sompop Saeheng, Sumalee Obchoei

Abstract read
In one paragraph

Article in Molecular medicine reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

7 authors.

Kandawasri PratummaneeDepartment of Biochemistry, Division of Health and Applied Sciences, Faculty of Science, Prince of Songkla University, Hatyai, Songkhla 90110, Thailand.
Kankamol KerdkumthongDepartment of Biochemistry, Division of Health and Applied Sciences, Faculty of Science, Prince of Songkla University, Hatyai, Songkhla 90110, Thailand.
Sittiruk RoytrakulFunctional Proteomics Technology Laboratory, National Center for Genetic Engineering and Biotechnology, National Science and Technology Development Agency, Pathumtani 12120, Thailand.
Phonprapavee TantimettaDepartment of Biochemistry, Division of Health and Applied Sciences, Faculty of Science, Prince of Songkla University, Hatyai, Songkhla 90110, Thailand.
Phanthipha RunsaengDepartment of Biochemistry, Division of Health and Applied Sciences, Faculty of Science, Prince of Songkla University, Hatyai, Songkhla 90110, Thailand.
Sompop SaehengDepartment of Biochemistry, Division of Health and Applied Sciences, Faculty of Science, Prince of Songkla University, Hatyai, Songkhla 90110, Thailand.
Sumalee ObchoeiDepartment of Biochemistry, Division of Health and Applied Sciences, Faculty of Science, Prince of Songkla University, Hatyai, Songkhla 90110, Thailand.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cholangiocarcinoma (CCA) is an extremely aggressive malignancy arising from the epithelial cells lining the bile ducts. It presents a substantial global health issue, with the highest incidence rates, ranging from 40‑100 cases/100,000 individuals, found in Southeast Asia, where liver fluke infection is endemic. In Europe and America, incidence rates range from 0.4‑2 cases/100,000 individuals. Globally, mortality rates range from 0.2‑2 deaths/100,000 person‑years and are increasing in most countries. Chemotherapy is the primary treatment for advanced CCA due to limited options from late‑stage diagnosis, but its efficacy is hindered by drug‑resistant phenotypes. In a previous study, proteomics analysis of drug‑resistant CCA cell lines (KKU‑213A‑FR and KKU‑213A‑GR) and the parental KKU‑213A line identified cullin 3 (Cul3) as markedly overexpressed in drug‑resistant cells. Cul3, a scaffold protein within CUL3‑RING ubiquitin ligase complexes, is crucial for ubiquitination and proteasome degradation, yet its role in drug‑resistant CCA remains to be elucidated. The present study aimed to elucidate the role of Cul3 in drug‑resistant CCA cell lines. Reverse transcription‑quantitative PCR and western blot analyses confirmed significantly elevated Cul3 mRNA and protein levels in drug‑resistant cell lines compared with the parental control. Short interfering RNA‑mediated Cul3 knockdown sensitized cells to 5‑fluorouracil and gemcitabine and inhibited cell proliferation, colony formation, migration and invasion. In addition, Cul3 knockdown induced G

Indexed as

Bile Duct NeoplasmsCell ProliferationCholangiocarcinomaCullin ProteinsDrug Resistance, NeoplasmAntineoplastic AgentsApoptosisCell Line, TumorCell MovementDeoxycytidineGemcitabineGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansPhenotypeAntineoplastic AgentsCUL3 protein, humanCullin ProteinsDeoxycytidineGemcitabine5‑fluoruracilcholangiocarcinomacullin 3drug resistancegemcitabine

Identifiers

PMID39239747
PMCPMC11406421

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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.