Evidence map›Paper›PMID 23865481›Full record

ArticleBMC genomics2013

Oxaliplatin induces different cellular and molecular chemoresistance patterns in colorectal cancer cell lines of identical origins.

Piroska Virag, Eva Fischer-Fodor, Maria Perde-Schrepler, Ioana Brie, Corina Tatomir, Loredana Balacescu, Ioana Berindan-Neagoe, Bogdan Victor, Ovidiu Balacescu

Open access · goldAbstract read
In one paragraph

Article in BMC genomics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

20 citing papers in PubMed, 31 citations in OpenAlex.

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  7. Computational Tactics for Precision Cancer Network Biology.International journal of molecular sciences · 2022
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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

9 authors at 2 institutions in 1 country.

Piroska ViragThe Oncology Institute Prof.Dr.I. Chiricuta, 400015 Republicii Str,, nr, 34-36, Cluj-Napoca, Romania. vpiroska@yahoo.com
Eva Fischer-Fodor
Maria Perde-Schrepler
Ioana Brie
Corina Tatomir
Loredana Balacescu
Ioana Berindan-Neagoe
Bogdan Victor
Ovidiu Balacescu
Institute of Oncology Prof. Dr. Ion Chiricuta · ROIuliu Hațieganu University of Medicine and Pharmacy · RO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCancer cells frequently adopt cellular and molecular alterations and acquire resistance to cytostatic drugs. Chemotherapy with oxaliplatin is among the leading treatments for colorectal cancer with a response rate of 50%, inducing intrastrand cross-links on the DNA. Despite of this drug's efficiency, resistance develops in nearly all metastatic patients. Chemoresistance being of crucial importance for the drug's clinical efficiency this study aimed to contribute to the identification and description of some cellular and molecular alterations induced by prolonged oxaliplatin therapy. Resistance to oxaliplatin was induced in Colo320 (Colo320R) and HT-29 (HT-29R) colorectal adenocarcinoma cell lines by exposing the cells to increasing concentrations of the drug. Alterations in morphology, cytotoxicity, DNA cross-links formation and gene expression profiles were assessed in the parental and resistant variants with microscopy, MTT, alkaline comet and pangenomic microarray assays, respectively.

resultsMorphology analysis revealed epithelial-to-mesenchymal transition in the resistant vs parental cells suggesting alterations of the cells' adhesion complexes, through which they acquire increased invasiveness and adherence. Cytotoxicity measurements demonstrated resistance to oxaliplatin in both cell lines; Colo320 being more sensitive than HT-29 to this drug (P < 0.001). The treatment with oxaliplatin caused major DNA cross-links in both parental cell lines; in Colo320R small amounts of DNA cross-links were still detectable, while in HT-29R not. We identified 441 differentially expressed genes in Colo320R and 613 in HT-29R as compared to their parental counterparts (at least 1.5 -fold up- or down- regulation, p < 0.05). More disrupted functions and pathways were detected in HT-29R cell line than in Colo320R, involving genes responsible for apoptosis inhibition, cellular proliferation and epithelial-to-mesenchymal transition. Several upstream regulators were detected as activated in HT-29R cell line, but not in Colo320R.

conclusionsOur findings revealed a more resistant phenotype in HT-29R as compared to Colo320R and different cellular and molecular chemoresistance patterns induced by prolonged treatment with oxaliplatin in cell lines with identical origins (colorectal adenocarcinomas).

Indexed as

Drug Resistance, NeoplasmAntineoplastic AgentsCell Line, TumorCell MovementColorectal NeoplasmsCross-Linking ReagentsHumansNeoplasm InvasivenessOrganoplatinum CompoundsOxaliplatinPhenotypeReproducibility of ResultsTime FactorsTranscriptomeAntineoplastic AgentsCross-Linking ReagentsOrganoplatinum CompoundsOxaliplatin

Identifiers

PMID23865481
PMCPMC3776436
OpenAlexW1973610643

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LicenceCC BY
Read underepoch 390

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.