Evidence map›Paper›PMID 34067290›Full record

ArticleCurrent issues in molecular biology2021

A Comparison of Doxorubicin-Resistant Colon Cancer LoVo and Leukemia HL60 Cells: Common Features, Different Underlying Mechanisms.

Laura Locatelli, Alessandra Cazzaniga, Giorgia Fedele, Monica Zocchi, Roberta Scrimieri, Claudia Moscheni, Sara Castiglioni, Jeanette A Maier

Open access · goldAbstract readComparative Study
In one paragraph

Article in Current issues in molecular biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.1field-weighted citation impact, top 26% 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

9 citing papers in PubMed, 15 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Laura LocatelliDepartment of Biomedical and Clinical Sciences L. Sacco, Università di Milano, Via G.B. Grassi 74, 20157 Milano, Italy.ORCID 0000-0002-4568-7825
Alessandra CazzanigaDepartment of Biomedical and Clinical Sciences L. Sacco, Università di Milano, Via G.B. Grassi 74, 20157 Milano, Italy.ORCID 0000-0001-7153-2256
Giorgia FedeleDepartment of Biomedical and Clinical Sciences L. Sacco, Università di Milano, Via G.B. Grassi 74, 20157 Milano, Italy.
Monica ZocchiDepartment of Biomedical and Clinical Sciences L. Sacco, Università di Milano, Via G.B. Grassi 74, 20157 Milano, Italy.ORCID 0000-0002-0728-6676
Roberta ScrimieriDepartment of Biomedical and Clinical Sciences L. Sacco, Università di Milano, Via G.B. Grassi 74, 20157 Milano, Italy.ORCID 0000-0001-8888-2594
Claudia MoscheniDepartment of Biomedical and Clinical Sciences L. Sacco, Università di Milano, Via G.B. Grassi 74, 20157 Milano, Italy.ORCID 0000-0001-6614-665X
Sara CastiglioniDepartment of Biomedical and Clinical Sciences L. Sacco, Università di Milano, Via G.B. Grassi 74, 20157 Milano, Italy.ORCID 0000-0002-8785-9891
Jeanette A MaierDepartment of Biomedical and Clinical Sciences L. Sacco, Università di Milano, Via G.B. Grassi 74, 20157 Milano, Italy.
University of Milan · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemoresistance causes cancer relapse and metastasis, thus remaining the major obstacle to cancer therapy. While some light has been shed on the underlying mechanisms, it is clear that chemoresistance is a multifaceted problem strictly interconnected with the high heterogeneity of neoplastic cells. We utilized two different human cell lines, i.e., LoVo colon cancer and promyelocytic leukemia HL60 cells sensitive and resistant to doxorubicin (DXR), largely used as a chemotherapeutic and frequently leading to chemoresistance. LoVo and HL60 resistant cells accumulate less reactive oxygen species by differently modulating the levels of some pro- and antioxidant proteins. Moreover, the content of intracellular magnesium, known to contribute to protect cells from oxidative stress, is increased in DXR-resistant LoVo through the upregulation of MagT1 and in DXR-resistant HL60 because of the overexpression of TRPM7. In addition, while no major differences in mitochondrial mass are observed in resistant HL60 and LoVo cells, fragmented mitochondria due to increased fission and decreased fusion are detected only in resistant LoVo cells. We conclude that DXR-resistant cells evolve adaptive mechanisms to survive DXR cytotoxicity by activating different molecular pathways.

Indexed as

Antibiotics, AntineoplasticCell Line, TumorColonic NeoplasmsDoxorubicinDrug Resistance, NeoplasmHL-60 CellsHumansLeukemia, Promyelocytic, AcuteMagnesiumProtein Serine-Threonine KinasesReactive Oxygen SpeciesTRPM Cation ChannelsAntibiotics, AntineoplasticDoxorubicinMagnesiumProtein Serine-Threonine KinasesReactive Oxygen SpeciesTRPM7 protein, humanTRPM Cation ChannelsdoxorubicinHL60 cellsLoVo cellsMagT1mitochondriaROSTRPM7

Identifiers

PMID34067290
PMCPMC8929017
OpenAlexW3164898606

What Socratic holds

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LicenceCC BY
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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 Socratic graph.