Evidence map›Paper›PMID 36900165›Full record

ArticleCancers2023

Contribution of Mitochondrial Activity to Doxorubicin-Resistance in Osteosarcoma Cells.

Isabella Giacomini, Margherita Cortini, Mattia Tinazzi, Nicola Baldini, Veronica Cocetta, Eugenio Ragazzi, Sofia Avnet, Monica Montopoli

Full text read
In one paragraph

Article in Cancers, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Mitochondrial function meets oncology: the multifaceted role of TFAM across cancer types.Apoptosis : an international journal on programmed cell death · 2026
    Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. 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

8 authors.

Isabella GiacominiDepartment of Pharmaceutical and Pharmacological Sciences, University of Padua, 35131 Padova, Italy.ORCID 0000-0002-7154-7930
Margherita CortiniBiomedical Science and Technologies and Nanobiotechnology Lab, IRCCS Istituto Ortopedico Rizzoli, 40136 Bologna, Italy.ORCID 0000-0002-8151-8105
Mattia TinazziDepartment of Pharmaceutical and Pharmacological Sciences, University of Padua, 35131 Padova, Italy.
Nicola BaldiniBiomedical Science and Technologies and Nanobiotechnology Lab, IRCCS Istituto Ortopedico Rizzoli, 40136 Bologna, Italy.
Veronica CocettaDepartment of Pharmaceutical and Pharmacological Sciences, University of Padua, 35131 Padova, Italy.ORCID 0000-0002-0350-8403
Eugenio RagazziDepartment of Pharmaceutical and Pharmacological Sciences, University of Padua, 35131 Padova, Italy.ORCID 0000-0002-0390-6823
Sofia AvnetDepartment of Biomedical and Neuromotor Sciences, Alma Mater Studiorum, University of Bologna, 40126 Bologna, Italy.ORCID 0000-0002-7843-0591
Monica MontopoliDepartment of Pharmaceutical and Pharmacological Sciences, University of Padua, 35131 Padova, Italy.ORCID 0000-0001-6182-4132

Funding

Italian Association for Cancer Research IG 2018 - ID. 21403University of Padua RAGA_BIRD2020_01
6 · The paper itself

Abstract

Osteosarcoma is considered the most common bone tumor affecting children and young adults. The standard of care is chemotherapy; however, the onset of drug resistance still jeopardizes osteosarcoma patients, thus making it necessary to conduct a thorough investigation of the possible mechanisms behind this phenomenon. In the last decades, metabolic rewiring of cancer cells has been proposed as a cause of chemotherapy resistance. Our aim was to compare the mitochondrial phenotype of sensitive osteosarcoma cells (HOS and MG-63) versus their clones when continuously exposed to doxorubicin (resistant cells) and identify alterations exploitable for pharmacological approaches to overcome chemotherapy resistance. Compared with sensitive cells, doxorubicin-resistant clones showed sustained viability with less oxygen-dependent metabolisms, and significantly reduced mitochondrial membrane potential, mitochondrial mass, and ROS production. In addition, we found reduced expression of

Indexed as

cancerchemotherapydoxorubicindrug resistancemetabolismmitochondriaosteosarcomatargeting mitochondrial alterations

Identifiers

PMID36900165
PMCPMC10000149

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read37
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.