Evidence map›Paper›PMID 31432325›Full record

ArticlePathology oncology research : POR2020

Mcl-1 Inhibitor Induces Cells Death in BRAF-Mutant Amelanotic Melanoma Trough GSH Depletion, DNA Damage and Cell Cycle Changes.

Michalina Respondek, Artur Beberok, Zuzanna Rzepka, Jakub Rok, Dorota Wrześniok

Open access · hybridAbstract read
In one paragraph

Article in Pathology oncology research : POR, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

13 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Amelanotic Melanoma-Biochemical and Molecular Induction Pathways.International journal of molecular sciences · 2024
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. BH3-mimetics: recent developments in cancer therapy.Journal of experimental & clinical cancer research : CR · 2021
    Review
  12. Article
  13. Targeting MCL-1 in cancer: current status and perspectives.Journal of hematology & oncology · 2021
    Review
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

5 authors at 2 institutions in 1 country.

Michalina RespondekSchool of Pharmacy with the Division of Laboratory Medicine, Department of Pharmaceutical Chemistry, Medical University of Silesia, Jagiellońska 4, 41-200, Sosnowiec, Poland. mrespondek@sum.edu.pl.ORCID http://orcid.org/0000-0003-0844-9155
Artur BeberokSchool of Pharmacy with the Division of Laboratory Medicine, Department of Pharmaceutical Chemistry, Medical University of Silesia, Jagiellońska 4, 41-200, Sosnowiec, Poland.
Zuzanna RzepkaSchool of Pharmacy with the Division of Laboratory Medicine, Department of Pharmaceutical Chemistry, Medical University of Silesia, Jagiellońska 4, 41-200, Sosnowiec, Poland.
Jakub RokSchool of Pharmacy with the Division of Laboratory Medicine, Department of Pharmaceutical Chemistry, Medical University of Silesia, Jagiellońska 4, 41-200, Sosnowiec, Poland.
Dorota WrześniokSchool of Pharmacy with the Division of Laboratory Medicine, Department of Pharmaceutical Chemistry, Medical University of Silesia, Jagiellońska 4, 41-200, Sosnowiec, Poland.
Medical University of Silesia · PLJagiellonian University · PL

Funding

Medical University of Silesia KNW-1-085/N/8/OMedical University of Silesia KNW-2-031/D/8/N
6 · The paper itself

Abstract

Mcl-1 is a potent antiapoptotic protein and amplifies frequently in many human cancer. Currently, it is considered that the extensively expressed of Mcl-1 protein in melanoma cells is associated with rapid tumor progression, poor prognosis and low chemosensitivity. Therefore, the antiapoptotic protein Mcl-1 could be considered as a potential target for malignant melanoma treatment. The aim of this study was to assess the effect of MIM1 a specific low molecular Mcl-1 protein inhibitor and mixture of MIM1 and dacarbazine on the viability, cell cycle progression and apoptosis induction in amelanotic C32 melanoma cells. The cytotoxic activity of MIM1 towards C32 melanoma cells was examined by the WST-1 test. The Mcl-1 protein level as a drug target in amelanotic melanoma cells was defined by Western blot analysis. Cell cycle progression, DNA fragmentation as well as GSH depletion were determined by fluorescence image cytometer NucleoCounter NC-3000. The obtained results demonstrate that the specific Mcl-1 protein inhibitor - MIM1 decreases cell viability and induce apoptosis (S-phase arrest, DNA fragmentation and redox imbalance) in amelanotic melanoma cells and intensify the proapoptotic properties of DTIC, as a result of interactions with Mcl-1 protein. Taken together, the presented data suggest that Mcl-1 protein is a an important target in malignant melanoma treatment and provide for the first time convincing evidence that MIM1, which inhibits Mcl-1 antiapoptotic protein is able to induce apoptosis and sensitize melanoma cells to alkylating agent.

Indexed as

Antineoplastic AgentsCell CycleCell Line, TumorCell SurvivalDacarbazineDNA DamageGlutathioneHumansMelanoma, AmelanoticMyeloid Cell Leukemia Sequence 1 ProteinProto-Oncogene Proteins B-rafAntineoplastic AgentsBRAF protein, humanDacarbazineGlutathioneMCL1 protein, humanMyeloid Cell Leukemia Sequence 1 ProteinProto-Oncogene Proteins B-rafAmelanotic melanomaApoptosisBH3 mimeticsDacarbazine, image cytometryMIM1

Identifiers

PMID31432325
PMCPMC7297871
OpenAlexW2969435575

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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.