Evidence map›Paper›PMID 33396645›Full record

ArticleCancers2020

BCL2L10 Is Overexpressed in Melanoma Downstream of STAT3 and Promotes Cisplatin and ABT-737 Resistance.

María Josefina Quezada, María Elisa Picco, María Belén Villanueva, María Victoria Castro, Gastón Barbero, Natalia Brenda Fernández, Edith Illescas, Pablo Lopez-Bergami

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

12 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Evaluating the Diverse Anticancer Effects of LaosMedicina (Kaunas, Lithuania) · 2024
    Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. 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 at 1 institution in 1 country.

María Josefina QuezadaCentro de Estudios Biomédicos, Básicos, Aplicados y Desarrollo (CEBBAD), Universidad Maimónides, C1405BCK Buenos Aires, Argentina.ORCID 0000-0002-9676-1124
María Elisa PiccoInstituto de Medicina y Biología Experimental (IBYME), CONICET, C1428ADN Buenos Aires, Argentina.
María Belén VillanuevaCentro de Estudios Biomédicos, Básicos, Aplicados y Desarrollo (CEBBAD), Universidad Maimónides, C1405BCK Buenos Aires, Argentina.
María Victoria CastroCentro de Estudios Biomédicos, Básicos, Aplicados y Desarrollo (CEBBAD), Universidad Maimónides, C1405BCK Buenos Aires, Argentina.
Gastón BarberoCentro de Estudios Biomédicos, Básicos, Aplicados y Desarrollo (CEBBAD), Universidad Maimónides, C1405BCK Buenos Aires, Argentina.
Natalia Brenda FernándezInstituto de Medicina y Biología Experimental (IBYME), CONICET, C1428ADN Buenos Aires, Argentina.
Edith IllescasCentro de Estudios Biomédicos, Básicos, Aplicados y Desarrollo (CEBBAD), Universidad Maimónides, C1405BCK Buenos Aires, Argentina.
Pablo Lopez-BergamiCentro de Estudios Biomédicos, Básicos, Aplicados y Desarrollo (CEBBAD), Universidad Maimónides, C1405BCK Buenos Aires, Argentina.
Consejo Nacional de Investigaciones Científicas y Técnicas · AR

Funding

Agencia Nacional de Promoción Científica y Tecnológica BID-PICT-2007-1010Agencia Nacional de Promoción Científica y Tecnológica BID-PICT2011-1605Fundación Alberto Roemmers aInstituto Nacional de Cancer a
6 · The paper itself

Abstract

The anti-apoptotic proteins from the Bcl-2 family are important therapeutic targets since they convey resistance to anticancer regimens. Despite the suspected functional redundancy among the six proteins of this subfamily, both basic studies and therapeutic approaches have focused mainly on BCL2, Bcl-xL, and MCL1. The role of BCL2L10, another member of this group, has been poorly studied in cancer and never has been in melanoma. We describe here that BCL2L10 is abundantly and frequently expressed both in melanoma cell lines and tumor samples. We established that BCL2L10 expression is driven by STAT3-mediated transcription, and by using reporter assays, site-directed mutagenesis, and ChIP analysis, we identified the functional STAT3 responsive elements in the BCL2L10 promoter. BCL2L10 is a pro-survival factor in melanoma since its expression reduced the cytotoxic effects of cisplatin, dacarbazine, and ABT-737 (a BCL2, Bcl-xL, and Bcl-w inhibitor). Meanwhile, both genetic and pharmacological inhibition of BCL2L10 sensitized melanoma cells to cisplatin and ABT-737. Finally, BCL2L10 inhibited the cell death upon combination treatments of PLX-4032, a BRAF inhibitor, with ABT-737 or cisplatin. In summary, we determined that BCL2L10 is expressed in melanoma and contributes to cell survival. Hence, targeting BCL2L10 may enhance the clinical efficacy of other therapies for malignant melanoma.

Indexed as

ABT-737Bcl-2 familyBCL2L10cytotoxicitymelanomaML258STAT3survival

Identifiers

PMID33396645
PMCPMC7795116
OpenAlexW3117478370

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.