Evidence map›Paper›PMID 41596764›Full record

ReviewInternational journal of molecular sciences2026

BCL-2 and BCL-xL in Cancer: Regulation, Function, and Therapeutic Targeting.

João P N Silva, Bárbara Pinto, Patrícia M A Silva, Hassan Bousbaa

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Molecular Mechanisms of Cadmium-Induced Apoptosis in Fish Cells: A Review.International journal of molecular sciences · 2026
    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

4 authors.

João P N SilvaUNIPRO-Oral Pathology and Rehabilitation Research Unit, University Institute of Health Sciences (IUCS), Cooperativa de Ensino Superior Politécnico e Universitário (CESPU), 4585-116 Gandra, Portugal.ORCID 0000-0003-4455-4286
Bárbara PintoUNIPRO-Oral Pathology and Rehabilitation Research Unit, University Institute of Health Sciences (IUCS), Cooperativa de Ensino Superior Politécnico e Universitário (CESPU), 4585-116 Gandra, Portugal.ORCID 0000-0002-8804-6104
Patrícia M A SilvaUNIPRO-Oral Pathology and Rehabilitation Research Unit, University Institute of Health Sciences (IUCS), Cooperativa de Ensino Superior Politécnico e Universitário (CESPU), 4585-116 Gandra, Portugal.ORCID 0000-0002-0694-7321
Hassan BousbaaUNIPRO-Oral Pathology and Rehabilitation Research Unit, University Institute of Health Sciences (IUCS), Cooperativa de Ensino Superior Politécnico e Universitário (CESPU), 4585-116 Gandra, Portugal.ORCID 0000-0002-4006-5779

Funding

Cooperativa de Ensino Superior Politécnico e Universitário BD/CBAS/CESPU/01/2020Cooperativa de Ensino Superior Politécnico e Universitário BD/CBAS/CESPU/01/2021Cooperativa de Ensino Superior Politécnico e Universitário FlavCanAct-GI2-CESPU-2025Cooperativa de Ensino Superior Politécnico e Universitário TargetMito-GI2-CESPU-2025Fundação para a Ciência e Tecnologia 2022.09451.BD
6 · The paper itself

Abstract

The BCL-2 family of proteins plays a central role in the regulation of apoptosis, with BCL-2 and BCL-xL representing two of its most prominent antiapoptotic members. This review explores the molecular regulation of BCL-2 and BCL-xL genes, emphasizing the structural domains that define the functions of the broader BCL-2 family. Beyond their canonical roles in preventing mitochondrial outer membrane permeabilization, both proteins contribute significantly to cancer development. Their overexpression enhances invasiveness and tumor progression, supports angiogenesis, and critically modulates cellular responses to chemotherapy, often conferring drug resistance. Additional non-apoptotic functions, including roles in metabolism, mitochondrial dynamics, and cellular homeostasis, further expand their biological relevance. Clinical trials exploring strategies to inhibit BCL-2 and BCL-xL, including selective BH3 mimetics and combination regimens, are discussed with emphasis on their potential and limitations in oncology. Overall, this review highlights the multifaceted contributions of BCL-2 and BCL-xL to cancer biology and underscores the importance of continued efforts to refine targeted therapeutic approaches.

Indexed as

bcl-X ProteinNeoplasmsProto-Oncogene Proteins c-bcl-2AnimalsAntineoplastic AgentsApoptosisDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHumansMolecular Targeted TherapyAntineoplastic Agentsbcl-X ProteinProto-Oncogene Proteins c-bcl-2apoptosis regulationBCL-2BCL-xLBH3 mimeticscancer progressiondrug resistancetherapeutic targeting

Identifiers

PMID41596764
PMCPMC12842368

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.