ArticleCell cycle (Georgetown, Tex.)2013
Protect and serve: Bcl-2 proteins as guardians and rulers of cancer cell survival.
Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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.
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.
Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- IRF4 contributes to chemoresistance in IGH::BCL2-positive diffuse large B-cell lymphomas by mediating BCL2-induced SOX9 expression.Clinical and translational medicine · 2025Article
- Bcl-xL is required to protect endothelial cells latently infected with KSHV from virus induced intrinsic apoptosis.PLoS pathogens · 2023Article
- Oxymatrine inhibits TGF‑β1‑mediated mitochondrial apoptotic signaling in alveolar epithelial cells via activation of PI3K/AKT signaling.Experimental and therapeutic medicine · 2023Article
- Single-Cell Proteomics Analysis of Recurrent Low-Grade Serous Ovarian Carcinoma and Associated Brain Metastases.Frontiers in oncology · 2022Article
- Anti-proliferation and apoptosis-inducing effects of sodium aescinate on retinoblastoma Y79 cells.International journal of ophthalmology · 2020Article
- Targeting MYC activity in double-hit lymphoma with MYC and BCL2 and/or BCL6 rearrangements with epigenetic bromodomain inhibitors.Journal of hematology & oncology · 2019Article
- BCL-2 family isoforms in apoptosis and cancer.Cell death & disease · 2019Review
- New Perspectives on Diagnosis and Therapy of Malignant Pleural Mesothelioma.Frontiers in oncology · 2018Review
- The nuclear transcription factor RelB functions as an oncogene in human lung adenocarcinoma SPC-A1 cells.Cancer cell international · 2018Article
- BCL-XNature communications · 2017Article
- Article
- Inferring gene and protein interactions using PubMed citations and consensus Bayesian networks.PloS one · 2017Article
- Affinity purification-mass spectrometry analysis of bcl-2 interactome identified SLIRP as a novel interacting protein.Cell death & disease · 2016Article
- Article
- The importance of being dead: cell death mechanisms assessment in anti-sarcoma therapy.Frontiers in oncology · 2015Review
- Cucurbitacin B inhibits proliferation and induces apoptosis via STAT3 pathway inhibition in A549 lung cancer cells.Molecular medicine reports · 2014Article
- Protein kinase A type II-α regulatory subunit regulates the response of prostate cancer cells to taxane treatment.Cell cycle (Georgetown, Tex.) · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is widely accepted that anti-apoptotic Bcl-2 family members promote cancer cell survival by binding to their pro-apoptotic counterparts, thereby preventing mitochondrial outer membrane permeabilization (MOMP) and cytotoxic caspase activation. Yet, these proteins do not only function as guardians of mitochondrial permeability, preserving it, and maintaining cell survival in the face of acute or chronic stress, they also regulate non-apoptotic functions of caspases and biological processes beyond MOMP from diverse subcellular localizations and in complex with numerous binding partners outside of the Bcl-2 family. In particular, some of the non-canonical effects and functions of Bcl-2 homologs lead to an interplay with E2F-1, NFκB, and Myc transcriptional pathways, which themselves influence cancer cell growth and survival. We thus propose that, by feedback loops that we currently have only hints of, Bcl-2 proteins may act as rulers of survival signaling, predetermining the apoptotic threshold that they also directly scaffold. This underscores the robustness of the control exerted by Bcl-2 homologs over cancer cell survival, and implies that small molecules compounds currently used in the clinic to inhibit their mitochondrial activity may be not always be fully efficient to override this control.
Indexed as
Identifiers
What Socratic holds
Registered trials
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.