ArticleThe Biochemical journal2003
Bcl-2 activates a programme of premature senescence in human carcinoma cells.
Article in The Biochemical journal, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 64 citations in OpenAlex.
- Recent Advances in Senotherapeutics Delivery.Tissue engineering. Part B, Reviews · 2022Review
- Review
- Effect ofCurrent issues in molecular biology · 2021Article
- Translocation of intracellular CD24 constitutes a triggering event for drug resistance in breast cancer.Scientific reports · 2021Article
- Clearance of therapy-induced senescent tumor cells by the senolytic ABT-263 via interference with BCL-XMolecular oncology · 2020Article
- Mechanisms of Oncogene-Induced Replication Stress: Jigsaw Falling into Place.Cancer discovery · 2018Review
- The Quest for Osteoporosis Mechanisms and Rational Therapies: How Far We've Come, How Much Further We Need to Go.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2018Article
- Tumor cell senescence response produces aggressive variants.Cell death discovery · 2017Article
- Polyphenolic Profile and Targeted Bioactivity of Methanolic Extracts from Mediterranean Ethnomedicinal Plants on Human Cancer Cell Lines.Molecules (Basel, Switzerland) · 2016Article
- Bcl-2 family proteins as regulators of cancer cell invasion and metastasis: a review focusing on mitochondrial respiration and reactive oxygen species.Oncotarget · 2016Review
- BCL-2 family protein, BAD is down-regulated in breast cancer and inhibits cell invasion.Experimental cell research · 2015Article
- The Intricate Interplay between Mechanisms Underlying Aging and Cancer.Aging and disease · 2015Review
- Proteomic analysis reveals a role for Bcl2-associated athanogene 3 and major vault protein in resistance to apoptosis in senescent cells by regulating ERK1/2 activation.Molecular & cellular proteomics : MCP · 2015Article
- Initiation of premature senescence by Bcl-2 in hypoxic condition.International journal of clinical and experimental pathology · 2014Article
- Article
- Regulation of senescence by microRNA biogenesis factors.Ageing research reviews · 2012Review
- Long-term smoking mediated down-regulation of Smad3 induces resistance to carboplatin in non-small cell lung cancer.Neoplasia (New York, N.Y.) · 2012Article
- Context-Dependent Regulation of Autophagy by IKK-NF-κB Signaling: Impact on the Aging Process.International journal of cell biology · 2012Article
- Targets and mechanisms of photodynamic therapy in lung cancer cells: a brief overview.Cancers · 2011Article
- Therapy-induced senescence in cancer.Journal of the National Cancer Institute · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The apoptosis regulator Bcl-2 has been shown to modulate cell-cycle progression, favouring a quiescent state over a proliferative state, in both normal and tumour cells. We show here that constitutive expression of Bcl-2 in human carcinoma cells results in a cell-cycle arrest that within a few days can become irreversible. Arrested cells acquire a senescent-like phenotype, which consists of several characteristic morphological alterations and increased activity of senescence-associated beta-galactosidase. The induction of the premature senescence programme is mediated by inhibition of Cdk2 kinase activity, and p27(KIP1) is required to maintain the senescent phenotype. We propose that the ability to activate an endogenous premature senescence programme allows Bcl-2 to suppress tumour growth. These results suggest that the down-regulation of Bcl-2 expression, which has been observed during the development and progression of human carcinoma, is related to the ability of Bcl-2 to severely hamper the growth of carcinoma cells and to induce a permanent cell-cycle arrest, with the features of senescence.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.