ArticleExperimental and molecular pathology2014
An Oct-1-based, feed-forward mechanism of apoptosis inhibited by co-culture with Raji B-cells: towards a model of the cancer cell/B-cell microenvironment.
Article in Experimental and molecular pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- Diagnostic and Prognostic Value of Long Noncoding RNAs as Potential Novel Biomarkers in Intrahepatic Cholestasis of Pregnancy.BioMed research international · 2021Trial
- Systemic Adaptive Immune Parameters Associated with Neuroblastoma Outcomes: the Significance of Gamma-Delta T Cells.Journal of molecular neuroscience : MN · 2021Article
- A feed-forward regulatory network lncPCAT1/miR-106a-5p/E2F5 regulates the osteogenic differentiation of periodontal ligament stem cells.Journal of cellular physiology · 2019Article
- An age-based, RNA expression paradigm for survival biomarker identification for pediatric neuroblastoma and acute lymphoblastic leukemia.Cancer cell international · 2019Article
- Recovery of T-cell receptor V(D)J recombination reads from lower grade glioma exome files correlates with reduced survival and advanced cancer grade.Journal of neuro-oncology · 2018Article
- Elucidating feed-forward apoptosis signatures in breast cancer datasets: Higher FOS expression associated with a better outcome.Oncology letters · 2018Article
- Article
- Recovery of Immunoglobulin VJ Recombinations from Pancreatic Cancer Exome Files Strongly Correlates with Reduced Survival.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2018Article
- Molecular targets and signaling pathways regulated by nuclear translocation of syndecan-1.BMC cell biology · 2017Article
- Identification of immunoglobulin V(D)J recombinations in solid tumor specimen exome files: Evidence for high level B-cell infiltrates in breast cancer.Human vaccines & immunotherapeutics · 2017Article
- TCGA: Increased oncoprotein coding region mutations correlate with a greater expression of apoptosis-effector genes and a positive outcome for stomach adenocarcinoma.Cell cycle (Georgetown, Tex.) · 2016Article
- Impact of SNPs on CpG Islands in the MYC and HRAS oncogenes and in a wide variety of tumor suppressor genes: A multi-cancer approach.Cell cycle (Georgetown, Tex.) · 2016Article
- Elevated OCT1 participates in colon tumorigenesis and independently predicts poor prognoses of colorectal cancer patients.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Tumor suppressor genes are larger than apoptosis-effector genes and have more regions of active chromatin: Connection to a stochastic paradigm for sequential gene expression programs.Cell cycle (Georgetown, Tex.) · 2015Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
A continuing conundrum of cancer biology is the dichotomous function of transcription factors that regulate both proliferation and apoptosis, seemingly opposite results. Previous results have indicated that regulated entry into the S-phase of the cell cycle can be anti-apoptotic. Indeed, tumor suppressor genes can be amplified in tumors and certain, slow growing cancers can represent a relatively poor prognosis, both phenomena likely related to reduced cancer cell apoptosis, in turn due to reduced, unproductive entry into S-phase. In this report, we demonstrate that the Oct-1 transcription factor, commonly considered pro-proliferative, indeed facilitates IFN-γ induced apoptosis in 5637 bladder carcinoma cells, consistent with the role of the retinoblastoma protein in down-regulating Oct-1 DNA binding activity and in suppressing IFN-γ induced apoptosis. More importantly, despite the commonly appreciated process of IFN-γ induced apoptosis, IFN-γ at low concentrations stimulated bladder cancer cell proliferation, consistent with apoptosis being dependent on an overstimulation of what is otherwise a pro-proliferative pathway. This observation is in turn consistent with a feed forward mechanism of apoptosis, whereby transcription factors activate proliferation-effector genes at relatively low levels, then apoptosis-effector genes when the transcription factors over-accumulate. Finally, Oct-1 mediated apoptosis is inhibited by co-culture with Raji B-cells, raising the question of whether the normal lymph node environment, or other microenvironments with high concentrations of B-cells, is protective against Oct-1 facilitated apoptosis?
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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.