ReviewYonsei medical journal2008
FLIP as an anti-cancer therapeutic target.
Review in Yonsei medical journal, 2008. 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
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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, 59 citations in OpenAlex.
- Flavonoids as Chemosensitizers in Leukemias.Advances in experimental medicine and biology · 2025Review
- An engineered construct of cFLIP provides insight into DED1 structure and interactions.Structure (London, England : 1993) · 2022Article
- Expression of DR5 and c‑FLIP proteins as novel prognostic biomarkers for non‑small cell lung cancer patients treated with surgical resection and chemotherapy.Oncology reports · 2019Article
- Understanding Apoptosis and Apoptotic Pathways Targeted Cancer Therapeutics.Advanced pharmaceutical bulletin · 2019Review
- c-FLIP, a Novel Biomarker for Cancer Prognosis, Immunosuppression, Alzheimer's Disease, Chronic Obstructive Pulmonary Disease (COPD), and a Rationale Therapeutic Target.Biomarkers journal · 2019Article
- Sensitization of renal carcinoma cells to TRAIL-induced apoptosis by rocaglamide and analogs.Scientific reports · 2018Article
- Baicalein induces cervical cancer apoptosis through the NF-κB signaling pathway.Molecular medicine reports · 2018Article
- Treatment of Donor Rat Hearts Prior to Transplantation with FLIP (FADD-Like Interleukin Beta-Converting Enzyme (FLICE)-Like Inhibitory Protein) in Cardioplegic Solution Decreased Apoptosis at Thirty Minutes Post-transplantation and Decreased Total Tyrosine Phosphorylation Levels.Annals of transplantation · 2018Article
- A Genome-Wide Loss-of-Function Screen Identifies SLC26A2 as a Novel Mediator of TRAIL Resistance.Molecular cancer research : MCR · 2017Article
- hnRNPK inhibits GSK3β Ser9 phosphorylation, thereby stabilizing c-FLIP and contributes to TRAIL resistance in H1299 lung adenocarcinoma cells.Scientific reports · 2016Article
- Genetic stability of pluripotent stem cells during anti-cancer therapies.Experimental and therapeutic medicine · 2016Article
- Identification and Characterization of the Interaction Site between cFLIPL and Calmodulin.PloS one · 2015Article
- Cellular FLICE-like inhibitory protein long form (c-FLIPL) overexpression is related to cervical cancer progression.International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists · 2013Article
- Aldose reductase inhibition prevents colon cancer growth by restoring phosphatase and tensin homolog through modulation of miR-21 and FOXO3a.Antioxidants & redox signaling · 2013Article
- On the TRAIL to successful cancer therapy? Predicting and counteracting resistance against TRAIL-based therapeutics.Oncogene · 2013Review
- Roles of c-FLIP in Apoptosis, Necroptosis, and Autophagy.Journal of carcinogenesis & mutagenesis · 2013Article
- Epigenetic regulation of the TRAIL/Apo2L apoptotic pathway by histone deacetylase inhibitors: an attractive approach to bypass melanoma immunotherapy resistance.American journal of clinical and experimental immunology · 2013Article
- c-FLIP, a master anti-apoptotic regulator.Experimental oncology · 2012Review
- The role of apoptosis-induced proliferation for regeneration and cancer.Cold Spring Harbor perspectives in biology · 2012Review
- Tumor necrosis factor (TNF) receptor-associated factor 7 is required for TNFα-induced Jun NH2-terminal kinase activation and promotes cell death by regulating polyubiquitination and lysosomal degradation of c-FLIP protein.The Journal of biological chemistry · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Suppression of apoptosis is one of the hallmarks of carcinogenesis. Tumor cells endure apoptotic pressure by overexpressing several antiapoptotic proteins, and FLICE inhibitory protein (FLIP) is one of the important antiapoptotic proteins that have been shown to be overexpressed in various primary tumor cells. FLIP has two death-effector domains in tandem, mimicking the prodomain of procaspase-8. It is recruited to Fadd in death-inducing signaling complex, thereby preventing the activation of procaspase-8. To date, three isoforms of human cytosolic FLIP (c-FLIP) and six viral homologs (v-FLIP) have been identified. Recently, the crystal structure of v-FLIP MC159 was determined for the first time as an atomic-detail FLIP structure, which revealed that two death effector domains are packed tightly against each other mainly through conserved hydrophobic interactions. The overexpression of c-FLIP in tumor cells has been shown to be the determinant of the tumor's resistance to death ligands such as FasL and TRAIL. It has also been shown that the down-regulation of c-FLIP results in sensitizing resistant tumor cells. Therefore, the agents directly targeting c-FLIP at mRNA and protein levels are expected to be developed in near future and tested for the potential as a new class of anti-cancer drugs.
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.