ArticleNeoplasia (New York, N.Y.)2007
Targeting antiapoptotic Bcl-2 family members with cell-permeable BH3 peptides induces apoptosis signaling and death in head and neck squamous cell carcinoma cells.
Article in Neoplasia (New York, N.Y.), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 53 citations in OpenAlex.
- Overcoming Resistance to Standard-of-Care Therapies for Head and Neck Squamous Cell Carcinomas.Cells · 2024Review
- Roles and Regulation of BCL-xL in Hematological Malignancies.International journal of molecular sciences · 2022Review
- Apoptosis signaling molecules as treatment targets in head and neck squamous cell carcinoma.The Laryngoscope · 2020Article
- Cell-Permeable Bak BH3 Peptide Induces Chemosensitization of Hematologic Malignant Cells.Journal of oncology · 2020Article
- Article
- Optimal targeting of BCL-family proteins in head and neck squamous cell carcinoma requires inhibition of both BCL-xL and MCL-1.Oncotarget · 2019Article
- Live AttenuatedFrontiers in immunology · 2019Article
- Preferential targeting of cancer stem cells in the radiosensitizing effect of ABT-737 on HNSCC.Oncotarget · 2016Article
- Direct Activation of Bax Protein for Cancer Therapy.Medicinal research reviews · 2016Review
- Wee-1 kinase inhibition overcomes cisplatin resistance associated with high-risk TP53 mutations in head and neck cancer through mitotic arrest followed by senescence.Molecular cancer therapeutics · 2015Article
- Improving the therapeutic potential of endostatin by fusing it with the BAX BH3 death domain.Cell death & disease · 2014Article
- HOXC6 is deregulated in human head and neck squamous cell carcinoma and modulates Bcl-2 expression.The Journal of biological chemistry · 2012Article
- Targeting proliferation and survival pathways in head and neck cancer for therapeutic benefit.Chinese journal of cancer · 2012Review
- Celecoxib and Bcl-2: emerging possibilities for anticancer drug design.Future medicinal chemistry · 2012Review
- Intracellular delivery of a proapoptotic peptide via conjugation to a RAFT synthesized endosomolytic polymer.Molecular pharmaceutics · 2010Article
- Cyanide-induced apoptosis of dopaminergic cells is promoted by BNIP3 and Bax modulation of endoplasmic reticulum-mitochondrial Ca2+ levels.The Journal of pharmacology and experimental therapeutics · 2010Article
- The War on Cancer rages on.Neoplasia (New York, N.Y.) · 2009Article
- Review
- Synthetic galectin-3 inhibitor increases metastatic cancer cell sensitivity to taxol-induced apoptosis in vitro and in vivo.Neoplasia (New York, N.Y.) · 2009Article
- The mitochondrial death pathway: a promising therapeutic target in diseases.Journal of cellular and molecular medicine · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Head and neck squamous cell carcinomas (HNSCC) are frequently characterized by chemotherapy and radiation resistance, and by overexpression of Bcl-XL, an antiapoptotic member of the Bcl-2 protein family. In this report we examined whether cell-permeable peptides derived from the BH3 domains of proapoptotic Bax, Bad, or Bak could be used to target Bcl-XL and/or Bcl-2 in HNSCC cells, and induce apoptotic death in these cells. To render the peptides cell permeable, Antennapedia (Ant) or polyarginine (R8) peptide transduction domains were fused to the amino termini. Fluorescence microscopy of peptide-treated HNSCC cells revealed that the BH3 peptides colocalized with mitochondria, the site of Bcl-XL and Bcl-2 expression. By contrast, a mutant peptide (BaxE BH3) which cannot bind Bcl-XL or Bcl-2 was diffusely localized throughout the cytoplasm. Treatment of three HNSCC cell lines (1483, UM-22A, UM-22B) with the wild-type BH3 peptides resulted in loss of viability and induction of apoptosis, as assessed by MTS assays and annexin V staining. In general, Ant-conjugated peptides were more potent than R8-conjugated peptides, and Bad BH3 peptide was typically more potent than Bax BH3 or Bak BH3. Treatment of purified HNSCC mitochondria with BH3 peptides resulted in robust release of cytochrome c. Thus, the relative apoptosis resistance of HNSCC cells is not due to a deficit in this step of the intrinsic, mitochondrial-mediated apoptosis pathway. We conclude that cell-permeable BH3 peptides can be used to target Bcl-XL and/or Bcl-2 in HNSCC, and targeting of these proteins may have therapeutic value in the treatment of this disease.
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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.