ArticleCancer research2013
Application of a proapoptotic peptide to intratumorally spreading cancer therapy.
Article in Cancer research, 2013. 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, 57 citations in OpenAlex.
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- Recent Studies and Progress in the Intratumoral Administration of Nano-Sized Drug Delivery Systems.Nanomaterials (Basel, Switzerland) · 2023Review
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- Engineered Polymeric Nanovector for Intracellular Peptide Delivery in Antitumor Therapy.International journal of nanomedicine · 2023Article
- A Synthetic CPP33-ConjugatedBiomolecules · 2020Article
- PTRH2: an adhesion regulated molecular switch at the nexus of life, death, and differentiation.Cell death discovery · 2020Review
- Cellular internalization of bystander nanomaterial induced by TAT-nanoparticles and regulated by extracellular cysteine.Nature communications · 2019Article
- iRGD: A Promising Peptide for Cancer Imaging and a Potential Therapeutic Agent for Various Cancers.Journal of oncology · 2019Review
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- Peritoneal Carcinomatosis Targeting with Tumor Homing Peptides.Molecules (Basel, Switzerland) · 2018Review
- Co-administration of iRGD with peptide HPRP-A1 to improve anticancer activity and membrane penetrability.Scientific reports · 2018Article
- Cell Penetrating Peptides as Molecular Carriers for Anti-Cancer Agents.Molecules (Basel, Switzerland) · 2018Review
- Anti-EGFR-iRGD recombinant protein modified biomimetic nanoparticles loaded with gambogic acid to enhance targeting and antitumor ability in colorectal cancer treatment.International journal of nanomedicine · 2018Article
- Downregulation of Bit1 expression promotes growth, anoikis resistance, and transformation of immortalized human bronchial epithelial cells via Erk activation-dependent suppression of E-cadherin.Biochemical and biophysical research communications · 2018Article
- Tumor penetrating peptides for improved drug delivery.Advanced drug delivery reviews · 2017Review
- Article
- iRGD-targeted delivery of a pro-apoptotic peptide activated by cathepsin B inhibits tumor growth and metastasis in mice.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Strategies for improving the intratumoral distribution of liposomal drugs in cancer therapy.Expert opinion on drug delivery · 2016Review
- The Anoikis Effector Bit1 Inhibits EMT through Attenuation of TLE1-Mediated Repression of E-Cadherin in Lung Cancer Cells.PloS one · 2016Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Bit1 is a proapoptotic mitochondrial protein associated with anoikis. Upon cell detachment, Bit1 is released into the cytoplasm and triggers caspase-independent cell death. Bit1 consists of 179 amino acids; for the C-terminal, two thirds of the molecule functions as a peptidyl-tRNA hydrolase, whereas the N-terminus contains a mitochondrial localization signal. Here, we localize the cell death domain (CDD) to the N-terminal 62 amino acids of Bit1 by transfecting cells with truncated Bit1 cDNA constructs. CDD was more potent in killing cells than the full-length Bit1 protein when equivalent amounts of cDNA were transfected. To develop Bit1 CDD into a cancer therapeutic, we engineered a recombinant protein consisting of the CDD fused to iRGD, which is a tumor-specific peptide with unique tumor-penetrating and cell-internalizing properties. iRGD-CDD internalized into cultured tumor cells through a neuropilin-1-activated pathway and triggered cell death. Importantly, iRGD-CDD spread extensively within the tumor when injected intratumorally into orthotopically implanted breast tumors in mice. Repeated treatment with iRGD-CDD strongly inhibited tumor growth, resulting in an average reduction of 77% in tumor volume and eradication of some tumors. The caspase independence of Bit1-induced cell death makes CDD a potentially attractive anticancer agent, because tumor resistance to the main mechanisms of apoptosis is circumvented. Using iRGD to facilitate the spreading of a therapeutic agent throughout the tumor mass may be a useful adjunct to local therapy for tumors that are surgically inoperable or difficult to treat systemically.
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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.