ArticleScientific reports2022
PLP2-derived peptide Rb4 triggers PARP-1-mediated necrotic death in murine melanoma cells.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Design of synthetic selenopeptides with antioxidant activity for the treatment of XP and non-melanoma skin cancer.Frontiers in systems biology · 2026Article
- Identification of biological significance of different stages of varicose vein development based on mRNA sequencing.Scientific reports · 2024Article
- A limitless Brazilian scientist: Professor Travassos and his contribution to cancer biology.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2023Review
- Recent advances and applications of peptide-agent conjugates for targeting tumor cells.Journal of cancer research and clinical oncology · 2023Review
- PLP2 Could Be a Prognostic Biomarker and Potential Treatment Target in Glioblastoma Multiforme.Pharmacogenomics and personalized medicine · 2023Article
- Role of HMGB1 in Cutaneous Melanoma: State of the Art.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Malignant melanoma is the main cause of death in patients with skin cancer. Overexpression of Proteolipid protein 2 (PLP2) increased tumor metastasis and the knockdown of PLP2 inhibited the growth and metastasis of melanoma cells. In the present work, we studied the antitumor activity of peptide Rb4 derived from protein PLP2. In vitro, Rb4 induced F-actin polymerization, prevented F-actin depolymerization and increased the ER-derived cytosolic calcium. Such effects were associated with necrosis of murine melanoma B16F10-Nex2 cells and with inhibition of the viability of human cancer cell lines. Loss of plasma membrane integrity, dilation of mitochondria, cytoplasm vacuolation and absence of chromatin condensation characterized tumor cell necrosis. Cleavage of PARP-1 and inhibition of RIP1 expression were also observed. In vivo, peptide Rb4 reduced the lung metastasis of tumor cells and delayed the subcutaneous melanoma growth in a syngeneic model. Rb4 induced the expression of two DAMPs molecules, HMGB1 and calreticulin, in B16F10-Nex2. Our results suggest that peptide Rb4 acts directly on tumor cells inducing the expression of DAMPs, which trigger the immunoprotective effect in vivo against melanoma cells. We suggest that peptide Rb4 is a promising compound to be developed as an anticancer drug.
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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.