ArticleOncogene2005
Growth factors rescue cutaneous melanoma cells from apoptosis induced by knockdown of mutated (V 600 E) B-RAF.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 49 citations in OpenAlex.
- A Positive Feedback DNA-PK/MYT1L-CXCR1-ERK1/2 Proliferative Signaling Loop in Glioblastoma.International journal of molecular sciences · 2025Article
- Inhibition of endothelin-B receptor signaling synergizes with MAPK pathway inhibitors in BRAF mutated melanoma.Oncogene · 2021Article
- HGF/c-MET Signaling in Melanocytes and Melanoma.International journal of molecular sciences · 2018Review
- Developmental pathways activated in melanocytes and melanoma.Archives of biochemistry and biophysics · 2014Review
- Dysfunctional oxidative phosphorylation makes malignant melanoma cells addicted to glycolysis driven by the (V600E)BRAF oncogene.Oncotarget · 2013Article
- Comparative exome sequencing of metastatic lesions provides insights into the mutational progression of melanoma.BMC genomics · 2012Article
- The helicase HAGE expressed by malignant melanoma-initiating cells is required for tumor cell proliferation in vivo.The Journal of biological chemistry · 2012Article
- The current state of targeted therapy in melanoma: this time it's personal.Seminars in oncology · 2012Review
- Pharmacodynamic characterization of the efficacy signals due to selective BRAF inhibition with PLX4032 in malignant melanoma.Neoplasia (New York, N.Y.) · 2010Article
- Recovery of phospho-ERK activity allows melanoma cells to escape from BRAF inhibitor therapy.British journal of cancer · 2010Article
- Melanocytes in development and cancer.Journal of cellular physiology · 2010Review
- Proliferation and survival molecules implicated in the inhibition of BRAF pathway in thyroid cancer cells harbouring different genetic mutations.BMC cancer · 2009Article
- Distinct genetic alterations in the mitogen-activated protein kinase pathway dictate sensitivity of thyroid cancer cells to mitogen-activated protein kinase kinase 1/2 inhibition.Thyroid : official journal of the American Thyroid Association · 2009Article
- Melanoma biology and the promise of zebrafish.Zebrafish · 2008Review
- Deoxyribonucleic acid profiling analysis of 40 human thyroid cancer cell lines reveals cross-contamination resulting in cell line redundancy and misidentification.The Journal of clinical endocrinology and metabolism · 2008Article
- Oncogenic BRAF(V600E) inhibits BIM expression to promote melanoma cell survival.Pigment cell & melanoma research · 2008Article
- Targeting V600EB-Raf and Akt3 using nanoliposomal-small interfering RNA inhibits cutaneous melanocytic lesion development.Cancer research · 2008Article
- Akt3 and mutant V600E B-Raf cooperate to promote early melanoma development.Cancer research · 2008Article
- Human cutaneous melanoma; a review of NRAS and BRAF mutation frequencies in relation to histogenetic subclass and body site.Molecular oncology · 2008Article
- BRAF(E600) in benign and malignant human tumours.Oncogene · 2008Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Constitutive activation of the RAS-RAF-MEK-ERK signaling cascade is a hallmark of cutaneous malignant melanoma. A single activating mutation (c.1799 T>A; p.V 600 E) in the gene encoding the serine/threonine kinase B-RAF occurs in >60% of the tumors. Previous work has shown that knockdown of (V 600 E)B-RAF by RNA interference induces a variety of phenotypic changes in cultured melanoma cells, including lower proliferation rates, reduced anchorage-independent growth and apoptosis. Here, we show that the majority of melanomas harboring the (V 600 E)B-RAF mutation have retained the wild-type (WT) B-RAF allele, and that these cells can be rescued from the effects of (V 600 E)B-RAF knockdown by stimulation with growth factors. Ectopic expression of short hairpin RNAs specifically suppressing (V 600 E)B-RAF in melanoma cell lines reduced colony formation by approximately 80%. This response could be rescued by basic fibroblast growth factor, hepatocyte growth factor or, to a lesser extent, endothelin-1. Rescue with growth factors was not possible in cell lines lacking (WT)B-RAF. Single-cell clones with efficient knockdown of (V 600 E)B-RAF could be propagated in the presence of basic fibroblast growth factor but underwent apoptosis or senescence-like growth arrest upon withdrawal of this growth factor. The ability of growth factors to modulate the response of (V 600 E)B-RAF knockdown in melanoma cells may have both experimental and therapeutic implications.
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