ArticleOncogene2018
ACTN4 regulates the stability of RIPK1 in melanoma.
Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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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.
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Who cites it
12 citing papers in PubMed, 30 citations in OpenAlex.
- Review
- Diagnostic and prognostic value of disulfidptosis-related genes in sepsis.Infectious medicine · 2024Article
- PHF23 promotes NSCLC proliferation, metastasis, and chemoresistance via stabilization of ACTN4 and activation of the ERK pathway.Cell death & disease · 2023Article
- Placental proteome in late‑onset of fetal growth restriction.Molecular medicine reports · 2022Article
- RNF38 suppress growth and metastasis via ubiquitination of ACTN4 in nasopharyngeal carcinoma.BMC cancer · 2022Article
- LncRNA TP73-AS1 Exacerbates the Non-Small-Cell Lung Cancer (NSCLC) Process via Regulating miR-125a-3p-Mediated ACTN4.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Alpha-actinin-4 is essential for maintaining normal trophoblast proliferation and differentiation during early pregnancy.Reproductive biology and endocrinology : RB&E · 2021Article
- Tumor-intrinsic determinants of immunogenic cell death modalities.Oncoimmunology · 2021Review
- E3 Ubiquitin Ligase UBR5 Promotes the Metastasis of Pancreatic CancerFrontiers in oncology · 2021Article
- Cylindromatosis Is Required for Survival of a Subset of Melanoma Cells.Oncology research · 2020Article
- Review
- Focal segmental glomerulosclerosis ACTN4 mutants binding to actin: regulation by phosphomimetic mutations.Scientific reports · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The actin crosslinking protein α-actinin-4 (ACTN4) is emerging as an important contributor to the pathogenesis of cancer. This has largely been attributed to its role in regulating cytoskeleton organization and its involvement in transcriptional regulation of gene expression. Here we report a novel function of ACTN4 as a scaffold necessary for stabilization of receptor-interacting protein kinase 1 (RIPK1) that we have recently found to be an oncogenic driver in melanoma. ACTN4 bound to RIPK1 and cellular inhibitor of apoptosis protein 1 (cIAP1) with its actin-binding domain at the N-terminus and the CaM-like domain at the C-terminus, respectively. This facilitated the physical association between RIPK1 and cIAP1 and was critical for stabilization of RIPK1 that in turn activated NF-κB. Functional investigations showed that silencing of ACTN4 suppressed melanoma cell proliferation and retarded melanoma xenograft growth. In contrast, overexpression of ACTN4 promoted melanocyte and melanoma cell proliferation and moreover, prompted melanocyte anchorage-independent growth. Of note, the expression of ACTN4 was transcriptionally activated by NF-κB. Taken together, our findings identify ACTN4 as an oncogenic regulator through driving a feedforward signaling axis of ACTN4-RIPK1-NF-κB, with potential implications for targeting ACTN4 in the treatment of melanoma.
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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.