ArticleAmerican journal of physiology. Cell physiology2020
Suppression of long noncoding RNA MALAT1 inhibits the development of uveal melanoma via microRNA-608-mediated inhibition of HOXC4.
Article in American journal of physiology. Cell physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 27 citations in OpenAlex.
- Article
- Review
- MALAT1 as a molecular driver of tumor progression, immune evasion, and resistance to therapy.Molecular cancer · 2025Review
- STAT6/LINC01637 axis regulates tumor growth via autophagy and pharmacological targeting STAT6 as a novel strategy for uveal melanoma.Cell death & disease · 2024Article
- HOXC4 promotes proliferation of pancreatic cancer cells by increasing LDHA-mediated glycolysis.Aging · 2024Article
- The Role of Autophagy in Human Uveal Melanoma and the Development of Potential Disease Biomarkers and Novel Therapeutic Paradigms.Biomedicines · 2024Review
- Potential roles of lncRNA MALAT1-miRNA interactions in ocular diseases.Journal of cell communication and signaling · 2023Review
- Deconstructing the role of MALAT1 in MAPK-signaling in melanoma: insights from antisense oligonucleotide treatment.Oncotarget · 2023Article
- Genetics and RNA Regulation of Uveal Melanoma.Cancers · 2023Review
- LINC01278 Induces Autophagy to Inhibit Tumour Progression by Suppressing the mTOR Signalling Pathway.Oxidative medicine and cellular longevity · 2023Article
- MiR-520a-5p/PPP5C regulation pattern is identified as the key to gemcitabine resistance in pancreatic cancer.Frontiers in oncology · 2022Article
- Biological Functions and Molecular Mechanisms of MiR-608 in Cancer.Frontiers in oncology · 2022Review
- Review
- The Role of LncRNAs in Uveal Melanoma.Cancers · 2021Review
- Comprehensive Review on the Clinical Relevance of Long Non-Coding RNAs in Cutaneous Melanoma.International journal of molecular sciences · 2021Review
- Autophagy-Related Long Non-coding RNA Signature as Indicators for the Prognosis of Uveal Melanoma.Frontiers in genetics · 2021Article
- LncRNACancers · 2020Article
- Long non-coding RNA SNHG6 promotes tumorigenesis in melanoma cells via the microRNA-101-3p/RAP2B axis.Oncology letters · 2020Article
- Single-Cell RNA Sequencing Unravels Heterogeneity of the Stromal Niche in Cutaneous Melanoma Heterogeneous Spheroids.Cancers · 2020Article
- The Role of Non-Coding RNAs in Uveal Melanoma.Cancers · 2020Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study explored the effects of the metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) on the development of uveal melanoma. Moreover, the role of the MALAT1/microRNA-608 (miR-608)/homeobox C4 (HOXC4) axis was assessed by evaluating the proliferation, invasion, and migration, as well as the cell cycle distribution of uveal melanoma in vitro after knocking down MALAT1 or HOXC4 and/or overexpression of miR-608 in uveal melanoma cells (MUM-2B and C918). Moreover, the effects of the MALAT1/miR-608/HOXC4 axis in uveal melanoma in vivo were further evaluated by injecting the C918 cells into the NOD/SCID mice. HOXC4 was found to be a gene upregulated in uveal melanoma, while knockdown of its expression resulted in suppression of uveal melanoma cell migration, proliferation, and invasion, as well as cell cycle progression. In addition, the upregulation of miR-608 reduced the expression of HOXC4 in the uveal melanoma cells, which was rescued by overexpression of MALAT1. Hence, MALAT1 could upregulate the HOXC4 by binding to miR-608. The suppressed progression of uveal melanoma in vitro by miR-608 was rescued by overexpression of MALAT1. Additionally, in vivo assays demonstrated that downregulation of MALAT1 could suppress tumor growth through downregulation of HOXC4 expression via increasing miR-608 in uveal melanoma. In summary, MALAT1 downregulation functions to restrain the development of uveal melanoma via miR-608-mediated inhibition of HOXC4.
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