ArticleInternational journal of clinical and experimental pathology2019
Interference from LncRNA SPRY4-IT1 restrains the proliferation, migration, and invasion of melanoma cells through inactivating MAPK pathway by up-regulating miR-22-3p.
Article in International journal of clinical and experimental pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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.
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Who cites it
13 citing papers in PubMed, 24 citations in OpenAlex.
- Review
- Novel Biological Strategies for Melanoma Therapy: A Focus on lncRNAs and Their Targeting.Cancers · 2025Review
- [Effect of phosphorylated HSP27 on the proliferation and metastasis of nasopharyngeal carcinoma and its mechanism].Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology head and neck surgery · 2024Article
- Pancreatic Neuroendocrine Tumors: Signaling Pathways and Epigenetic Regulation.International journal of molecular sciences · 2024Review
- LncRNAs in melanoma phenotypic plasticity: emerging targets for promising therapies.RNA biology · 2024Review
- Pathogenic roles of long noncoding RNAs in melanoma: Implications in diagnosis and therapies.Genes & diseases · 2023Review
- Long non-coding RNAs involved in different steps of cancer metastasis.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022Review
- Review
- The pleiotropic roles of circular and long noncoding RNAs in cutaneous melanoma.Molecular oncology · 2022Review
- A Review on the Role of SPRY4-IT1 in the Carcinogenesis.Frontiers in oncology · 2021Review
- Article
- Long Non-Coding RNAs: Role in Testicular Cancers.Frontiers in oncology · 2021Review
- SPRY4-IT1 promotes survival of colorectal cancer cells through regulating PDK1-mediated glycolysis.Animal cells and systems · 2020Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Melanoma is a common malignancy with a low survival rate worldwide. Long non-coding RNA Sprouty4-Intron 1 (SPRY4-IT1) is correlated with various cancers, including melanoma. Herein, the underlying molecular mechanisms of SPRY4-IT1 in melanoma were characterized. We found that SPRY4-IT1 level was upregulated in melanoma cells lines compared to the normal skin cells, while miR-22-3p was downregulated. According to of bioinformatics analysis, SPRY4-IT1 was a hypothetic target of miR-22-3p, and knockdown SPRY4-IT1 by sh-RNA (sh-SPRY4-IT1) markedly elevated the miR-22-3p level. Also, the target relationship was further confirmed by dual luciferase reporter assay. In addition, low-expression of SPRY4-IT1 impeded cell proliferation, invasion, migration, and epithelial-mesenchymal transition. Furthermore, western blot assay indicated that the enhanced miR-22-3p further decelerated the phosphorylation of p38MAPK, MAPKAPK and Hsp27, which indicates that miR-22-3p could inactivate the p38MAPK/MAPKAPK/Hsp27 signaling pathway. Overall, our results show that sh-SPRY4-IT1 inhibits cell proliferation and motility through inactivating MAPK signaling by up-regulating miR-22-3p. Therefore, designing targeted drugs against SPRY4-IT1 provides a new direction for the treatment of melanoma.
Indexed as
Identifiers
31933852PMC6945084W3028115925What Socratic holds
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 Socratic graph.