ArticleBioengineered2022
Long non-coding RNA breast cancer-associated transcript 54 sponges microRNA-1269b to suppress the proliferation of hemangioma-derived endothelial cells.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- hsa_circ_0001776 regulates the progression of acute myeloid leukemia through the miR-1269b/PTEN axis.Turkish journal of biology = Turk biyoloji dergisi · 2025Article
- Non-coding RNA in infantile hemangioma.Pediatric research · 2024Review
- miRNAs in Heart Development and Disease.International journal of molecular sciences · 2024Review
- Transcriptional data analysis reveals the association between infantile hemangiomas and venous malformations.Frontiers in genetics · 2022Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long non-coding RNA (lncRNA) breast cancer-associated transcript 54 (BRCAT54) and microRNA-1269b (miR-1269b) are two critical ncRNAs in cancer biology, while their roles in hemangioma are unknown. Our preliminary sequencing data revealed their altered expression in hemangioma and predicted they could interact with each other. This study was therefore carried out to investigate the roles of BRCAT54 and miR-1269b in hemangioma, with a focus on their interaction. In this study, hemangioma samples donated by 20 infantile hemangioma patients at proliferating-phase and 20 infantile hemangioma patients at involuting-phase were used. The expression of BRCAT54 and miR-1269b in hemangioma samples, as well as hemangioma-derived endothelial cells (HDECs) and human umbilical vein endothelial cells (HUVECs) were detected by RT-qPCR. IntaRNA 2.0 was applied to predict the interaction between BRCAT54 and miR-1269b, which was then confirmed by RNA-RNA pulldown assay. Accumulation of BRCAT54 in the subcellular location of HDECs was detected by subcellular fractionation assay. The role of BRCAT54 and miR-1269b in cell proliferation has been explored by the BrdU assay. Compared to proliferating-phase tissues, involuting-phase tissues exhibited decreased expression levels of BRCAT54 and increased expression levels of miR-1269b. HDECs had decreased expression levels of BRCAT54 and increased expression levels of miR-1269b compared to that of HUVECs. In HDECs, BRCAT54, which was detected in both nuclear and cytoplasm fractions, directly interacted with miR-1269b. BRCAT54 and miR-1269b did not affect the expression of each other, while BRCAT54 suppressed the role of miR-1269b in enhancing the proliferation of HDECs. BRCAT54 may sponge miR-1269b to suppress the proliferation of HDECs.
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