ArticleCell death & disease2014
MicroRNA-181a-mediated downregulation of AC9 protein decreases intracellular cAMP level and inhibits ATRA-induced APL cell differentiation.
Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- Modulation of all-trans retinoic acid-induced MiRNA expression in neoplastic cell lines: a systematic review.BMC cancer · 2019Pooled it
- Biochemical pharmacology of adenylyl cyclases in cancer.Biochemical pharmacology · 2024Review
- cAMP-PKA/EPAC signaling and cancer: the interplay in tumor microenvironment.Journal of hematology & oncology · 2024Review
- MiR92b-3p synthetic analogue impairs zebrafish embryonic development, leading to ocular defects, decreased movement and hatching rate, and increased mortality.Journal of applied genetics · 2023Article
- Physiological roles of mammalian transmembrane adenylyl cyclase isoforms.Physiological reviews · 2022Review
- Targeting Adenylate Cyclase Family: New Concept of Targeted Cancer Therapy.Frontiers in oncology · 2022Review
- A CREB1-miR-181a-5p loop regulates the pathophysiologic features of bone marrow stromal cells in fibrous dysplasia of bone.Molecular medicine (Cambridge, Mass.) · 2021Article
- Two Worlds Colliding: The Interplay Between Natural Compounds and Non-Coding Transcripts in Cancer Therapy.Frontiers in pharmacology · 2021Review
- Piceatannol suppresses proliferation and induces apoptosis by regulation of the microRNA‑21/phosphatase and tensin homolog/protein kinase B signaling pathway in osteosarcoma cells.Molecular medicine reports · 2020Article
- miR-188-5p Promotes Tumor Growth by Targeting CD2AP Through PI3K/AKT/mTOR Signaling in Children with Acute Promyelocytic Leukemia.OncoTargets and therapy · 2020Article
- Retinoic acid and microRNA.Methods in enzymology · 2020Article
- MicroRNA‑98 suppresses cell growth and invasion of retinoblastoma via targeting the IGF1R/k‑Ras/Raf/MEK/ERK signaling pathway.International journal of oncology · 2019Article
- The epithelial-to-mesenchymal transition activator ZEB1 initiates a prometastatic competing endogenous RNA network.The Journal of clinical investigation · 2018Article
- Long non-coding RNA SNHG1 regulates NOB1 expression by sponging miR-326 and promotes tumorigenesis in osteosarcoma.International journal of oncology · 2018Article
- International Union of Basic and Clinical Pharmacology. CI. Structures and Small Molecule Modulators of Mammalian Adenylyl Cyclases.Pharmacological reviews · 2017Review
- MicroRNA-92b promotes hepatocellular carcinoma progression by targeting Smad7 and is mediated by long non-coding RNA XIST.Cell death & disease · 2016Article
- miR-181a promotes G1/S transition and cell proliferation in pediatric acute myeloid leukemia by targeting ATM.Journal of cancer research and clinical oncology · 2016Article
- MicroRNA-155 and Its Role in Malignant Hematopoiesis.Biomarker insights · 2015Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
AC9 is one of the adenylate cyclase (AC) isoforms, which catalyze the conversion of ATP to cAMP, an important second messenger. We previously found that the integration of cAMP/PKA pathway with nuclear receptor-mediated signaling was required during all-trans retinoic acid (ATRA)-induced maturation of acute promyelocytic leukemia (APL) cells. Here we showed that AC9 could affect intracellular cAMP level and enhance the trans-activity of retinoic acid receptor. Knockdown of AC9 in APL cell line NB4 could obviously inhibit ATRA-induced differentiation. We also demonstrated that miR-181a could decrease AC9 expression by targeting 3'UTR of AC9 mRNA, finally controlling the production of intracellular cAMP. The expression of miR-181a itself could be inhibited by CEBPα, probably accounting for the differential expression of miR-181a in NB4 and ATRA-resistant NB4-R1 cells. Moreover, we found that AC9 expression was relatively lower in newly diagnosed or relapsed APL patients than in both complete remission and non-leukemia cases, closely correlating with the leukemogenesis of APL. Taken together, our studies revealed for the first time the importance of miR-181a-mediated AC9 downregulation in APL. We also suggested the potential value of AC9 as a biomarker in the clinical diagnosis and treatment of leukemia.
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