ArticleOncology letters2018
MicroRNA-433 targets AKT3 and inhibits cell proliferation and viability in breast cancer.
Article in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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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.
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Who cites it
24 citing papers in PubMed, 42 citations in OpenAlex.
- Article
- Cellular and Exosomal MicroRNAs: Emerging Clinical Relevance as Targets for Breast Cancer Diagnosis and Prognosis.Advanced biology · 2024Review
- Review
- Combinatorial Effects of miRNAs in HSV-2 Infection of Macrophages: An In Silico and In Vitro Integration Approach.Vaccines · 2023Article
- Evidence and Metabolic Implications for a New Non-Canonical Role of Cu-Zn Superoxide Dismutase.International journal of molecular sciences · 2023Article
- MiR-22-3p and miR-29a-3p synergistically inhibit hepatic stellate cell activation by targeting AKT3.Experimental biology and medicine (Maywood, N.J.) · 2022Article
- The role of MiRNA-433 in malignant tumors of digestive tract as tumor suppressor.Cancer reports (Hoboken, N.J.) · 2022Review
- miR-3614-3p suppresses cell aggressiveness of human breast cancer by targetingTranslational cancer research · 2022Article
- Akt Isoforms: A Family Affair in Breast Cancer.Cancers · 2021Review
- The epigenetic silencing of microRNA-433 facilitates the malignant phenotypes of non-small cell lung cancer by targeting CREB1.American journal of translational research · 2021Article
- MiR-485-3p serves as a biomarker and therapeutic target of Alzheimer's disease via regulating neuronal cell viability and neuroinflammation by targeting AKT3.Molecular genetics & genomic medicine · 2021Article
- RP11-480I12.5-004 Promotes Growth and Tumorigenesis of Breast Cancer by Relieving miR-29c-3p-Mediated AKT3 and CDK6 Degradation.Molecular therapy. Nucleic acids · 2020Article
- Potential miRNAs for miRNA-Based Therapeutics in Breast Cancer.Non-coding RNA · 2020Review
- Expression and role of miR-338-3p in peripheral blood and placenta of patients with pregnancy-induced hypertension.Experimental and therapeutic medicine · 2020Article
- miR-185-5p response to usnic acid suppresses proliferation and regulating apoptosis in breast cancer cell by targeting Bcl2.Biological research · 2020Article
- Linc01234 promotes cell proliferation and metastasis in oral squamous cell carcinoma via miR-433/PAK4 axis.BMC cancer · 2020Article
- MicroRNA-33b Suppresses Epithelial-Mesenchymal Transition Repressing the MYC-EZH2 Pathway in HER2+ Breast Carcinoma.Frontiers in oncology · 2020Article
- Distinct functions of AKT isoforms in breast cancer: a comprehensive review.Cell communication and signaling : CCS · 2019Review
- Review
- MiR-16-5p inhibits breast cancer by reducing AKT3 to restrain NF-κB pathway.Bioscience reports · 2019Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Breast cancer is the most frequently diagnosed malignancy in women. However, the molecular mechanisms underlying breast cancer pathogenesis are not fully understood. The present study examined the role of miR-433 in breast cancer and investigated its underlying molecular mechanisms of action. Reverse transcription-quantitative polymerase chain reaction and western blot analysis were performed to analyze the level of microRNA (miRNA/miR)/mRNA and protein expression, respectively. Additionally, MTT assay was used to determined cell proliferation and viability. Cell apoptosis was measured by flow cytometry. A dual-luciferase reporter assay was used to confirm the identity of the downstream target of miR-433. The results revealed that miR-433 was downregulated in breast cancer tissues and cell lines. Overexpression of miR-433 inhibited cell proliferation and cell viability in BT-549 cells, whereas downregulation of miR-433 increased cell proliferation and cell viability in MDA-MB-231 cells. Further flow cytometry analysis revealed that miR-433 was able to induce apoptosis and also alter the levels of proteins expression of B-cell lymphoma-2 and Bcl-associated X. Bioinformatics analysis showed that RAC-γ serine/threonine-protein kinase (AKT3) was one of the downstream targets of miR-433, and luciferase reporter assay further confirmed that AKT3 is a direct target of miR-433. The knockdown of AKT3 was able to inhibit proliferation and viability in BT-549 cells. Overexpression of AKT3 prevented the inhibitory effects of miR-433 on proliferation and viability in BT-549 cells. The level of AKT3 mRNA expression was upregulated in breast cancer tissues compared with normal tissues and was inversely correlated with miR-433 expression levels. In summary, the results of the present study results indicate that the tumor-suppressive role of miR-433 may be mediated by regulating AKT3. miR-433 may therefore serve as a potential therapeutic target for breast cancer.
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Registered trials
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