ArticleOncotarget2015
AKT3 promotes prostate cancer proliferation cells through regulation of Akt, B-Raf, and TSC1/TSC2.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 43 citations in OpenAlex.
- Comprehensive Epigenome-Wide Profiling Reveals Distinctive DNA Methylation Signatures and Potential Prognostic Biomarkers in Mexican Pediatric B-ALL.International journal of molecular sciences · 2025Article
- The impact of zinc and testosterone co-treatment on tumourigenesis in prostate cancer: a novel model.BMC cancer · 2025Article
- MYB/AKT3 axis is a key driver of ovarian cancer growth, aggressiveness, and chemoresistance.Journal of ovarian research · 2025Article
- Review
- Potential Drug Synergy Through the ERBB2 Pathway in HER2+ Breast Tumors.International journal of molecular sciences · 2024Article
- Important Roles of PI3K/AKT Signaling Pathway and Relevant Inhibitors in Prostate Cancer Progression.Cancer medicine · 2024Review
- PTEN-regulated PI3K-p110 and AKT isoform plasticity controls metastatic prostate cancer progression.Oncogene · 2024Article
- Article
- LINC01207 promotes prostate cancer progression by sponging miR-1182 to upregulate AKT3.Oncology letters · 2022Article
- Hsa_circ_0000520 Promotes Non-Small Cell Lung Cancer Progression through the miR-1258/AKT3 Axis.Journal of oncology · 2022Article
- Hypomethylation-driven AKT Serine/Threonine Kinase 3 promotes testicular germ cell tumors proliferation and negatively correlates to immune infiltration.Bioengineered · 2021Article
- Ultrasound-Based Method for the Identification of Novel MicroRNA Biomarkers in Prostate Cancer.Genes · 2021Article
- The potent AMPK inhibitor BAY-3827 shows strong efficacy in androgen-dependent prostate cancer models.Cellular oncology (Dordrecht, Netherlands) · 2021Article
- AKT3 is a key regulator of head and neck squamous cell carcinoma.Cancer science · 2021Article
- Role of TSC1 in physiology and diseases.Molecular and cellular biochemistry · 2021Review
- Oncogenic role of MiR-130a in oral squamous cell carcinoma.Scientific reports · 2021Article
- Article
- RHPN1-AS1 promotes cell proliferation and migration via miR-665/Akt3 in ovarian cancer.Cancer gene therapy · 2021Article
- Inferring Differential Networks by Integrating Gene Expression Data With Additional Knowledge.Frontiers in genetics · 2021Article
- Identification of biomarkers and pathways in hypertensive nephropathy based on the ceRNA regulatory network.BMC nephrology · 2020Article
Corrections and comments
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Authors and funding
16 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The qRT-PCR analysis of 139 clinical samples and analysis of 150 on-line database clinical samples indicated that AKT3 mRNA expression level was elevated in primary prostate tumors. Immunohistochemical staining of 65 clinical samples revealed that AKT3 protein expression was higher in prostate tumors of stage I, II, III as compared to nearby normal tissues. Plasmid overexpression of AKT3 promoted cell proliferation of LNCaP, PC-3, DU-145, and CA-HPV-10 human prostate cancer (PCa) cells, while knockdown of AKT3 by siRNA reduced cell proliferation. Overexpression of AKT3 increased the protein expression of total AKT, phospho-AKT S473, phospho-AKT T308, B-Raf, c-Myc, Skp2, cyclin E, GSK3β, phospho-GSK3β S9, phospho-mTOR S2448, and phospho-p70S6K T421/S424, but decreased TSC1 (tuberous sclerosis 1) and TSC2 (tuberous Sclerosis Complex 2) proteins in PC-3 PCa cells. Overexpression of AKT3 also increased protein abundance of phospho-AKT S473, phospho-AKT T308, and B-Raf but decreased expression of TSC1 and TSC2 proteins in LNCaP, DU-145, and CA-HPV-10 PCa cells. Oncomine datasets analysis suggested that AKT3 mRNA level was positively correlated to BRAF. Knockdown of AKT3 in DU-145 cells with siRNA increased the sensitivity of DU-145 cells to B-Raf inhibitor treatment. Knockdown of TSC1 or TSC2 promoted the proliferation of PCa cells. Our observations implied that AKT3 may be a potential therapeutic target for PCa treatment.
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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 OpenQuestion graph.