ArticleMolecular cancer therapeutics2016
AKT Inhibition Promotes Nonautonomous Cancer Cell Survival.
Article in Molecular cancer therapeutics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- An enrichment-based approach to interpreting metabolomic data using differential metabolomic profiles within the iDMET framework.BMC bioinformatics · 2026Article
- iDMET: network-based approach for integrating differential analysis of cancer metabolomics.BMC bioinformatics · 2022Article
- Article
- Isoliensinine induces cervical cancer cell cycle arrest and apoptosis by inhibiting the AKT/GSK3α pathway.Oncology letters · 2022Article
- Adaptive Mechanisms of Tumor Therapy Resistance Driven by Tumor Microenvironment.Frontiers in cell and developmental biology · 2021Review
- Resistance to Neoadjuvant Treatment in Breast Cancer: Clinicopathological and Molecular Predictors.Cancers · 2020Review
- A post-transcriptional program of chemoresistance by AU-rich elements and TTP in quiescent leukemic cells.Genome biology · 2020Article
- Tumor microenvironment-driven non-cell-autonomous resistance to antineoplastic treatment.Molecular cancer · 2019Review
- Blocking AMPK/ULK1-dependent autophagy promoted apoptosis and suppressed colon cancer growth.Cancer cell international · 2019Article
- Identification and removal of sequencing artifacts produced by mispriming during reverse transcription in multiple RNA-seq technologies.RNA (New York, N.Y.) · 2018Article
- AKT1Molecular cancer therapeutics · 2018Article
- Analysis of MicroRNA-Mediated Translation Activation of In Vitro Transcribed Reporters in Quiescent Cells.Methods in molecular biology (Clifton, N.J.) · 2018Article
- AKT1Breast cancer research : BCR · 2017Article
- Somatic PI3K activity regulates transition to the spermatocyte stages in Drosophila testis.Journal of biosciences · 2017Article
- Dual inhibition of Akt and c-Met as a second-line therapy following acquired resistance to sorafenib in hepatocellular carcinoma cells.Molecular oncology · 2017Article
- Fetal Bovine Serum RNA Interferes with the Cell Culture derived Extracellular RNA.Scientific reports · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Small molecule inhibitors of AKT (v-akt murine thymoma viral oncogene homolog) signaling are being evaluated in patients with various cancer types, but have so far proven therapeutically disappointing for reasons that remain unclear. Here, we treat cancer cells with subtherapeutic doses of Akti-1/2, an allosteric small molecule AKT inhibitor, in order to experimentally model pharmacologic inhibition of AKT signaling in vitro. We then apply a combined RNA, protein, and metabolite profiling approach to develop an integrated, multiscale, molecular snapshot of this "AKT(low)" cancer cell state. We find that AKT-inhibited cancer cells suppress thousands of mRNA transcripts, and proteins related to the cell cycle, ribosome, and protein translation. Surprisingly, however, these AKT-inhibited cells simultaneously upregulate a host of other proteins and metabolites posttranscriptionally, reflecting activation of their endo-vesiculo-membrane system, secretion of inflammatory proteins, and elaboration of extracellular microvesicles. Importantly, these microvesicles enable rapidly proliferating cancer cells of various types to better withstand different stress conditions, including serum deprivation, hypoxia, or cytotoxic chemotherapy in vitro and xenografting in vivo. These findings suggest a model whereby cancer cells experiencing a partial inhibition of AKT signaling may actually promote the survival of neighbors through non-cell autonomous communication.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.