Evidence map›Paper›PMID 35892586›Full record

ArticleCells2022

AKT1 Transcriptomic Landscape in Breast Cancer Cells.

Bijesh George, Bin Gui, Rajeswari Raguraman, Aswathy Mary Paul, Harikrishna Nakshatri, Madhavan Radhakrishna Pillai, Rakesh Kumar

Open access · goldAbstract read
In one paragraph

Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 8% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
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  16. Public neoantigens in breast cancer immunotherapy (Review).International journal of molecular medicine · 2024
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 5 institutions in 2 countries.

Bijesh GeorgeCancer Research Program, Rajiv Gandhi Centre for Biotechnology, Trivandrum 695014, India.
Bin GuiBiological Sciences, Ribon Therapeutics, Inc., Cambridge, MA 02140, USA.
Rajeswari RaguramanCancer Research Program, Rajiv Gandhi Centre for Biotechnology, Trivandrum 695014, India.
Aswathy Mary PaulCancer Research Program, Rajiv Gandhi Centre for Biotechnology, Trivandrum 695014, India.
Harikrishna NakshatriDepartment of Surgery, Indiana University of School of Medicine, Indianapolis, IN 46202, USA.
Madhavan Radhakrishna PillaiCancer Research Program, Rajiv Gandhi Centre for Biotechnology, Trivandrum 695014, India.
Rakesh KumarCancer Research Program, Rajiv Gandhi Centre for Biotechnology, Trivandrum 695014, India.
Rajiv Gandhi Centre for Biotechnology · INIndiana University – Purdue University Indianapolis · USManipal Academy of Higher Education · INRibon Therapeutics (United States) · USRutgers New Jersey Medical School

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Overexpression and hyperactivation of the serine/threonine protein kinase B (AKT) pathway is one of the most common cellular events in breast cancer progression. However, the nature of AKT1-specific genome-wide transcriptomic alterations in breast cancer cells and breast cancer remains unknown to this point. Here, we delineate the impact of selective AKT1 knock down using gene-specific siRNAs or inhibiting the AKT activity with a pan-AKT inhibitor VIII on the nature of transcriptomic changes in breast cancer cells using the genome-wide RNA-sequencing analysis. We found that changes in the cellular levels of AKT1 lead to changes in the levels of a set of differentially expressed genes and, in turn, imply resulting AKT1 cellular functions. In addition to an expected positive relationship between the status of AKT1 and co-expressed cellular genes, our study unexpectedly discovered an inherent role of AKT1 in inhibiting the expression of a subset of genes in both unstimulated and growth factor stimulated breast cancer cells. We found that depletion of AKT1 leads to upregulation of a subset of genes-many of which are also found to be downregulated in breast tumors with elevated high AKT1 as well as upregulated in breast tumors with no detectable AKT expression. Representative experimental validation studies in two breast cancer cell lines showed a reasonable concurrence between the expression data from the RNA-sequencing and qRT-PCR or data from ex vivo inhibition of AKT1 activity in cancer patient-derived cells. In brief, findings presented here provide a resource for further understanding of AKT1-dependent modulation of gene expression in breast cancer cells and broaden the scope and significance of AKT1 targets and their functions.

Indexed as

Breast NeoplasmsProto-Oncogene Proteins c-aktFemaleHumansRNATranscriptomeAKT1 protein, humanProto-Oncogene Proteins c-aktRNAAKT1breast cancercancer therapeuticsemerging functions and targetsRNA-sequencingtranscriptome

Identifiers

PMID35892586
PMCPMC9332453
OpenAlexW4287837708

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.