Evidence map›Paper›PMID 28176758›Full record

ArticleNature communications2017

LncRNA AK023948 is a positive regulator of AKT.

Pratirodh Koirala, Jianguo Huang, Tsui-Ting Ho, Fangting Wu, Xianfeng Ding, Yin-Yuan Mo

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
5.4field-weighted citation impact, top 3% 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

72 citing papers in PubMed, 114 citations in OpenAlex.

  1. Article
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  3. Tuning epigenetics to enhance cancer virotherapy.Acta pharmaceutica Sinica. B · 2026
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  10. Frontiers in immunology · 2025
    Article
  11. Review
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  16. Article
  17. Advances in CRISPR therapeutics.Nature reviews. Nephrology · 2023
    Review
  18. Review
  19. Article
  20. Long noncoding RNA-mediated activation of PROTOR1/PRR5-AKT signaling shunt downstream of PI3K in triple-negative breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article

12 more citing papers are in PubMed but not listed here.

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

6 authors at 2 institutions in 2 countries.

Pratirodh KoiralaCancer Institute, University of Mississippi Medical Center, Jackson, Mississippi 39216, USA.
Jianguo HuangCancer Institute, University of Mississippi Medical Center, Jackson, Mississippi 39216, USA.
Tsui-Ting HoCancer Institute, University of Mississippi Medical Center, Jackson, Mississippi 39216, USA.
Fangting WuSystem Biosciences, Mountain View, California 94041, USA.
Xianfeng DingCancer Institute, University of Mississippi Medical Center, Jackson, Mississippi 39216, USA.
Yin-Yuan MoCancer Institute, University of Mississippi Medical Center, Jackson, Mississippi 39216, USA.
University of Mississippi Medical Center · USSystem Biosciences (United States) · US

Funding

The Akt-associated microRNAs in cancer cellsR01CA154989 · NCI · UNIVERSITY OF MISSISSIPPI MED CTR · PI MO, YIN-YUAN · 2011 to 2015
$1.5M
NCI NIH HHS R01 CA154989
6 · The paper itself

Abstract

Despite the overwhelming number of human long non-coding RNAs (lncRNAs) reported so far, little is known about their physiological functions for the majority of them. The present study uses a CRISPR/Cas9-based synergistic activation mediator (SAM) system to identify potential lncRNAs capable of regulating AKT activity. Among lncRNAs identified from this screen, we demonstrate that AK023948 is a positive regulator for AKT. Knockout of AK023948 suppresses, whereas rescue with AK023948 restores the AKT activity. Mechanistically, AK023948 functionally interacts with DHX9 and p85. Importantly, AK023948 is required for the interaction between DHX9 and p85 to hence the p85 stability and promote AKT activity. Finally, AK023948 is upregulated in breast cancer; interrogation of TCGA data set indicates that upregulation of DHX9 in breast cancer is associated with poor survival. Together, this study demonstrates two previously uncharacterized factors AK023948 and DHX9 as important players in the AKT pathway, and that their upregulation may contribute to breast tumour progression.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsBreastBreast NeoplasmsClass Ia Phosphatidylinositol 3-KinaseCRISPR-Cas SystemsDEAD-box RNA HelicasesDisease ProgressionFemaleGene Knockout TechniquesHumansMCF-7 CellsMice, NudeNeoplasm ProteinsProto-Oncogene Proteins c-aktRNA, Long NoncodingClass Ia Phosphatidylinositol 3-KinaseDEAD-box RNA HelicasesDHX9 protein, humanNeoplasm ProteinsProto-Oncogene Proteins c-aktRNA, Long NoncodingRNA, Small Interfering

Identifiers

PMID28176758
PMCPMC5309785
OpenAlexW2587669339

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.