Evidence map›Paper›PMID 40790586›Full record

ArticleJournal of ovarian research2025

MYB/AKT3 axis is a key driver of ovarian cancer growth, aggressiveness, and chemoresistance.

Kunwar Somesh Vikramdeo, Orlandric Miree, Shashi Anand, Amod Sharma, Sanjeev Kumar Srivastava, Seema Singh, Rodney P Rocconi, Ajay Pratap Singh

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of ovarian research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Article
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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

8 authors.

Kunwar Somesh Vikramdeo *Cancer Center and Research Institute, University of Mississippi Medical Center, Jackson, MS, USA.
Orlandric Miree *Mitchell Cancer Institute, University of South Alabama, Mobile, AL, USA.
Shashi AnandCancer Center and Research Institute, University of Mississippi Medical Center, Jackson, MS, USA.
Amod SharmaCancer Center and Research Institute, University of Mississippi Medical Center, Jackson, MS, USA.
Sanjeev Kumar SrivastavaMitchell Cancer Institute, University of South Alabama, Mobile, AL, USA.
Seema SinghCancer Center and Research Institute, University of Mississippi Medical Center, Jackson, MS, USA.
Rodney P RocconiCancer Center and Research Institute, University of Mississippi Medical Center, Jackson, MS, USA.
Ajay Pratap SinghCancer Center and Research Institute, University of Mississippi Medical Center, Jackson, MS, USA. asingh1@umc.edu.

Funding

Molecular determinant of racial disparity in prostate cancerU01CA185490 · NCI · UNIVERSITY OF SOUTH ALABAMA · PI SINGH, AJAY PRATAP · 2014 to 2018
$1.7M
NCI NIH HHS U01 CA185490NIH HHS U01CA185490NIH HHS U01CA185490-04S1
6 · The paper itself

Abstract

backgroundOvarian cancer (OC) remains the most lethal gynecologic malignancy in the United States due to its late diagnosis, aggressive nature, and poor responsiveness to existing therapies. Dissecting the molecular mechanisms and identifying molecular drivers of aggressiveness and therapy resistance is critical for devising new therapies and improving patient outcomes.

methodsMYB expression was evaluated in a panel of OC cell lines by immunoblotting. Gain and loss of function studies were performed by developing stable control and forced-MYB-expressing and -silenced cell lines, respectively. Functional assays included growth kinetics, clonogenicity, cell cycle, live-dead cell measurements, and annexin-V staining, followed by flow cytometry, migration and invasion assays, and MTT assays following drug treatment. Gene expression profiling was done using the nanoString PanCancer Progression panel. Chromatin immunoprecipitation (ChIP) was performed to confirm MYB binding to the responsive gene promoter, followed by siRNA-mediated silencing to establish the intermediary role in potentiating the downstream effects.

resultsLow to high MYB expression was reported in all OC cell lines, with negligible expression reported in normal ovarian surface epithelial cells. MYB expression was significantly higher in aggressive (SKOV3-ip) and chemoresistant (A2780-CP) OC cell lines compared to the parental (SKOV3 and A2780) cells. Functional assays in MYB-overexpressing and -silenced OC cell lines demonstrated a role of MYB overexpression in increased cell proliferation, survival, migration, invasion, EMT, and chemoresistance. nanoString analysis and comparison of transcriptomic data of MYB-silenced SKOV3-ip and MYB-overexpressing SKOV3 cells with their respective control cells identified MYB-dependent genes. Interestingly, these target genes showed a limited overlap between cell lines, suggesting a cell-specific MYB-regulated gene regulation. AKT3 was consistently identified as a common MYB-regulated gene in multiple OC cell lines and confirmed as a direct transcriptional MYB target through confirmation of MYB binding to its promoter. Pathway analysis using the MYB-regulated transcriptomic data also identified PI3K/Akt signaling to be activated in MYB-overexpressing cells. siRNA-mediated silencing of AKT3 confirmed its role in potentiating the oncogenic actions of MYB in OC cells.

conclusionMYB/AKT3 axis drives ovarian cancer growth, aggressiveness, and chemoresistance, highlighting its potential as a therapeutic target in ovarian cancer.

Indexed as

Drug Resistance, NeoplasmOvarian NeoplasmsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-mybCell Line, TumorCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansSignal TransductionAKT3 protein, humanMYB protein, humanProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-mybAKT3MYBOvarian cancer

Identifiers

PMID40790586
PMCPMC12337402

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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.