Evidence map›Paper›PMID 39123360›Full record

ArticleCancers2024

High Mobility Group AT-hook 2: A Biomarker Associated with Resistance to Enzalutamide in Prostate Cancer Cells.

Yusuf Mansur Liadi, Taaliah Campbell, Bor-Jang Hwang, Bethtrice Elliott, Valerie Odero-Marah

Abstract read
In one paragraph

Article in Cancers, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. AI/ML-Assisted Detection ofInternational journal of molecular sciences · 2025
    Article
  2. HMGA2 regulates GPX4 expression and ferroptosis in prostate cancer cells.Biochemical and biophysical research communications · 2024
    Article
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

5 authors.

Yusuf Mansur LiadiCenter for Urban Health Disparities Research and Innovation, Department of Biology, Morgan State University, Baltimore, MD 21251, USA.
Taaliah CampbellCenter for Cancer Research and Therapeutic Development, Department of Biological Sciences, Clark Atlanta University, Atlanta, GA 30314, USA.
Bor-Jang HwangCenter for Urban Health Disparities Research and Innovation, Department of Biology, Morgan State University, Baltimore, MD 21251, USA.
Bethtrice ElliottCenter for Urban Health Disparities Research and Innovation, Department of Biology, Morgan State University, Baltimore, MD 21251, USA.
Valerie Odero-MarahCenter for Urban Health Disparities Research and Innovation, Department of Biology, Morgan State University, Baltimore, MD 21251, USA.ORCID 0000-0001-7525-4652

Funding

Wastewater surveillance for addressing environmental health disparitiesU54MD013376 · NIMHD · MORGAN STATE UNIVERSITY · PI Payam Sheikhattari · 2019 to 2026
$33.5M
To Investigate Molecular Mechanisms of Aging-Related Growth of the Prostate - Implications in Prostate Tumorigenesis and Cancer TreatmentU54MD007590 · NIMHD · CLARK ATLANTA UNIVERSITY · PI Cimona Vaughn Hinton Dirickson · 2019 to 2026
$17.1M
HMGA2 mediates resistance to therapy in prostate cancerR16GM149265 · NIGMS · MORGAN STATE UNIVERSITY · PI ODERO-MARAH, VALERIE · 2023 to 2023
$151k
National Institutes of Health, NIGMS R16GM149265National Institutes of Health, NIH/NIMHD 2U54MD007590National Institutes of Health, NIMHD U54MD013376NIGMS NIH HHS R16 GM149265NIMHD NIH HHS U54 MD007590NIMHD NIH HHS U54 MD013376
6 · The paper itself

Abstract

Metastatic prostate cancer (mPCa) is a leading cause of mortality, partly due to its resistance to anti-androgens like enzalutamide. Snail can promote this resistance by increasing full-length AR and AR-V7. High Mobility Group AT-hook 2 (HMGA2), a DNA-binding protein upstream of Snail, is crucial in proliferation and epithelial-mesenchymal transition (EMT). This study examines HMGA2's role in enzalutamide resistance. LNCaP and 22Rv1 cells overexpressing wild-type HMGA2, but not truncated HMGA2, showed EMT. Both variants led to a decreased sensitivity to enzalutamide but not alisertib compared to Neo control cells. The overexpression of HMGA2 did not alter AR expression. Enzalutamide-resistant C4-2B cells (C4-2B MDVR) had higher HMGA2 and AR/AR variant expression than enzalutamide-sensitive C4-2B cells but remained sensitive to alisertib. The HMGA2 knockdown in C4-2B MDVR cells increased sensitivity to both enzalutamide and alisertib without changing AR expression. A clinical analysis via cBioPortal revealed HMGA2 alterations in 3% and AR alterations in 59% of patients. The HMGA2 changes were linked to treatments like enzalutamide, abiraterone, or alisertib, with amplifications more prevalent in bone, lymph node, and liver metastases. Conclusively, HMGA2 is a potential biomarker for enzalutamide resistance in mPCa, independent of Snail and AR signaling, and alisertib may be an effective treatment for mPCa that expresses HMGA2.

Indexed as

alisertibandrogen receptor (AR)enzalutamideenzalutamide-resistantepithelial to mesenchymal transition (EMT)high mobility group AT-hook 2 (HMGA2)metastatic prostate cancerSnail

Identifiers

PMID39123360
PMCPMC11311100

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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.