Evidence map›Paper›PMID 40522370›Full record

ArticleMedical oncology (Northwood, London, England)2025

Hypoxanthine activates PI3K/AKT pathway and lipid metabolism, hallmarks in breast cancer metastasis.

Sarra B Shakartalla, Amal Bouzid, Alaa M Altaie, Naglaa S Ashmawy, Zainab M Al Shareef, Mohamed I Husseiny, Sameh S M Soliman

Abstract read
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In one paragraph

Article in Medical oncology (Northwood, London, England), 2025. 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. Article
  2. 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

7 authors.

Sarra B ShakartallaResearch Institute for Medical and Health Sciences, University of Sharjah, P.O. Box 27272, Sharjah, United Arab Emirates.
Amal BouzidResearch Institute for Medical and Health Sciences, University of Sharjah, P.O. Box 27272, Sharjah, United Arab Emirates.
Alaa M AltaieResearch Institute for Medical and Health Sciences, University of Sharjah, P.O. Box 27272, Sharjah, United Arab Emirates.
Naglaa S AshmawyDepartment of Pharmaceutical Sciences, College of Pharmacy, Dubai Medical University, Dubai, United Arab Emirates.
Zainab M Al ShareefCollege of Medicine, University of Sharjah, P.O. Box 27272, Sharjah, United Arab Emirates.
Mohamed I HusseinyDepartment of Translational Research & Cellular Therapeutics, Arthur Riggs Diabetes & Metabolism Research Institute, Beckman Research Institute, City of Hope National Medical Center, Duarte, CA, 91010, USA.
Sameh S M SolimanResearch Institute for Medical and Health Sciences, University of Sharjah, P.O. Box 27272, Sharjah, United Arab Emirates. ssoliman@sharjah.ac.ae.

Funding

Al Jalila Foundation AJF2023-078‎
6 · The paper itself

Abstract

Metastasis is the primary cause of death in women with breast cancer, which ranks among the most prevalent malignant diseases. Recently, we identified the significant metastatic role of hypoxanthine (HYP) in cancer cells. HYP is a naturally occurring purine derivative that actively participates in the synthesis of nucleic acids via the nucleotide salvage pathway. To gain a deeper insight onto the metastatic mechanism of HYP, integrated transcriptomics and metabolomics were conducted following the treatment of MCF-7 cells with HYP. HYP significantly activates PI3K/AKT pathway, a hallmark of cancer metastasis. Glycerolipid and fatty acid metabolisms are among the top-upregulated lipid metabolic pathways, while glycolysis is dysregulated. Seahorse real-time ATP rate analysis revealed a significant decrease in ATP production from the glycolysis pathway in HYP-treated cancer cells. On the other hand, genetic information processes including gene transcription and protein translation were downregulated. Collectively, our results highlight the contribution of HYP to cancer cell metastasis through the PI3K/AKT pathway. Consequently, manipulating HYP release could serve as a therapeutic target for the management of breast cancer.

Indexed as

Breast NeoplasmsHypoxanthineLipid MetabolismPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktFemaleGene Expression Regulation, NeoplasticGlycolysisHumansMCF-7 CellsNeoplasm MetastasisSignal TransductionHypoxanthinePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktBreast cancerHypoxanthineMetabolomicsMetastasisTranscriptomics

Identifiers

PMID40522370

What Socratic holds

Textmetadata
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 Socratic graph.