Evidence map›Paper›PMID 39757677›Full record

ArticleAnti-cancer agents in medicinal chemistry2025

Cucurbitacin E Glucoside as an Apoptosis Inducer in Melanoma Cancer Cells by Modulating AMPK/PGK1/PKM2 Pathway.

Mohammed Abdalla Hussein, Aya Sayed Sallam, Shaza Ahmed Mohamed, Amera Mahmoud Abdel-Rady, Adam Mostafa Maghrabe, Abdelrahman Wahdan Soltan, Hanan Mohamed Abdelhamid, Gaber E Eldesoky, Seikh Mafiz Alam, Mohammad Shahidul Islam

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Article in Anti-cancer agents in medicinal chemistry, 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. Review
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4 · The record

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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

10 authors.

Mohammed Abdalla HusseinDepartment of Biotechnology, Faculty of Applied Health Science, October 6 University, Giza, Egypt.
Aya Sayed SallamDepartment of Biotechnology, Faculty of Applied Health Science, October 6 University, Giza, Egypt.
Shaza Ahmed MohamedDepartment of Biotechnology, Faculty of Applied Health Science, October 6 University, Giza, Egypt.
Amera Mahmoud Abdel-RadyDepartment of Biotechnology, Faculty of Applied Health Science, October 6 University, Giza, Egypt.
Adam Mostafa MaghrabeDepartment of Biotechnology, Faculty of Applied Health Science, October 6 University, Giza, Egypt.
Abdelrahman Wahdan SoltanDepartment of Biotechnology, Faculty of Applied Health Science, October 6 University, Giza, Egypt.
Hanan Mohamed AbdelhamidDepartment of Biotechnology, Faculty of Applied Health Science, October 6 University, Giza, Egypt.
Gaber E EldesokyDepartment of Chemistry, College of Science, King Saud University, P.O. Box 2455, Riyadh, 11451, Saudi Arabia.
Seikh Mafiz AlamDepartment of Chemistry, Aliah University, New Town, Kolkata, 700 156, India.
Mohammad Shahidul IslamDepartment of Chemistry, College of Science, King Saud University, P.O. Box 2455, Riyadh, 11451, Saudi Arabia.

Funding

King Saud University, Riyadh, Saudi Arabia RSPD2025R1100
6 · The paper itself

Abstract

backgroundCucurbitacin E glucoside (CEG), a prominent constituent of Cucurbitaceae plants, exhibits notable effects on cancer cell behavior, including inhibition of invasion and migration, achieved through mechanisms such as apoptosis induction, autophagy, cell cycle arrest, and disruption of the actin cytoskeleton.

objectiveMelanoma, the fastest-growing malignancy among young individuals in the United States and the predominant cancer among young adults aged 25 to 29, poses a significant health threat.

aimThis study aims to elucidate the apoptotic mechanism of CEG against the melanoma cancer cell line (A375).

methodsThe study estimated the IC

resultsThe IC

conclusionCEG induces apoptosis in melanoma cancer cells (A375) through various mechanisms, including enhanced production of p53 and MDA, inhibition of key enzymes (GR, SOD, GPx, CAT) involved in oxidative stress defense and production of cell cycle regulating enzymes (cyclin D1, cyclin E2, cdk2, cdk4, and upregulation of AMPK and downregulation PGK1, and PKM2 in A375 tumor cells pathways. The downregulation of PKM2 in CEG-treated A375 cells inhibits ATP generation via aerobic glycolysis, a metabolic preference of cancer cells.

Indexed as

AMP-Activated Protein KinasesAntineoplastic AgentsAntineoplastic Agents, PhytogenicApoptosisGlucosidesMelanomaMembrane ProteinsPhosphoglycerate KinaseTriterpenesCell Line, TumorCell ProliferationCell SurvivalDose-Response Relationship, DrugDrug Screening Assays, AntitumorHumansMolecular StructureAMP-Activated Protein KinasesAntineoplastic AgentsAntineoplastic Agents, Phytogeniccucurbitacin EGlucosidesMembrane ProteinsPhosphoglycerate KinasePyruvate KinaseThyroid Hormone-Binding ProteinsThyroid HormonesTriterpenesA375AMPKCucurbitacin E glucoside (CEG)melanoma cancerPGK1PKM2.

Identifiers

PMID39757677

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