Evidence map›Paper›PMID 42210139›Full record

ArticleBMC cancer2026

Isatin-mediated inhibition of the PI3K/AKT/EMT signaling axis confers antitumor efficacy in Ehrlich solid carcinoma-bearing mice.

Heba Effat, Marwa A Ibrahim, Rehab S Abohashem, Yasmin M Attia, Fatma M Abdelwahed

Abstract read
In one paragraph

Article in BMC cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Heba EffatMedical Biochemistry and Molecular Biology Unit, Cancer Biology Department, National Cancer Institute, Cairo University, Cairo, Egypt. hebatullah.effat@nci.cu.edu.eg.
Marwa A IbrahimMedicinal and Aromatic Plants Department, Desert Research Center, Cairo, Egypt.
Rehab S AbohashemHormones Department, Medical Research and Clinical Studies Institute, National Research Centre, Giza, Egypt.
Yasmin M AttiaPharmacology Unit, Cancer Biology Department, National Cancer Institute, Cairo University, Kasr El Aini Street, Fom El Khalig, Cairo, 11796, Egypt.
Fatma M AbdelwahedMedical Biochemistry and Molecular Biology Unit, Cancer Biology Department, National Cancer Institute, Cairo University, Cairo, Egypt. fatma.abdelwahed@nci.cu.edu.eg.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite advances, detailed insight into cancer's biological mechanisms remains needed. Isatin, an indole-1 H-2,3-dione, is an attractive agent for new drug discovery. Here, the anticancer efficacy and potential toxicity of isatin in combination with doxorubicin (Dox) in a mouse Ehrlich solid carcinoma (ESC) model were examined by modulating the PI3K/AKT/EMT pathway. Five groups of fifty female mice were prepared: negative control, positive ESC-bearing mice, isatin-treated ESC group, Dox-treated ESC group, and isatin and Dox combination-treated ESC group. Treatments began after tumor formation. Inflammatory markers, kidney and liver enzyme activities, and EMT markers levels (vimentin and E-cadherin) were assessed by ELISA. HIF 1 α, NF-κB, PI3K, AKT, MMP2, and MMP9 gene expression was evaluated using qRT-PCR. Protein expression of MMP-9 and E-cadherin was assessed by IHC. Compared with the positive control, the combined treatment reduced tumor growth by 51%. Additionally, combined treatment showed a significant increase in the amount of necrotic tissue. Mechanistically, isatin exerted its therapeutic effect by increasing anti-inflammatory (IL-10) cytokine levels and suppressing pro-inflammatory (IL-6) cytokine levels, along with reductions in HIF-1α, NF-κB, PI3K, AKT, MMP2, and MMP9 mRNA levels. Also, a combined group of isatin and Dox showed reduced vimentin levels and elevated E-cadherin levels by ELISA. Co-administration of isatin and Dox significantly increased E-cadherin expression and attenuated MMP-9 expression compared with the untreated group, as assessed by IHC. Our results indicate that isatin, in combination with doxorubicin, exerts a synergistic anticancer effect against ESC, offering a promising therapeutic approach to enhance treatment efficacy.

Indexed as

Carcinoma, Ehrlich TumorDoxorubicinIsatinAnimalsAntineoplastic Combined Chemotherapy ProtocolsDrug SynergismEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticMicePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionDoxorubicinIsatinPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAnticancerDoxEhrlich solid carcinomaInflammationIsatinPI3k/AKT/EMT

Identifiers

PMID42210139
PMCPMC13221764

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Registered trials

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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.