Evidence mapPaperPMID 42428556Full record

ReviewJournal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques2026

The cross-talk between GSK-3β, RKIP, and PTEN as potential targets for therapeutic implications in cancer: a comprehensive insight.

Esraa M Mosalam, Mahmoud S Abdallah, Ahmed R Gardouh, Eman Hamza, Mostafa M Bahaa, Mahmoud Nazih, Reham A Al-Dhelaan, Noha Kamal

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In one paragraph

Review in Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques, 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

8 authors.

Esraa M MosalamDepartment of PharmD, Faculty of Pharmacy, Jadara University, Irbid, Jordan.
Mahmoud S AbdallahDepartment of PharmD, Faculty of Pharmacy, Jadara University, Irbid, Jordan.
Ahmed R GardouhDepartment of Pharmaceutical Sciences, Faculty of Pharmacy, Jadara University, Irbid, Jordan.
Eman HamzaDepartment of Biochemistry, College of Medicine, Imam Mohammad Ibn Saud Islamic University (IMSIU), Riyadh, Saudi Arabia.
Mostafa M BahaaPharmacy Practice Department, Faculty of Pharmacy, Horus University, New Damietta, Egypt.
Mahmoud NazihDepartment of Clinical Pharmacy, Faculty of Pharmacy, Deraya University, Minya, Egypt.
Reham A Al-DhelaanDepartment of Biochemistry, College of Medicine, Imam Mohammad Ibn Saud Islamic University (IMSIU), Riyadh, Saudi Arabia.
Noha KamalDepartment of Clinical Pharmacy, Faculty of Pharmacy, University of Sadat City (USC), Sadat, Egypt.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The serine/threonine kinase glycogen synthase kinase-3 (GSK-3) was initially identified and studied in the regulation of glycogen synthesis. In some cases, suppression of GSK-3 activity by phosphorylation by Akt and other kinases has been associated with cancer progression. In these cases, GSK-3 has tumor suppressor functions. In other cases, GSK-3 has been associated with tumor progression by stabilizing components of the beta-catenin complex. In these situations, GSK-3 has oncogenic properties. The Raf kinase inhibitor protein (RKIP) has been reported to be under expressed in many cancers and plays a role in the regulation of tumor cells' survival, proliferation, invasion, and metastasis, hence, a tumor suppressor. RKIP also regulates tumor cell resistance to cytotoxic drugs/cells. Likewise, the tumor suppressor, phosphatase and tensin homolog (PTEN), which inhibits the phosphatidylinositol 3 kinase (PI3K)/protein kinase B (Akt) pathway, is either mutated, under expressed, or deleted in many cancers and shares with RKIP its anti-tumor properties and its regulation in resistance. Several pathways are regulated by RKIP, GSK-3, PTEN, and the transcriptional and post-transcriptional regulations of RKIP, GSK-3, and PTEN are significantly altered in cancers. In addition, RKIP, GSK-3 and PTEN play a key role in the regulation of tumor cells response to chemotherapy and immunotherapy. In this review, we will focus on the roles that GSK-3, PTEN, and RKIP play in various human cancers. We will also discuss how this pivotal kinase interacts with multiple signaling pathways such as: PI3K/PTEN/Akt/mechanistic target of rapamycin complex 1 (mTORC1), nuclear Factor kappa-B (NF-κB)/Snail family transcriptional repressor 1 (Snail)/Yin Yang 1 (YY1) loop, and rat sarcoma virus oncogene (Ras)/rapidly accelerated fibrosarcoma (Raf)/mitogen-activated protein kinase (MEK)/extracellular signal-regulated kinase (ERK).

Indexed as

Antineoplastic AgentsGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaNeoplasmsPhosphatidylethanolamine Binding ProteinPTEN PhosphohydrolaseAnimalsHumansSignal TransductionAntineoplastic AgentsGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaPEBP1 protein, humanPhosphatidylethanolamine Binding ProteinPTEN PhosphohydrolasePTEN protein, humancancer mechanismsGSK-3GSK-3βkinasesmTORC1

Identifiers

PMID42428556
PMCPMC13345995

What Socratic holds

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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 Socratic graph.