ReviewOncology letters2026
STOML2 promotes hepatocellular carcinoma cell proliferation, invasion and migration by activating the PI3K/AKT signaling pathway (Review).
Review in Oncology letters, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed.
- Exosomal circ-ZNF652 Mediates TGF-β1-Induced Epithelial-Mesenchymal Transition and Glycolytic Reprogramming to Promote Hepatocellular Carcinoma Progression.Journal of microbiology and biotechnology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stomatin-like protein 2 (STOML2) has emerged as a key oncoprotein in hepatocellular carcinoma (HCC), with its regulation being associated with tumor progression and poor patient prognosis. The present mechanistic review delineates how STOML2 functions as a central hub to promote HCC malignancy, which is primarily through constitutive activation of the PI3K/AKT signaling pathway. Direct mechanisms are detailed, including how STOML2 binds to the PI3K p85 subunit to stabilize the PI3K complex, promoting indirect modulations. These include potential interactions with receptor tyrosine kinases and negative regulators, such as PTEN, a number of which, while plausible, await definitive validation in HCC-specific models. The subsequent activation of the PI3K/AKT cascade by STOML2 drives key hallmarks of cancer, enhancing cell proliferation, suppressing apoptosis, potentiating invasion and metastasis through epithelial-mesenchymal transition, and contributing to chemotherapy resistance. Furthermore, the present review summarizes the upstream regulatory networks controlling STOML2, encompassing transcriptional, epigenetic and post-translational mechanisms, in addition to evaluating the therapeutic potential of targeting the STOML2/PI3K/AKT axis. Through integrating established evidence with clearly defined knowledge gaps, the present review provides a foundational framework for future research and the development of STOML2-directed diagnostic and therapeutic strategies for HCC.
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Registered trials
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.