ArticleMedical oncology (Northwood, London, England)2025
Scutellarin triggers ferroptosis in ovarian cancer cells via inhibiting AKT/mTOR and JAK2/STAT3 pathways.
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. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
20 authors.
Funding
Abstract
Ovarian cancer (OC) ranks as the second most prevalent gynecologic malignancy worldwide, largely attributed to the difficulties in detecting early stages, frequent disease reappearance, and unresponsiveness to existing therapies. Contemporary treatment selections for individuals with OC remain limited. Scutellarin (Scu), an active compound, demonstrates suppressive properties against multiplication, invasion, and survival of certain cancer cell types. Nevertheless, the exact anti-cancer properties and molecular pathways of Scu in OC are still not fully understood. This investigation sought to examine the therapeutic impact of Scu and its potential mechanisms in OC. A series of assays, encompassing cell counting kit-8 (CCK-8), colony-formation assay, EdU staining, scratch/wound healing assay, matrigel invasion assay, DHE staining, flow cytometry, Western blotting, ferrous ion content assay kit, and immunofluorescence staining were employed to investigate the role and mechanisms of Scu in OC cell lines (SKOV3 and HO-8910). Scu markedly diminished cell viability, proliferation, and colony formation in both SKOV3 and HO-8910 cells. Scu substantially inhibited OC cells' migration, invasion, and epithelial-mesenchymal transition (EMT). Additionally, the flow cytometry data and Western blot results of Bax and Bcl-2 protein levels indicated that Scu induced cell apoptosis in both SKOV3 and HO-8910 cells. Furthermore, Scu induced cell ferroptosis by upregulating the levels of reactive oxygen species (ROS), 4-hydroxynonenal (4-HNE), and Fe2+ while downregulating the expression of specificity protein 1 (SP1), solute carrier family 7 member 11 (SLC7A11), and glutathione peroxidase 4 (GPX4). The anti-cancer capabilities of Scu were also linked to the inhibition of the phosphorylated forms of AKT, mTOR, JAK2, and STAT3. Lastly, cell apoptosis and ferroptosis induced by Scu were counteracted by AKT agonist SC79. The findings demonstrate that Scu effectively inhibited cell multiplication, migration, invasion, and EMT, while inducing oxidative stress, apoptosis, and ferroptosis in SKOV3 and HO-8910 cells. These effects were likely mediated by inhibiting the AKT/mTOR and JAK2/STAT3 signaling cascades. This investigation suggests that Scu holds potential as a promising chemotherapeutic agent for treating OC.
Indexed as
Identifiers
41288840What OpenQuestion holds
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.