ArticleScience progress
ULK2 suppresses glycolysis to attenuate cisplatin resistance in ovarian cancer organoid via c-Jun phosphorylation.
Article in Science progress. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
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Who cites it
1 citing paper in PubMed.
- Mechanistic role of glycolytic pathways in the tumor microenvironment in driving chemoresistance.Frontiers in cell and developmental biology · 2026Review
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Authors and funding
6 authors.
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No grant is acknowledged in the PubMed record.
Abstract
ObjectiveResistance to platinum-based chemotherapy remains a key obstacle in ovarian cancer treatment. This study aims to investigate the role of Uncoordinated 51-like kinase 2 (ULK2) in chemoresistance of ovarian cancer and elucidate its underlying mechanisms using 3D patient-derived organoids.MethodsSurvival analysis was first performed using the Kaplan‒Meier plotter database. Immunohistochemical profiling delineated differential ULK2 expression patterns between chemoresistant and chemosensitive ovarian cancer tissue samples and organoids. ULK2 overexpression was achieved in cisplatin-resistant ovarian cancer organoids via lentiviral vector transduction. Then, we conducted an in-depth examination of the alterations in phosphorylated proteins induced by ULK2 overexpression using phosphoproteomics technology. To investigate the influence of ULK2 on chemosensitivity in ovarian cancer, Cell Counting Kit-8 (CCK-8) and
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