ArticleCell death & disease2026
PABPC1-induced stabilization of PGK1 mRNA reduces apoptosis and sunitinib sensitivity in renal cell carcinoma by suppressing endoplasmic reticulum stress.
Article in Cell death & disease, 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
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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
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.
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Who cites it
1 citing paper in PubMed.
- PABPC1 in Cancer: From a Translational Housekeeper to a Stress-Responsive Regulatory Hub.Cancer science · 2026Review
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Sunitinib resistance poses a significant challenge in the management of advanced and metastatic clear cell renal cell carcinoma (ccRCC). Although RNA-binding proteins (RBPs) have recently emerged as important regulators of tumorigenesis, their roles in ccRCC progression and sunitinib resistance remain poorly understood. Through comprehensive bioinformatics analysis of clinical datasets, we identified PABPC1 as an RBP significantly upregulated in ccRCC. Functionally, PABPC1 promoted the proliferation, migration, invasion, and sunitinib resistance of ccRCC cells. Mechanistically, PABPC1 bound to and stabilized PGK1 mRNA, thereby upregulating PGK1 expression. This upregulation reduced endoplasmic reticulum (ER) stress, inhibited apoptosis, and consequently conferred sunitinib resistance in ccRCC cells. Importantly, treatment with Eeyarestatin I, a small-molecule ER stress agonist, restored sunitinib sensitivity in tumor cells. These findings reveal a novel PABPC1-PGK1 regulatory axis underlying sunitinib resistance and suggest a promising therapeutic strategy for overcoming drug resistance in ccRCC.
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