ArticleTranslational andrology and urology2022
PRRX1/FOXM1 reduces gemcitabin-induced cytotoxicity by regulating autophagy in bladder cancer.
Article in Translational andrology and urology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- The Regulatory Network of FOXM1: Orchestrating Cancer Progression and Resistance to Therapy.International journal of molecular sciences · 2026Review
- Hypomethylation-mediated upregulation of PHOX1 promotes gastric cancer progression via transactivation of NGFR.Cell death discovery · 2025Article
- Inhibiting NLRP3 enhances cellular autophagy induced by outer membrane vesicles fromMicrobiology spectrum · 2025Article
- LncRNAs as nodes for the cross-talk between autophagy and Wnt signaling in pancreatic cancer drug resistance.International journal of biological sciences · 2024Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Bladder cancer (BC) is a common urological malignancy with high mortality worldwide. Many proteins can influence tumorigenesis by participating in cellular processes. Recently, abundant evidence has illustrated that paired related homeobox 1 ( Methods: The expression of genes ( Results: In our study, PRRX1 was highly expressed in BC tissues and cells, and high PRRX1 expression resulted in poor overall survival in patients with BC. PRRX1 accelerated the viability and hindered the apoptosis of BC cells. It also weakened gemcitabine-induced cytotoxicity and strengthened gemcitabine-induced autophagy. PRRX1 was found to cooperate with forkhead box protein M1 (FOXM1) to influence downstream genes, and FOXM1 was found to regulate Beclin-1 and microtubule-associated protein 1 light chain 3 (LC3) genes to influence autophagy. PRRX1 up-regulated the expression of LC3 and Beclin-1 by cooperating with FOXM1. In rescue assays, FOXM1 reversed the effects of PRRX1 on gemcitabine-induced cytotoxicity and autophagy. Knockdown of PRRX1 enhanced the inhibitive effects of gemcitabine on tumor growth Conclusions: PRRX1 reduces gemcitabine-induced cytotoxicity in BC cells by regulating the expression of the autophagy proteins LC3 and Beclin-1. This discovery suggests that
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