PRC1 (Protein regulator of cytokinesis 1)

PRC1 silencing elicited ER stress, but this effect was partially rescued by the ROS scavenger N-acetylcysteine...In conclusion, this study verified that inhibition of PRC1 expression could induce ICD in CRC by triggering ER stress via the Wnt/β-catenin signaling pathway. These findings highlight a novel molecular pathway whereby PRC1 exerts carcinogenic role in tumor immune microenvironment through ICD in CRC.

This study demonstrates a critical oncogenic role of PRC1 in NSCLC. CCNY, which modulates PRC1 phosphorylation, and the TET2-BACH1 cascade, which modulates demethylation and transcription of PRC1, may serve as promising targets for NSCLC management.

In vitro, PRC1 knockdown in WIT-49 cells significantly impaired migratory capacity, invasive potential, EMT progression, and glycolytic metabolism. These findings collectively position PRC1 as a promising therapeutic target and prognostic biomarker in WT.

Mechanically, PRC1 could interact with RPL4, which caused a decrease in RPL4/MDM2 complex formation, resulting in the enhanced ubiquitination of p53 and a reduction of p53 proteins. These findings revealed that PRC1 was involved in the RPL4-MDM2-p53 pathway thus playing a tumorigenic role on OC.

BKT300 treatment led to 98% of tumor growth inhibition and 89.4% of tumor regression in mouse xenograft AML models, without notable impacts on normal hematopoiesis or biochemistry, even at high doses. As a first-in-class targeted therapy, BKT300 presents a promising new treatment option for advanced AML.

These results elucidate a mechanism wherein the PRC1 gene participates in the occurrence and development of HBV‑associated liver cancer by modulating autophagy. PRC1 could be a potential therapeutic target for liver cancer.

This study identified 10 key genes related to stemness and immune cell infiltration in HCC. These genes, primarily involved in cell cycle regulation, may serve as potential targets for developing more effective treatments to reduce HCC recurrence and improve patient outcomes.

These findings provide new insights into the pathogenesis of impaired hepatic lipid metabolism and abnormal development and the molecular origin of post-natal liver disease in IUGR due to maternal undernutrition. This information can support the development of new therapeutic strategies.

Subcutaneous and oral administration of 4Bb could effectively inhibit the growth of drug-resistant tumors in vivo, doubling the survival time of tumor bearing mice without side effects in normal tissues. Thus, our study offers an orally-available, structurally-novel PLK1 inhibitor for drug-resistant lung cancer therapy.

Moreover, PRC1 was found to exert regulatory control over glycolysis and the mammalian target of rapamycin complex 1 (mTORC1) pathway in the context of CHOL based on KEGG and GSEA analysis. Collectively, these results underscore the pivotal role of PRC1 in CHOL progression, wherein it modulates glycolysis and the mTORC1 pathway under the regulatory influence of FOXM1.

Further analysis through differential expression and survival analysis reaffirmed their strong correlation with the incidence of breast cancer. Consequently, the investigation of these 10 pertinent Hub genes presents novel prospects for potential biomarkers and valuable insights into the early diagnosis of breast cancer.

This work suggests that E2F3 renders an immunosuppressive TME in NPC by activating PRC1 and BIRC5. Suppression of any member involved might favor tumor elimination.