Increasing life expectancy imposes big challenges to the global health of the male population, because some disorders, such as tumours, tend to progress with age (Bell et al., 2015). Among them, prostate cancer (PCa) is a leading cause of cancer-associated mortality among men, specifically in Western countries; the lowest rates of this cancer are seen in Africa and Asia. PCa has the highest heritability, accounting for almost 10% of all new male tumours. More than 650,000 men worldwide are diagnosed with PCa annually (Fitzpatrick et al., 2009). In addition to family history and genetic factors, well-established risk factors for PCa include Lynch syndrome, country of origin, age and race/ethnicity (Grönberg, 2003; Teoh et al., 2019). Today, PCa is diagnosed based on the measurement of serum prostate-specific antigen (PSA), also known as DRE (Misawa et al., 2017). PC3 is a grade IV PCa cell line that does not respond to fibroblast growth factors (FGF), androgens or glucocorticoids and has potential metastatic activity. It is useful in studying curative interventions in progressive PCa cells (Ashtiani et al., 2017). Understanding the molecular mechanisms correlated with PCa development and progression is pivotal, where long noncoding RNAs (lncRNAs) are hopeful candidates in assessing PCa initiation and tumorigenesis. Only a small portion of transcripts are translated into proteins, while the majority of them are noncoding RNAs (ncRNAs) (Bray

Departmental sources Background: This study aimed to investigate the effects of the 6-nitroindazole compound and amino analog of ludartin, (11R)-13-(6-nitroindazole)-11,13-dihydroludartin (NDHL), on human prostate carcinoma cells in vitro and in mouse tumor xenografts in vivo. Material/Methods: DU-145 and LNCaP human prostate carcinoma cells were cultured with increasing concentrations of NDHL. Cell viability was measured using the MTT assay, and cell apoptosis was measured by fluorescence flow cytometry. Mouse tumor xenografts were created by implanting 2×10 6 of DU-145 cells subcutaneously in the left flank. On the second day following DU-145 cell implantation, the mice in the treatment groups were injected intraperitoneally with 2, 5, and 10 mg/kg of NDHL. Results: Treatment of DU-145 and LNCaP cells with NDHL (range, 2.5-20.0 μM) significantly reduced cell proliferation in vitro (P<0.05). The proliferation rate of DU-145 and LNCaP cells was reduced to 27% and 24%, respectively, following treatment with 20.0 μM of NDHL. Treatment with NDHL significantly increased cell apoptosis and the formation of reactive oxygen species (ROS) formation in DU-145 cells at 48 h (P<0.05). NDHL significantly increased the proportion of DU-145 cells in the G1 phase of the cell cycle and significantly increased the expression of cyclin D1 and p21 (P<0.05). Treatment of the mice in the xenograft tumor model with NDHL significantly increased survival and suppressed tumor growth (P<0.02). Conclusions: NDHL inhibited cell proliferation, increased apoptosis, and caused cell cycle arrest in human prostate carcinoma cells in vitro and inhibited mouse tumor xenograft growth in vivo.