Dihydroartemisinin Modulates Prostate Cancer Progression by Regulating Multiple Genes via the Transcription Factor NR2F2.

Objective: This study aimed to investigate the effect of dihydroartemisinin (DHA) on DU145 cells and the role of NR2F2 (COUP-TFII) and its potential target genes in this process.

Methods: GSE122625 was used to identify differentially expressed genes (DEGs) between the DHA-treated and control groups. Protein-protein interaction (PPI) network analysis was performed to identify hub genes, and the ChEA3 database was used to identify potential transcription factors.

SH3BP5-AS1/IGF2BP2/VDAC2 Axis Promotes the Apoptosis and Ferroptosis of Bladder Cancer Cells.

Background: Bladder cancer (BC) is the most common malignant tumor in the urinary system with a high incidence, imposing a burden on the healthcare system worldwide. The participation of long non-coding RNAs (lncRNAs) in BC has attracted increasing attention.

Objective: The aim in the current study was to explore the potential mechanism involving SH3BP5-AS1 in modulating BC cell proliferation, apoptosis and ferroptosis.

Antiproliferative activities of auraptenol against drug-resistant human prostate carcinoma cells are mediated via programmed cell death, endogenous ROS production, and targeting the JNK/p38 MAPK signal pathways.

The Editors of JBUON issue an Expression of Concern to 'Antiproliferative activities of auraptenol against drugresistant human prostate carcinoma cells are mediated via programmed cell death, endogenous ROS production, and targeting the JNK/p38 MAPK signal pathways', by Yunli Liu, Xuedong Li, Zhaoyan Chen, Yunhui Chan; JBUON 2020;25(1):454-459; PMID: 32277668. Following the publication of the above article, readers drew to our attention that part of the data was possibly unreliable. We sent emails to the authors with a request to provide the raw data to prove the originality, but received no reply.

Antiproliferative activities of auraptenol against drug-resistant human prostate carcinoma cells are mediated via programmed cell death, endogenous ROS production, and targeting the JNK/p38 MAPK signal pathways.

Purpose: Prostate cancer is considered to be one of the most common cancers in men and as such there is a pressing need for finding new therapeutic agents to treat this disease. Therefore, the main purpose of the current research work was to study the anticancer effects of a naturally occurring coumarin- Auraptenol- against drug-resistant human prostate cancer cells and evaluate its effects on programmed cell death, reactive oxygen species (ROS) production, and JNK/p38 MAPK signalling pathway.

Methods: Cell proliferation was examined by CCK8 cell viability assay.

Comprehensive characterization of immune- and inflammation-associated biomarkers based on multi-omics integration in kidney renal clear cell carcinoma.

Background: Kidney renal clear cell carcinoma (KIRC) is the most common type of kidney cancer in adults, and it is responsible for approximately 90-95% of cases. Although extensive evidence has suggested that many immune- and inflammation-related genes could serve as effective biomarkers in KIRC, the potential associations among immune-, inflammation- and KIRC-related genes has not been sufficiently understood.

Methods: Here, we integrated multiple levels of data to construct an immune-, inflammation- or KIRC-directed neighbour network (IIKDN network) and a KIRC-related gene-directed network (KIRCD network).

[Effects of 40H-tamoxifen on the proliferation and apoptosis of prostate stromal cells].

Objective: To investigate the effects of 4OH-Tamoxifen (OHT) on proliferation and apoptosis of primary cultured prostate stromal cells.

Methods: Primarily cultured prostate stromal cells in vitro were treated with various concentrations (10(-8) mol/L - 10(-5) mol/L) of estradiol (E2), diethylstilbestrol (DES), OHT and the mixture of E2 (10(-8) mol/L - 10(-6) mol/L) with OHT (10(-7) mol/L) and then MTT and TUNEL were used to detect their proliferation and apoptosis respectively.

Results: There was a significant difference (P < 0.