PMID- 32277668
OWN - NLM
STAT- MEDLINE
DCOM- 20201209
LR  - 20210908
IS  - 2241-6293 (Electronic)
IS  - 1107-0625 (Linking)
VI  - 25
IP  - 1
DP  - 2020 Jan-Feb
TI  - 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.
PG  - 454-459
AB  - 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. Apoptosis-related studies were checked by fluorescent microscopy 
      using acridine orange (AO)/ethidium bromide (EB) and Hoechst staining, as well as 
      flow cytometry using annexin V/propidium iodide (PI) assay. Western blot was used 
      to study the effects of Auraptenol on apoptosis-related protein expressions 
      including Bax, Bcl-2, as well as JNK/p38 MAPK signalling pathway. ROS production 
      was evaluated by flow cytometry. RESULTS: The results showed that Auraptenol 
      caused significant reduction in the viability of the human LNCaP prostate 
      carcinoma cells in a dose-dependent manner, exhibiting an IC50 of 25 microM in cancer 
      cells and IC50 of 100 microM in normal PNT2 cells. The AO/EB staining assay showed 
      that Auraptenol inhibited the viability of cancer cells via induction of 
      apoptotic cell death, which was associated with increase in Bax and decrease in 
      Bcl-2 levels. Hoechst staining results also confirmed that Auraptenol induced 
      programmed cell death. The apoptotic cells increased from 0.8% in the control to 
      32.5% in the study group at 50 microM concentration of Auraptenol. Auraptenol also 
      induced an increase in ROS production in a dose-dependent manner. Finally, this 
      molecule blocked the JNK/p38 MAPK signal pathway concentration-dependently in 
      human prostate cancer cells. CONCLUSION: In conclusion, the current study 
      indicates that this molecule could be developed as a potential anticancer drug 
      against human prostate carcinoma provided further studies are carried out.
FAU - Liu, Yunli
AU  - Liu Y
AD  - Department of Urological Surgery, the second affiliated hospital of Harbin 
      Medical University, Harbin, Heilongjiang, China, 150001.
FAU - Li, Xuedong
AU  - Li X
FAU - Chen, Zhaoyan
AU  - Chen Z
FAU - Chan, Yunhui
AU  - Chan Y
LA  - eng
PT  - Journal Article
PL  - Cyprus
TA  - J BUON
JT  - Journal of B.U.ON. : official journal of the Balkan Union of Oncology
JID - 100883428
RN  - 0 (Coumarins)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (auraptenol)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
SB  - IM
ECI - J BUON. 2021 May-Jun;26(3):1183. PMID: 34269000
MH  - Apoptosis/*drug effects
MH  - Coumarins/pharmacology/*therapeutic use
MH  - Humans
MH  - MAP Kinase Signaling System/*drug effects
MH  - Male
MH  - Prostatic Neoplasms/*drug therapy/pathology
MH  - Reactive Oxygen Species/metabolism
MH  - Signal Transduction/*drug effects
MH  - p38 Mitogen-Activated Protein Kinases/*metabolism
EDAT- 2020/04/12 06:00
MHDA- 2020/12/15 06:00
CRDT- 2020/04/12 06:00
PHST- 2020/04/12 06:00 [entrez]
PHST- 2020/04/12 06:00 [pubmed]
PHST- 2020/12/15 06:00 [medline]
PST - ppublish
SO  - J BUON. 2020 Jan-Feb;25(1):454-459.