C Lammer

CH Liao

Cheng-Yoong Pang

D Karan

D Newman

D Wang

DV Bulavin

EA Slee

G Iguchi

H Xiao

Horng-Jyh Harn

Hsueh-Hui Yang

JB Welsh

K Tomioka

K Yamaguchi

KF Macleod

KL Gould

L Du

M Shim

Mei-Jen Wang

MJ Hayat

PB Schiff

RP Singh

S Krajewski

SA Susin

SH Lee

Shee-Ping Chen

Sheng-Chun Chiu

Shinn-Zong Lin

SJ Baek

Sung-Ying Huang

TE Eling

VM Paralkar

Yi-Lin Chen

YL Chen

YL Cheng

BMC Cancer

English

PubMed

Abstract
          
            Background
            We explored the mechanisms of cell death induced by isochaihulactone treatment in LNCaP cells.
          
          
            Methods
            LNCaP cells were treated with isochaihulactone and growth inhibition was assessed. Cell cycle profiles after isochaihulactone treatment were determined by flow cytometry. Expression levels of cell cycle regulatory proteins, caspase 9, caspase 3, and PARP were determined after isochaihulactone treatment. Signaling pathway was verified by inhibitors pre-treatment. Expression levels of early growth response gene 1 (EGR-1) and nonsteroidal anti-inflammatory drug-activated gene 1 (NAG-1) were determined to investigate their role in LNCaP cell death. NAG-1 expression was knocked down by si-NAG-1 siRNA transfection. Rate of cell death and proliferation were obtained by MTT assay.
          
          
            Results
            Isochaihulactone caused cell cycle arrest at G2/M phase in LNCaP cells, which was correlated with an increase of p53 and p21 levels and downregulation of the checkpoint proteins cdc25c, cyclin B1, and cdc2. Bcl-2 phosphorylation and caspase activation were also observed. Isochaihulactone induced phosphorylation of c-Jun-N-terminal kinase (JNK), and JNK inhibitor partially reduced isochaihulactone-induced cell death. Isochaihulactone also induced the expressions of EGR-1 and NAG-1. Expression of NAG-1 was reduced by JNK inhibitor, and knocking down of NAG-1 inhibited isochaihulactone-induced cell death.
          
          
            Conclusions
            Isochaihulactone apparently induces G2/M cell cycle arrest via downregulation of cyclin B1 and cdc2, and induces cellular death by upregulation of NAG-1 via JNK activation in LNCaP cells.
          </jats:sec

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Activation of NAG-1 via JNK signaling revealed an isochaihulactone-triggered cell death in human LNCaP prostate cancer cells

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Activation of NAG-1 via JNK signaling revealed an isochaihulactone-triggered cell death in human LNCaP prostate cancer cells

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