Luteolin inhibited proliferation and induced apoptosis of prostate cancer cells through miR-301.
Luteolin is a falvonoid compound derived from Lonicera japonica Thunb. Numerous reports have demonstrated that luteolin has anticancer effects on many kinds of tumors. This study investigated the effects of luteolin on prostate cancer (PCa), assessing the PC3 and LNCaP cells. The cell viability and apoptosis were assessed by performing Cell Counting Kit-8 assay and Annexin V-fluorescein isothiocyanate/propidium iodide double staining. Luteolin was found to inhibit androgen-sensitive and androgen-independent PCa cell lines' growth and induced apoptosis. To uncover the exact mechanisms and molecular targets, microRNA (miR) array analysis was performed. miR-301 was found to be markedly downregulated. Then, the expression of miR-301 was retrospectively analyzed in the primary PCa tissues by quantitative reverse transcription polymerase chain reaction and in situ hybridization methods. According to the quantitative reverse transcription polymerase chain reaction results of miR-301, the 54 PCa patients were divided into two groups: high and low miR-301 groups. The division indicator is a relative expression ≥5. Compared to the low-expression group, high miR-301 expression was associated with a significantly shorter overall survival (P=0.029). The proapoptotic gene, DEDD2, was predicted to be the direct target of miR-301. It was clarified in accordance with bioinformatics and luciferase activity analyses. The overexpression of miR-301 by plasmid decreased the luteolin effect. Taken together, these results suggest that luteolin inhibits PCa cell proliferation through miR-301, the poor predictive factor of PCa.
Oncology Department, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, People's Republic of China.
Kun
K
Han
Institute of Genetic Engineering of Southern Medical University, Guangzhou, Guangdong, People's Republic of China.
Wei
W
Meng
Oncology Department, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, People's Republic of China.
Jian-Jun
JJ
Zhang
Oncology Department, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, People's Republic of China.
Yan
Y
Zhou
Oncology Department, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, People's Republic of China.
Ya-Ling
YL
Wang
Oncology Department, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, People's Republic of China.
Yang
Y
Su
Oncology Department, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, People's Republic of China.
Shu-Chen
SC
Lin
Oncology Department, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, People's Republic of China.
Zhi-Hua
ZH
Gan
Oncology Department, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, People's Republic of China.
Yong-Ning
YN
Sun
Oncology Department, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, People's Republic of China.
Da-Liu
DL
Min
DEDD2; apoptosis; luteolin; miR-301; prostate cancer