Investigation of effect of psoralen on proliferation of prostate cancer LNCap-AD cells and its underlying molecular mechanism

doi:10.3877/cma.j.issn.2095-1221.2017.04.006

Abstract

Abstract:

Objective

To explore the influence of psoralen on the proliferation of prostate cancer LNCaP-AD cells and its mechanism.

Methods

Psoralen with different concentration was added into LNCaP-AD cells cultured in vitro. The effect of psoralen on the proliferation inhibition of LNCaP-AD cells was detected by CCK-8. The expressions of AR mRNA and protein, as well as PCNA protein, were respectively determined by real time PCR and Western blot.

Results

CCK-8 test showed that psoralen significantly inhibited the proliferation of LNCaP-AD cells in a dose- and time-dependent manner (P < 0.05) . Real time PCR showed that the expression of AR mRNA in LNCaP-AD cells was up-regulated by 30 μg/ml psoralen (1.63±0.04, t = 17.72, P < 0.01) , down-regulated by 100 μg/ml psoralen (0.46±0.07, t = 15.18, P < 0.01) and had no difference by 50 μg/ml psoralen (0.98±0.04, t = 0.66, P = 0.53) when compared with the control group (1.00±0.00) . Western blot showed that the protein expression of PCNA was down-regulated by 30 μg/ml, 50 μg/ml and 100 μg/ml psoralen in a dose-dependent manner compared (11.88?± 0.21 vs 10.61±0.17 vs 6.62?±?0.13 vs 2.71±0.43, F = 68.53, P < 0.01) . The protein expression level of AR was significantly down-regulated by 100 μg/ml psoralen compared with the control group (0.43?±0.06 vs 0.87±0.04, t = 6.04, P < 0.01) .

Conclusion

Psoralen can inhibit the proliferation of LNCaP-AD cells in a dose- and time-dependent manner in vitro. The possible mechanism lays in the down-regulation of PCNA and the influence of AR expression in LNCaP-AD cells.

Key words: Psoralens, Prostatic neoplasms, Proliferating cell nuclear antigen, Receptors, androgen

Shushang Chen, Mingfang Weng, Shuiliang Wang, Jun Lu, Jianming Tan. Investigation of effect of psoralen on proliferation of prostate cancer LNCap-AD cells and its underlying molecular mechanism[J]. Chinese Journal of Cell and Stem Cell(Electronic Edition), 2017, 07(04): 219-223.

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References 16

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基因	引物
AR	F:5'-AGTCAATGGGCAAAACATGG-3'
?	R: 5'- TTGTGTCAAAAGCGAAATGG-3'
β-actin	F: 5'- GTTGTCGACGACGAGCG-3'
?	R: 5'- GCACAGAGCCTCGCCTT-3'

基因	引物
AR	F:5'-AGTCAATGGGCAAAACATGG-3'
?	R: 5'- TTGTGTCAAAAGCGAAATGG-3'
β-actin	F: 5'- GTTGTCGACGACGAGCG-3'
?	R: 5'- GCACAGAGCCTCGCCTT-3'

分组	例数	24 h	48 h	72 h	96 h	F值	P值
10 μg/ml	15	0.96±0.07	0.84±0.05	0.82±0.08	0.65±0.07	19.03	< 0.01
30 μg/ml	15	0.94±0.07	0.80±0.04^a	0.77±0.04^a	0.63±0.06^a	26.03	< 0.01
50 μg/ml	15	0.89±0.09^a	0.76±0.13^a	0.72±0.09^a	0.61±0.08^a	6.92	< 0.01
100 μg/ml	15	0.78±0.05^a	0.60±0.02^a	0.56±0.03^a	0.42±0.05^a	59.45	< 0.01
F值	?	8.77	24.54	38.95	60.95	?	?
P值	?	< 0.01	< 0.01	< 0.01	< 0.01	?	?

分组	例数	24 h	48 h	72 h	96 h	F值	P值
10 μg/ml	15	0.96±0.07	0.84±0.05	0.82±0.08	0.65±0.07	19.03	< 0.01
30 μg/ml	15	0.94±0.07	0.80±0.04^a	0.77±0.04^a	0.63±0.06^a	26.03	< 0.01
50 μg/ml	15	0.89±0.09^a	0.76±0.13^a	0.72±0.09^a	0.61±0.08^a	6.92	< 0.01
100 μg/ml	15	0.78±0.05^a	0.60±0.02^a	0.56±0.03^a	0.42±0.05^a	59.45	< 0.01
F值	?	8.77	24.54	38.95	60.95	?	?
P值	?	< 0.01	< 0.01	< 0.01	< 0.01	?	?

分组	例数	PCNA	AR
对照组	3	0.89±0.05	0.87±0.04
30 μg/ml	3	0.77±0.03^a	1.58±0.14^a
50 μg/ml	3	0.48±0.08^a	0.81±0.08
100 μg/ml	3	0.29±0.07^a	0.43±0.06^a
F值	?	68.53	89.55
P值	?	< 0.01	< 0.01

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