miR-155对前列腺癌放射治疗的增敏作用

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Abstract Objective To explore the effects of miR-155 on radiosensitivity enhancement of prostate cancer in vitro.Methods Cell viability and adhesion of DU145 and PC-3 cells were evaluated after anti-miR-155 transfection combined with irradiation therapy. Flow cytometry was performed to evaluate the cell apoptosis. The expression and activity of Caspase-3 and Caspase-9 were also observed after the above treatment.Results The results evidenced that cell viability(25.6%±2.0% and 21.6±1.0% in irradiated group;20.5%±1.0% and 15.5%±1.0% in anti-miR-155 transfected group) and adhesion of DU145 and PC-3 cells(0.8%±0.1% and 0.7%±0.1% in irradiated group;0.7%±0.1% and 0.6%±0.1% in anti-miR-155 transfected group) were inhibited obviously after anti-miR-155 transfection. The apoptosis rate(3.3%±0.3% and 4.2%±0.3% in irradiated group;4.1%±0.1% and 3.9%±0.2% in anti-miR-155 transfected group), Caspase-3 and Caspase-9 expression and activity were enhanced obviously compared with the control group(P<0.01).After combinative treatment, cell viability (10.1%±0.5% in irradiated group and 6.1%±0.5% in anti-miR-155 transfected group) and adhesion (0.4%±0.1% in irradiated group and 0.4%±0.1% in anti-miR-155 transfected group)decreased significantly(P<0.01,n=6).The apoptosis rate(6.9%±0.4% in irradiated group;6.8%±0.3% in anti-miR-155 transfected group) and the expression of Caspase-3 and Caspase-9 were also higher than the signal treated group(P<0.01).Conclusions Our results suggested that miR-155 can increase the radiosensitivity of DU145 and PC-3 cells and increase the efficiency of radiotherapy of γ-ray irradiation on prostate cancer in vitro.

Key words： miR-155 prostate cancer radiosensitivity Caspase-3 Caspase-9

Received: 20 June 2016

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	Articles by authors
	DONG Qingchuan
	ZHANG Zhiguo
	CHENG Ji
	WANG Zhigang
	ZHAO Huacai
	ZHAO Wencai
	ZHANG Haiyan
	and CHENG Yongyi

Cite this article:

DONG Qingchuan,ZHANG Zhiguo,CHENG Ji等. Effect of miR-155 on radiosensitivity enhancement of prostate cancer in vitro[J]. Med. J. Chin. Peop. Armed Poli. Forc., 2017, 28(1): 60-63.

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http://journal08.magtechjournal.com/Jwk_wjyx/EN/ OR http://journal08.magtechjournal.com/Jwk_wjyx/EN/Y2017/V28/I1/60

[1]	Brody H. Prostate cancer [J]. Nature, 2015, 528(7582): S117.
[2]	Xin L. Cells of origin for cancer: an updated view from prostate cancer [J]. Oncogene, 2013, 32(32): 3655-3663.
[3]	Jerónimo C, Bastian P J, Bjartell A, et al. Epigenetics in prostate cancer: biologic and clinical relevance [J]. Eur Urol, 2011, 60(4): 753-766.
[4]	Bertoli G, Cava C, Castiglioni I. MicroRNAs as biomarkers for diagnosis, prognosis and theranostics in prostate cancer [J]. Int J Mol Sci, 2016, 17(3): 245-251.
[5]	Tutar Y. miRNA and cancer; computational and experimental approaches [J]. Curr Pharm Biotechnol, 2014, 15(5): 429-436.
[6]	Cai Z K, Chen Q, Chen Y B, et al. microRNA-155 promotes the proliferation of prostate cancer cells by targeting annexin 7 [J]. Mol Med Rep, 2015, 11(1): 533-538.
[7]	Ji H, Li Y, Jiang F, et al. Inhibition of transforming growth factor beta/SMAD signal by MiR-155 is involved in arsenic trioxide-induced anti-angiogenesis in prostate cancer [J]. Cancer Sci, 2014, 105(12):1541-1549.
[8]	Babar I A, Czochor J, Steinmetz A, et al. Inhibition of hypoxia-induced miR-155 radiosensitizes hypoxic lung cancer cells [J]. Cancer Biol Ther, 2011, 12(10): 908-914.
[9]	Challagundla K B, Wise P M, Neviani P, et al. Exosome-mediated transfer of microRNAs within the tumor microenvironment and neuroblastoma resistance to chemotherapy [J]. J Natl Cancer Inst, 2015, 107(7):1093-1098.
[10]	Barbieri C E, Demichelis F, Rubin M A. Molecular genetics of prostate cancer: emerging appreciation of genetic complexity [J]. Histopathology, 2012, 60(1):187-198.
[11]	Chang L, Graham P H, Ni J, et al. Targeting PI3K/Akt/mTOR signaling pathway in the treatment of prostate cancer radioresistance [J]. Crit Rev Oncol Hematol, 2015, 96(3): 507-517.
[12]	Kiliccioglu I, Konac E, Varol N, et al. Apoptotic effects of proteasome and histone deacetylase inhibitors in prostate cancer cell lines [J]. Genet Mol Res, 2014, 13(2): 3721-3731.
[13]	Das T P, Suman S, Alatassi H, et al. Inhibition of AKT promotes FOXO3a-dependent apoptosis in prostate cancer [J]. Cell Death Dis, 2016, 7: e2111.
[14]	Jain A, Jain S, Jain R, et al. Coated chitosan nanoparticles encapsulating caspase 3 activator for effective treatment of colorectral cancer [J]. Drug Deliv Transl Res, 2015, 5(6): 596-610.
[15]	Yan J, Ma C, Cheng J, et al. HAX-1 inhibits apoptosis in prostate cancer through the suppression of caspase-9 activation [J]. Oncol Rep, 2015, 34(5): 2776-2781.
[16]	Lu T, Stark G R. NF-κB: regulation by methylation [J]. Cancer Res, 2015, 75(18): 3692-3695.
[17]	Turturro F. Constitutive NF- κ B activation underlines major mechanism of drug resistance in relapsed refractory diffuse large B cell lymphoma [J]. Biomed Res Int, 2015,2015:484537.