Expression and significance of apoptosis inhibitor 5 in ovarian cancer

WANG Juan HUA Xiao-tang

Acta Anatomica Sinica ›› 2017, Vol. 48 ›› Issue (3) : 303-309.

PDF(576 KB)
Welcome to visit Acta Anatomica Sinica! Today is Chinese
PDF(576 KB)
Acta Anatomica Sinica ›› 2017, Vol. 48 ›› Issue (3) : 303-309. DOI: 10.16098/j.issn.0529-1356.2017.03.009
Cancer Biology

Expression and significance of apoptosis inhibitor 5 in ovarian cancer

  • WANG Juan1 HUA Xiao-tang 2*
Author information +
History +

Abstract

Objective The study is designed to investigate the expression of apoptosis inhibitor 5(API5)in ovarian cancer(OC), and to analysis its association with clinical pathologic variables. Methods API5 expression was evaluated by Western blotting in two normal ovarian tissues and six different fresh OC tissues. Immunohistochemistry analysis was performed on formalin-fixed paraffinembedded sections of 10 normal tissues and 119 cases of OCs (including 61 serous papillary adenocarcinoma, 10 endometrioid adenocarcinoma, 10 clear cell carcinoma, 5 mucinous papillary carcinoma, and 33 specimens were classified as undifferentiated carcinoma). SiRNA transfection and flow cytometry showed the impact of API5 and cisplatin on ovarian cancer cells. Results The expression of API5 was higher in the cancer samples compared with that in the normal ovary tissues. API5 was significantly associated with clinical pathologic variables(P<0.05). Kaplan-Meier curve showed that high expression of API5 was related to poor prognosis of OC patients than that low expression. Decreasing the expression of API5 enhanced EOC cell line’s sensibility to cisplatin by flow cytometry. Conclusion Our findings suggest that API5 is involved in the progression of OC and has a potential clinical application value in the assessment of prognosis, which may be a target of therapy in OC.

Key words

Ovarian cancer / Apoptosis inhibitor 5 / Cisplatin / Immunohistochemistry / Human

Cite this article

Download Citations
WANG Juan HUA Xiao-tang. Expression and significance of apoptosis inhibitor 5 in ovarian cancer[J]. Acta Anatomica Sinica. 2017, 48(3): 303-309 https://doi.org/10.16098/j.issn.0529-1356.2017.03.009

References

[1]Siegel R, Ma J, Zou Z, et al. Cancer statistics, 2014[J]. CA Cancer J Clin, 2014, 64(1):9-29.
[2]Anuradha S,Webb PM, Blomfield P, et al. Survival of Australian women with invasive epithelial ovarian cancer: a population-based study[J]. Med J Aust, 2014, 201(5): 283-288.
[3]Garcia-Jove Navarro M, Basset C, Arconde’guy T, et al. Api5 contributes to E2F1 control of the G1/S cell cycle phase transition[J]. PLoeS One, 2013, 8(8):e71443.
[4]Gong YQ, Han FJ, Wu XK, et al. Progress in study on etiology of ovarian epithelial cancer[J].Frontiers of Medicine, 2010,39(5):18-20. (in Chinese)
宫艳秋,韩凤娟,吴效科,等. 卵巢上皮性癌病因学研究进展[J]. 医学前沿,2010,39(5):18-20.
[5]Walters Haygood, CL, Arend RC, Straughn JM, et al. Ovarian cancer stem cells: Can targeted therapy lead to improved progression-free survival[J]? World J Stem Cells, 2014, 6(4):441-447.
[6]Ma RQ, Ye X, Cheng HY,et al. Expressions and clinical significance of ROBO4 in both serum and tumor tissues in patients with epithelial ovarian cancer[J]. Acta Anatomica Sinica, 2014, 45(1):64-69. (in Chinese)
马瑞琼,叶雪,程洪艳,等. ROBO4在上皮性卵巢癌组织和血清中的表达及临床意义[J]. 解剖学报,2014,45(1):64-69.
[7]Lim S, Kaldis P. Cdks, cyclins and CKIs: roles beyond cell cycle regulation[J]. Development, 2013, 140(15):3079-3093.
[8]Stone A, Sutherland RL, Musgrove EA. Inhibitors of cell cycle kinases: recent advances and future prospects as cancer therapeutics[J]. Crit Rev Oncog, 2012,17(2):175-198.
[9]Zhao HL, Zhao XX, Wang YQ. The progress of API5[J]. Anhui Agricultural Science Bulleti, 2011,17(7):46. (in Chinese)
赵慧玲,赵鑫鑫,汪艳秋. API5相关的研究进展[J]. 安徽农学通,2011,17(7):46.
[10]Morris EJ, Michaud WA, Ji JY, et al. Functional identification of Api5 as a suppressor of E2F-dependent apoptosis in vivo[J]. PLoS Genet, 2006, 2(11):e196.
[11]Noh KH, Kim SH, Kim JH, et al. API5 confers tumoral immune escape through FGF2-dependent cell survival pathway[J]. Cancer Res, 2014, 74(13):3556-3566.
[12]Tewari M1, Yu M, Ross B, et al. AAC-11, a novel cDNA that inhibits apoptosis after growth factor withdrawal[J]. Cancer Res, 1997, 57(18):4063-4069.
[13]Kim JW, Cho HS, Kim JH, et al. AAC-11 overexpression induces invasion and protects cervical cancer cells from apoptosis[J]. Lab Invest, 2000, 80(4):587-594.
[14]Cho H, Chung JY, Song KH, et al. Apoptosis inhibitor-5 overexpression is associated with tumor progression and poor prognosis in patients with cervical cancer[J]. BMC Cancer, 2014, 14(1):545.
[15]Clegg N, Ferguson C, True LD, et al. Molecular characterization of prostatic small-cell neuroendocrine carcinoma[J]. Prostate, 2003, 55(1):55-64. 
[16]Sasaki H, Moriyama S, Yukiue H, et al. Expression of the antiapoptosis gene, AAC-11, as a prognosis marker in nonsmall cell lung cancer[J]. Lung Cancer, 2001, 34(1):53-57.
[17]Wang Z, Liu H, Liu B, et al. Gene expression levels of CSNK1A1 and AAC-11, but not NME1, in tumor tissues as prognostic factors in NSCLC patients[J]. Med Sci Monit, 2010, 16(8):357-364.
[18]Li D, Liu Y, Li H, et al. MicroRNA-1 promotes apoptosis of hepatocarcinoma cells by targeting apoptosis inhibitor-5 (API-5)[J]. FEBS Lett, 2015, 589(1):68-76.
[19]Upraity S, Kazi S, Padul V, et al. MiR-224 expression increases radiation sensitivity of glioblastoma cells[J]. Biochem Biophys Res Commun, 2014, 448(2):225-230.
[20]Ren K, Zhang W, Shi Y, et al. Pim-2 activates API-5 to inhibit the apoptosis of hepatocellular carcinoma cells through NF-kappaB pathway[J]. Pathol Oncol Res, 2010,16(2):229-237.
PDF(576 KB)

Accesses

Citation

Detail

Sections
Recommended

/