Expression of survivin in adenoid cystic carcinoma of the lacrimal gland and the effect of intervention with arsenic trioxide in vitro
- Authors:
- Yingzhe Pan
- Yiqiao Xing
- Hui Wang
View Affiliations
Affiliations: Department of Xiangyang Hospital, Hubei University of Medicine, Xiangyang, Hubei 441000, P.R. China, Department of Ophthalmology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China
- Published online on: April 30, 2015 https://doi.org/10.3892/etm.2015.2466
-
Pages:
330-334
Metrics: Total
Views: 0 (Spandidos Publications: | PMC Statistics: )
Metrics: Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
Abstract
The aim of the present study was to investigate the role of survivin in adenoid cystic carcinoma of the lacrimal gland (LGACC) and the effect of arsenic trioxide (As2O3) intervention in vitro. In total, 13 patients with LGACC were recruited from Renmin Hospital of Wuhan University between 2007 and 2012. The patients were divided into different groups, namely tumor‑node‑metastasis (TNM)1‑2 and TNM3‑4, according to the TNM classification. A total of eight samples were included in the TNM1‑2 group, while five samples were included in the TNM3‑4 group. In addition, six patients that suffered from other diseases (no tumor), but underwent eye surgery, were selected as the controls. The mRNA and protein expression levels of survivin were analyzed. In addition, primary adenoid cystic carcinoma (ACC) cells were cultured and the expression of survivin was silenced using short interfering RNA (siRNA), after which the cell proliferation was determined. Furthermore, the primary cultured ACC cells were treated with different doses of As2O3 to observe the effect on the apoptosis rate. The mRNA and protein expression levels of survivin in the LGACC groups were higher when compared with the controls (P<0.01). In addition, the expression levels were higher in the TNM3‑4 group when compared with the TNM1‑2 group (P<0.01). After silencing survivin expression using siRNA, the rate of ACC cell proliferation was shown to decrease at days 2, 3, 4 and 5 following culture, particularly in the TNM3‑4 group at days 2 and 3 (P<0.05), day 4 (P<0.01 vs. TNM1‑2 + siRNA); and days 3 and 5 (P<0.05), and day 2 (P<0.01 vs. TNM3‑4 + siRNA). The mRNA expression levels of survivin in the TNM1‑2 and TNM3‑4 groups were significantly decreased following treatment with the various doses of As2O3 (2, 4 and 6 µΜ) for 48 h, and the apoptosis rate of the ACC cells was markedly increased (TNM1‑2 and 3‑4: As2O3 6 µM vs. As2O3 2 µM, As2O3 6 µM vs. As2O3 4 Μm, P<0.01; TNF3‑4, As2O3 4 µM VS. As2O3 2 µM, P<0.01; TNM1‑2, As2O3 4 µM vs. As2O3 2 µM, P<0.05). Therefore, survivin was demonstrated to be highly expressed in ACC cells of the lacrimal gland, and inhibition of survivin gene expression was found to suppress the proliferation of the ACC cells. Furthermore, As2O3 treatment was demonstrated to inhibit the mRNA expression of survivin in the ACC cells, while significantly increasing the apoptosis rate.
View References
|
1
|
Kokemueller H, Eckardt A, Brachvogel P and
Hausamen JE: Adenoid cystic carcinoma of the head and neck - a 20
years experience. Int J Oral Maxillofac Surg. 33:25–31. 2004.
View Article : Google Scholar : PubMed/NCBI
|
|
2
|
Zhou Q, Chang H, Han YD, Gao Y and Liu HG:
High-grade transformation in adenoid cystic carcinoma: A
clinicopathologic study. Zhonghua Bing Li Xue Za Zhi. 42:106–110.
2013.(In Chinese). PubMed/NCBI
|
|
3
|
Zeng J, Shi JT, Li B, Sun XL, An YZ, Li
LQ, Gao F, Xu JP and Jonas JB: Epithelial tumors of the lacrimal
gland in the Chinese: a clinicopathologic study of 298 patients.
Graefes Arch Clin Exp Ophthalmol. 248:1345–1349. 2010. View Article : Google Scholar : PubMed/NCBI
|
|
4
|
Civit T, Klein O and Baylac F: Lacrimal
gland epithelial tumors. Neurochirurgie. 56:152–157. 2010.(In
French). View Article : Google Scholar : PubMed/NCBI
|
|
5
|
Lee JI, Kim YZ, Lee EH and Kim KH: Skull
base invasion of adenoid cystic carcinoma of the lacrimal gland: a
case report. J Korean Neurosurg Soc. 44:273–276. 2008. View Article : Google Scholar : PubMed/NCBI
|
|
6
|
McKenzie JA and Grossman D: Role of the
apoptotic and mitotic regulator survivin in melanoma. Anticancer
Res. 32:397–404. 2012.PubMed/NCBI
|
|
7
|
Kanwar JR, Kamalapuram SK and Kanwar RK:
Targeting survivin in cancer: Patent review. Expert Opin Ther Pat.
20:1723–1737. 2010. View Article : Google Scholar : PubMed/NCBI
|
|
8
|
Kanwar JR, Kamalapuram SK and Kanwar RK:
Targeting survivin in cancer: The cell-signalling perspective. Drug
Discov Today. 16:485–494. 2011. View Article : Google Scholar : PubMed/NCBI
|
|
9
|
Altieri DC: Survivin, cancer networks and
pathway-directed drug discovery. Nat Rev Cancer. 8:61–70. 2008.
View Article : Google Scholar : PubMed/NCBI
|
|
10
|
Zhang B, Mu HB, Xu XG, Liu W and Hu NR:
Role of survivin gene on the apoptosis of adenoid cystic
carcinoma-2 cells induced by arsenic trioxide. Hua Xi Kou Qiang Yi
Xue Za Zhi. 28:246–249. 2010.(In Chinese). PubMed/NCBI
|
|
11
|
Adida C, Crotty PL, McGrath J, Berrebi D,
Diebold J and Altieri DC: Developmentally regulated expression of
the novel cancer anti-apoptosis gene survivin in human and mouse
differentiation. Am J Pathol. 152:43–49. 1998.PubMed/NCBI
|
|
12
|
Ryan BM, O'Donovan N and Duffy MJ:
Survivin: a new target for anti-cancer therapy. Cancer Treat Rev.
35:553–562. 2009. View Article : Google Scholar : PubMed/NCBI
|
|
13
|
Shin S, Sung BJ, Cho YS, Kim HJ, Ha NC,
Hwang JI, Chung CW, Jung YK and Oh BH: An anti-apoptotic protein
human survivin is a direct inhibitor of caspase-3 and −7.
Biochemistry. 40:1117–1123. 2001. View Article : Google Scholar : PubMed/NCBI
|
|
14
|
Tamm I, Wang Y, Sausville E, Scudiero DA,
Vigna N, Oltersdorf T and Reed JC: IAP-family protein survivin
inhibits caspase activity and apoptosis induced by Fas (CD95), Bax,
caspases and anticancer drugs. Cancer Res. 58:5315–5320.
1998.PubMed/NCBI
|
|
15
|
Mirza A, McGuirk M, Hockenberry TN, Wu Q,
Ashar H, Black S, Wen SF, Wang L, Kirschmeier P, Bishop WR, Nielsen
LL, Pickett CB and Liu S: Human survivin is negatively regulated by
wild-type p53 and participates in p53-dependent apoptotic pathway.
Oncogene. 21:2613–2622. 2002. View Article : Google Scholar : PubMed/NCBI
|
|
16
|
Yang D, Welm A and Bishop JM: Cell
division and cell survival in the absence of survivin. Proc Natl
Acad Sci USA. 101:15100–15105. 2004. View Article : Google Scholar : PubMed/NCBI
|
|
17
|
Yang CH, Kuo ML, Chen JC and Chen YC:
Arsenic trioxide sensitivity is associated with low level of
glutathione in cancer cells. Br J Cancer. 81:796–799. 1999.
View Article : Google Scholar : PubMed/NCBI
|
