Increased survivin expression in high‐grade oral squamous cell carcinoma: a study in Indian tobacco chewers

Fifty outbred Syrian golden hamsters were equally divided into three experimental groups and two control groups. The pouches of the experimental groups were painted bilaterally with a 0.5% 7,12-dimethylbenz[a]anthracene (DMBA) solution thrice a week for 3, 7 and 14 weeks. One of the control groups was applied with mineral oil while another control group remained untreated throughout the experiment. Neither survivin nor cIAP2 could be detected in any of the control tissues, whereas survivin and cIAP2 were found to be significantly increased in 3-, 7- and 14-week DMBA-treated pouches compared with the control pouches. Expression of XIAP, cIAP1 and NAIP were noted for both the control and 3-, 7- and 14-week DMBA-treated pouches, but levels were found to be significantly elevated in the experimental groups compared with the control pouches. p53 was not detected in any control tissues, but was significantly increased in 3-, 7- and 14-week DMBA-treated pouches. Direct sequencing revealed a point mutation (C-->G) of p53 for pouch tissues treated with DMBA for 3 and 7 weeks, and there was a wide variation in the p53 sequence of the 14-week DMBA-treated pouch tissues, as compared with the control tissues. The control tissues had a survivin- and cIAP2-methylated allele, whereas the DMBA-treated tissues showed no evidence of survivin- and cIAP2-methylation. Neither the control nor DMBA-treated pouches showed evidence of XIAP-, cIAP1- or NAIP-methylation. Our results suggest that the expression of inhibitors of apoptosis family in DMBA-induced hamster buccal-pouch squamous-cell carcinogenesis may be modulated by both genetic (mutant p53) and epigenetic mechanisms.

show abstract

“…These findings are consistent with the results for human oral carcinogenesis (Tanimotoa et al. 2005; Jane et al. 2006).…”

Section: Discussionsupporting

confidence: 93%

“…1998), and the association of IAP family members, chiefly survivin, with human oral squamous‐cell carcinomas has also been studied (Tanimotoa et al. 2005; Jane et al. 2006).…”

Section: Discussionmentioning

confidence: 99%

Expression of inhibitors of apoptosis family protein in 7,12‐dimethylbenz[a]anthracene‐induced hamster buccal‐pouch squamous‐cell carcinogenesis is associated with mutant p53 accumulation and epigenetic changes

Hsue

Wang

Chen

et al. 2008

Int J Experimental Path

View full text Add to dashboard Cite

show abstract

“…[35][36][37] Since the function of cytoplasmic survivin is to inhibit apoptosis, evasion from apoptosis may play a key role in the early event of oral carcinogenesis. 24,28,39 Interestingly, the high rate of cytoplasmic survivin expression (72% to 100%) in OSCC was consistently reported from various studies, [22][23][24]40 despite the differences in risk factors, geographic factors, criteria of evaluation of survivin expression, and antibody sources. It has been shown that apoptosis inhibited by survivin led to p53 mutant clones after ultraviolet B irradiation in a skin tumor model.…”

Section: Discussionmentioning

confidence: 74%

Overexpression of Survivin and Caspase 3 in Oral Carcinogenesis

Poomsawat

Punyasingh

Vejchapipat

2014

Applied Immunohistochemistry &Amp; Molecular Morphology

View full text Add to dashboard Cite

Survivin is an inhibitor of apoptosis protein that inhibits caspase 3 function. While cytoplasmic survivin suppresses apoptosis, nuclear survivin regulates cell division. Little is known about the subcellular localization of survivin in oral carcinogenesis. This study examined the subcellular distribution of these 2 proteins in oral squamous cell carcinoma (OSCC) and premalignant lesions including oral leukoplakia (OL) with and without dysplasia. Expression of survivin and caspase 3 were immunohistochemically analyzed in 114 samples including OSCC, OL with and without dysplasia, and normal oral mucosa (NM). Cytoplasmic and nuclear positive cells were counted separately. The results were presented as the frequency of positive cases. The positive expression rates of cytoplasmic and nuclear survivin in OSCC were significantly higher than in NM, OL with and without dysplasia. NM showed a low rate of cytoplasmic survivin expression compared to OL with and without dysplasia. The numbers of cytoplasmic and nuclear expression of caspase 3 in OSCC were significantly higher than that of NM, OL with and without dysplasia. In conclusion, the overexpression of cytoplasmic survivin in OSCC and premalignant lesions suggest that suppression of apoptosis by survivin occurs at early and late stages of oral carcinogenesis. The elevated expression of nuclear survivin and caspase 3 in OSCC indicate that at the late stage survivin increases cell proliferation whereas caspase 3 promotes apoptosis.

show abstract

“…2 An important reason for poor prognosis of OSCC is the lack of molecular prognostic markers available to assess the aggressiveness of this tumour, probability of recurrence and disease progression. 3 Apoptosis has become one of the basic tools in cancer research and establishing cancer pathways. 4 Survivin is a protein that inhibits apoptosis and regulates cell division.…”

Section: Introductionmentioning

confidence: 99%

Expression of survivin in dysplasia and different grades of oral squamous cell carcinoma

Deo

Deshmukh

2017

Translational Research in Oral Oncology

View full text Add to dashboard Cite

Background: Survivin is a protein that inhibits apoptosis and regulates cell division. Studies examining the expression of survivin in oral cancer are limited. Correlation between the expression of survivin in dysplasia and different grades of oral squamous cell carcinoma (OSCC) could help us to assess its use as a biomarker. Objectives: The objectives of this research were to evaluate the expression of survivin in dysplasia and in different grades of OSCC keeping in mind that when comparison is made between these two groups, it may highlight the use of this biomarker.

show abstract

Increased survivin expression in high‐grade oral squamous cell carcinoma: a study in Indian tobacco chewers

Abstract: Increased expression of anti-apoptotic survivin in high-grade tumors suggests that survivin is likely to contribute significantly to apoptosis resistance in response to therapy.

Cited by 30 publications

References 37 publications

Expression of inhibitors of apoptosis family protein in 7,12‐dimethylbenz[a]anthracene‐induced hamster buccal‐pouch squamous‐cell carcinogenesis is associated with mutant p53 accumulation and epigenetic changes

Expression of inhibitors of apoptosis family protein in 7,12‐dimethylbenz[a]anthracene‐induced hamster buccal‐pouch squamous‐cell carcinogenesis is associated with mutant p53 accumulation and epigenetic changes

Overexpression of Survivin and Caspase 3 in Oral Carcinogenesis

Expression of survivin in dysplasia and different grades of oral squamous cell carcinoma

Contact Info

Product

Resources

About