Research ArticleClinical Studies

Significant Association of Caveolin-1 (CAV1) Genotypes with Prostate Cancer Susceptibility in Taiwan

HSI-CHIN WU, CHAO-HSIANG CHANG, YUNG-AN TSOU, CHIA-WEN TSAI, CHENG-CHIEH LIN and DA-TIAN BAU
Anticancer Research February 2011, 31 (2) 745-749;

Abstract

Background: Multiple lines of evidence have implicated the Caveolin-1 (CAV1) gene in prostate cancer progression. CAV1 is located within the locus at 7q31-33 associated with prostate cancer aggressiveness, and was identified as being overexpressed in prostate tumors. Therefore, this study evaluated the relationship between the polymorphism of CAV1 and the risk of prostate cancer in Taiwan. Patients and Methods: Two hundred and fifty patients with prostate cancer and five hundred age-matched healthy controls recruited were genotyped. Results: There were significant differences between prostate cancer and control groups in the distributions of their genotypes (p=0.0004) and allelic frequencies (p=4.9×10−5) in the CAV1 T29107A (rs7804372) polymorphisms. Conclusion: This study provides evidence for the relationship of this variant of CAV1 and risk of prostate cancer which might merit further study as a genomic marker for early detection of prostate cancer.

Prostate cancer has become the most frequently diagnosed malignancy among men and one of the most common causes of cancer death in men in recent years. The etiology of prostate cancer is largely unknown, with both genetic and environmental factors likely to be involved (1). Nevertheless, confirmed risk factors for prostate cancer include age, ethnicity, country of origin, and family history.

In tumors, several genetic alterations have been associated with allelotyping and chromosome deletion. Loss of heterozygosity studies of specific chromosomal regions were performed to identify genomic sites harboring tumor suppressor genes (2-8). The region of 7q31 appears to play a critical role for the clinical aggressiveness and progression of prostate tumors (9), and several potential tumor suppressor genes have been suggested (10).

Caveolin-1 (CAV1) is located within this critical region and has been implicated in prostate cancer progression. CAV1 consists of three exons and is located at 7q31.1 telomeric of the microsatellite marker D7S522. Down-regulation or loss of CAV1 expression has been reported in many types of human cancer and cancer cell lines (11-17). CAV1 is the major structural and functional protein component of caveolae and the marker protein for this organelle (18). It plays an important role in many signaling pathways, molecular transport, and cellular proliferation and differentiation. The specific functions of the CAV1 protein/caveolae are highly cell- and context-specific (19). Biochemical and molecular analyses of prostate cancer tissues and cell lines identified CAV1 as being mostly up-regulated in metastatic prostate cancer (20, 21). It has also been shown that CAV1 expression is increased in metastatic human prostate cancer and that CAV1 cellular protein expression is predictive of recurrence of the disease after radical prostatectomy (22).

The emerging evidence pointing to the role of CAV1 in carcinogenesis led us to investigate whether different alleles of this gene are associated with prostate cancer. Thus, the aims of the current study were to determine the genotypic frequency of six polymorphisms of the CAV1 gene at C239A (rs1997623), G14713A (rs3807987), G21985A (12672038), T28608A (rs3757733), T29107A (rs7804372), and G32124A (rs3807992), and find their associations with prostate cancer susceptibility. To the best of our knowledge, this is the most valuable study carried out to evaluate the contribution of CAV1 polymorphisms in prostate oncology in Taiwan.

Patients and Methods

Study population and sample collection. The study population consisted of 250 prostate cancer patients and 500 cancer-free control volunteers. The patients were recruited at the outpatient clinics of general surgery between 2004 and 2010 at the China Medical University Hospital, Taichung, Taiwan, Republic of China. The clinical characteristics of the patients, including their histological details, were all graded and defined by expert surgeons (Dr. Wu and Chang's team). All the patients voluntarily participated, completed a self-administered questionnaire and provided peripheral blood samples. The controls were selected from the Health Examination Cohort of the hospital. The exclusion criteria of the control group included previous malignancy, metastases from known or unknown primary cancer and any familial or genetic diseases, and those whose genotypes could not be identified in our system. The study was approved by the Institutional Review Board of the China Medical University Hospital and written-informed consent was obtained from all the participants.

Genotyping conditions. Genomic DNA was prepared from peripheral blood leucocytes using a QIAmp Blood Mini Kit (Blossom, Taipei, Taiwan) and further processed according to our previous methods (23-30). In brief, the following primers were used: for CAV1 C239A (rs1997623), 5’-GTGTCCGCTTCTGCTATCTG-3’ and 5’-GCCAAGATGCAGAAGGAGTT-3’; for CAV1 G14713A (rs3807987), 5’-CCTTCCAGTAAGCAAGCTGT-3’ and 5’-CCTC TCAATCTTGCCATAGT-3’; for CAV1 G21985A (12672038), 5’-GGTGTCAGCAAGGCTATGCT-3’ and 5’-CCAGACACTCAGAA TGTGAC-3’; for CAV1 T28608A (rs3757733), 5’-GCTCAA CCTCATCTGAGGCA-3’ and 5’-GGCCTATTGT TGAGTGGATG-3’; for CAV1 T29107A (rs7804372), 5’-GCCTGAATTG CAATCCTGTG-3’ and 5’-ACGGTGTGAAC ACGGACATT-3’; and for CAV1 G32124A (rs3807992), 5’-GGTGTCTTGCAGTTGAATG-3’ and 5’-ACGGAG CTACTCAGTGCCAA-3’. The following cycling conditions were performed: one cycle at 94°C for 5 min; 35 cycles of 94°C for 30 s, 55°C for 30 s, and 72°C for 30 s; and a final extension at 72°C for 10 min. The PCR products were studied after digestion with Avr II, Bfa I, Hae III, Tsp509 I, Sau3AI and Nla III, restriction enzymes for CAV1 C239A (cut from 485 bp C type into 170+315 bp T type), CAV1 G14713A (cut from 268 bp A type into 66+202 bp G type), CAV1 G21985A (cut from 251+43 bp A type into 153+98+43 bp G type), CAV1 T28608A (cut from 298 bp T type into 100+198 bp A type), CAV1 T29107A (cut from 336 bp A type into 172+164 bp T type), and CAV1 G32124A (cut from 213+142+67 bp A type into 142+118+95+67 bp T type), respectively.

Statistical analyses. Only those with all the SNPs data (case/control=250/500) were selected for the final analysis. To ensure that the controls used were representative of the general population and to exclude the possibility of genotyping error, the deviation of the genotype frequencies of CAV1 single nucleotide polymorphisms (SNP) in the controls from those expected under the Hardy-Weinberg equilibrium was assessed using the goodness-of-fit test. Pearson's Chi-square test or Fisher's exact test (when the expected number in any cell was less than five) was used to compare the distribution of the CAV1 genotypes between cases and controls. The data was recognized as significant when the statistical p-value was less than 0.05. All statistical tests were performed using SAS, Version 9.1.3 (SAS Institute Inc., Cary, NC, USA) on two-sided probabilities.

Results

The frequencies of the genotypes for the CAV1 C239A, G14713A, G21985A, T28608A, T29107A and G32124A between controls and prostate cancer patients are presented in Table I. Genotype distributions of various genetic polymorphisms of CAV1 T29107A were significantly different between prostate cancer and control groups (p=0.0004), while those for CAV1 C239A, G14713A, G21985A, T28608A and G32124A were not statistically significant (p>0.05) (Table II).

The frequencies of the alleles for the CAV1 C239A, G14713A, G21985A, T28608A, T29107A and G32124A between controls and prostate cancer patients are shown in Table II. The CAV1 T29107A polymorphism was found to be significantly differently distributed between patients with prostate cancer and controls (Table I). It was also found to be associated with prostate cancer susceptibility in the allele frequency analysis model (p=4.9×10−5), confirming the previous finding. In particular, the frequency of the T allele was higher in prostate cancer patients. As for the other five SNPs, the distributions of their allele frequencies were not significantly different in controls and prostate cancer patients (Table II).

Discussion

Expression of the caveolin gene family, particularly CAV1, has been assessed in relationship to several human types of cancer, but few data consider CAV1 for genetic predisposition to these cancer types (31, 32). Williams and Lisanti interbred CAV1−/− null mice with TRAMP mice, which spontaneously develop advanced prostate cancer (33). They found that the loss of CAV1 reduced progression to metastasis. In order to determine the role of CAV1 and to find potential biomarkers of prostate cancer, six SNPs of the CAV1 gene were selected from the NCBI website and their associations with the susceptibility for prostate cancer were investigated in a population in central Taiwan. In the present study, we found that the CAV1 T29107A (rs7804372) SNP was closely associated with the susceptibility to prostate cancer (Table I and II), while the other five polymorphisms were not.

The CAV1 gene is on the long arm of chromosome 7, in a region associated with tumor suppression and with loss of heterozygosity in several types of cancer (34). In a recent study, among the eleven SNPs of the CAV1 gene evaluated (35), only one in CAV1 (rs9920, chr7:115987328; ORCT+CC=1.37, 95% CI=1.12, 1.68) was found to be associated with prostate cancer risk among Caucasians (from a sample of 1458 cases and 1351 controls). Compared with their results, we found the SNP in CAV1 (rs7804372, chr7:116194228; p=0.0004) was associated with prostate cancer risk in Taiwanese. There is a long genetic distance between these two SNP sites. This may indicate that the rs7804372 in CAV1 is associated with prostate cancer risk specifically of Taiwanese. However, Langeberg et al. also found that two SNPs (rs3807986 and rs3907989) of CAV1 were not associated with prostate cancer risk (35). This result was similarly to ours for the two SNPs rs3807987 and rs3807992 which lie very close to these two. As for this region in CAV1, the results are coincident between Caucasians and Taiwanese. To sum up these findings, we suggest that CAV1 variant distribution might depend on the ethnic type, and the genetic etiology of prostate cancer may be different among ethnicities.

View this table:
Table I.

Distribution of CAV1 genotypes among prostate cancer patients and controls.

The overexpression of CAV1 was reported in various malignancies, including prostate cancer (20, 36). The molecular basis for the initiation of CAV1 expression in prostate cancer is not clear. The CAV1 gene promoter has multiple CpG sites, and alterations in gene methylation have been shown in prostate cancer (37). However, patterns of CAV1 gene methylation have not, thus far, provided a convincing argument for the up-regulation of CAV1 in prostate cancer. In general, CAV1 has been associated with the stimulatory effects of steroid receptors, including the androgen receptor, suggesting a point of convergence for further mechanistic studies (38).

View this table:
Table II.

Distribution of CAV1 alleles among prostate cancer patients and controls.

In conclusion, this is the first study focused in the case–control comparison of CAV1 SNPs and prostate cancer in Taiwan, and individuals carrying the T allele of T29107A appear to be at a higher risk of prostate cancer. In the future, the T allele of T29107A might be a useful marker in prostate oncology.

Acknowledgements

We are grateful to Wen-Shin Chang, and the Tissue Bank in China Medical University Hospital for their technical assistance. This study was supported by research grants from the China Medical University and Hospital (DMR-99-069), the Terry Fox Cancer Research Foundation and the National Science Council (NSC 98-2320-B-039-010-MY3).

  • Received July 29, 2010.
  • Revision received November 1, 2010.
  • Accepted January 25, 2011.

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Significant Association of Caveolin-1 (CAV1) Genotypes with Prostate Cancer Susceptibility in Taiwan
HSI-CHIN WU, CHAO-HSIANG CHANG, YUNG-AN TSOU, CHIA-WEN TSAI, CHENG-CHIEH LIN, DA-TIAN BAU
Anticancer Research Feb 2011, 31 (2) 745-749;
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