| General information | Literature | Expression | Regulation | Mutation | Homolog | Interaction |
Basic Information | |
|---|---|
Gene ID | 1636 |
Name | ACE |
Synonymous | angiotensin I converting enzyme;ACE;angiotensin I converting enzyme |
Definition | CD143 antigen|angiotensin I converting enzyme (peptidyl-dipeptidase A) 1|angiotensin I converting enzyme peptidyl-dipeptidase A 1 transcript|angiotensin converting enzyme, somatic isoform|angiotensin-converting enzyme|carboxycathepsin|dipeptidyl carboxype |
Position | 17q23.3 |
Gene type | protein-coding |
Title | Abstract |
| breast cancer | It has been indicated that renin-angiotensin system (RAS) has role in various steps of cancer progression. The presence of RAS components has been shown in normal and breast cancer tissue. insertion/deletion (I/D) is one of angiotensin I converting enzyme (ACE) polymorphisms and A1166C is one of angiotensin II type-1 receptor (AT1R) polymorphisms which have been associated with various diseases such as cardiovascular diseases. In the present study, we aimed to substantiate the putative significance of ACE and AT1R on breast cancer biology by investigating the influence of their gene polymorphisms on breast cancer progression. The I/D and A1166C polymorphisms were evaluated by using polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP), respectively in 70 breast cancer patients diagnosed with invasive breast cancer and 70 healthy women. Breast cancer prognostic factors were obtained from medical and pathology reports of patients. There was no significant difference between cases and controls for ACE (I/D) (P = 0.15) and AT1R (A1166C) genotypes (P = 0.86). In breast cancer patients, when DD genotype was used as reference group, the combination of II and ID genotypes was associated with increased HER-2 expression (P = 0.020; OR, 4.58; 95% CI, 1.26-16.60). Also, when AA genotype was used as reference group, the AC genotype was associated with higher tumor TNM stage (P = 0.024; OR, 4.66; 95% CI, 1.18-18.35). This is the first study indicating that ACE (I/D) polymorphism is associated with HER-2 expression and AT1R (A1166C) polymorphism is associated with tumor TNM stage in breast cancer patients. |
| gastric cancer | PURPOSE: In the present study, we aimed to substantiate the putative significance of angiotensin I-converting enzyme (ACE) on gastric cancer biology by investigating the influence of its gene polymorphism on gastric cancer progression. EXPERIMENTAL DESIGN: Genomic DNA was purified from peripheral blood mononuclear cells or tissue specimens. Amplified ACE gene fragments were separated on agarose gels. D or I alleles were identified by the presence of 190- or 490-bp fragments, respectively. Local expression of ACE was investigated by immunohistochemistry. RESULTS: Twenty-four of 113 (21%) gastric cancer patients had the II, 57 (51%) the ID, and 32 (28%) the DD genotype. The distribution of the ACE genotypes did not differ significantly from the control group of 189 patients without gastric cancer. However, the ACE genotypes correlated with the number of lymph node metastases and the Unio Internationale Contra Cancrum (UICC) tumor stage. Patients with the II genotype had a highly significantly smaller number of lymph node metastases (P < 0.001) and a significantly lower UICC tumor stage (P = 0.01) than patients with the DD genotype. No correlation was found between tumor type, tumor location, local tumor growth, distant metastases, and the ACE genotype. The expression of ACE in gastric cancer was investigated by immunohistochemistry in 100 of 113 patients. ACE was expressed by endothelial cells in all (100%) specimens and by tumor cells in 56 (56%) specimens. CONCLUSIONS: Our study shows that ACE is expressed locally in gastric cancer and that the gene polymorphism influences metastatic behavior. |
| oral cancer | OBJECTIVES: Angiotensin I-converting enzyme (ACE), a type I cell surface zinc metallopeptidase, is differentially expressed in several malignancies and plays a role in tumor cell proliferation, tumor cell migration, angiogenesis, and metastatic behavior. We aimed to investigate the effects of ACE gene (rs1799752) variants on oral cancer risk. MATERIALS AND METHODS: Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) 32 was used to measure ACE gene polymorphisms in 88 patients with oral precancerous lesion (OPL), 186 33 patients with oral cancer, and 120 control subjects without any oral lesions. All study subjects were male 34 betel quid chewers. RESULTS: Patients with oral cancer or OPL had a higher frequency of the DD genotype than the control patients did. Oral cancer patients with the DD genotype had a significantly higher prevalence of lymph node metastases than patients with the II/ID genotype did. After adjusting for age, smoking, drinking, and betel quid chewing status, we found that individuals with the DD genotype of the ACE gene had a 5.46-fold and 3.13-fold higher risk of developing oral cancer or OPL, respectively, than those with the II genotype did. Furthermore, oral cancer patients with the DD genotype of the ACE gene had a 2.16-fold higher likelihood of lymph node metastasis. CONCLUSION: Our data suggest that the ACE gene polymorphisms may be associated with increased susceptibility to OPL and oral cancer and lymph node metastasis from oral cancer. |
| prostate cancer | The aim was to substantiate the putative significance of angiotensin-converting enzyme (ACE) (insertion/deletion) I/D polymorphism on prostate cancer risk, BTPSA-A TPSA (before treatment-after treatment prostate-specific antigen) levels and tumor development. MATERIALS AND METHODS: 48 prostate cancer patients and 51 healthy volunteers were included. The ACE I/D genotypes were determined by PCR (polymerase chain reaction) and RFLP (restriction fragment length polymorphism) techniques. RESULTS: The DD genotype may have detrimental and the II genotype may have protective effect on prostate cancer (p = 0.03). The highest before treatment PSA (BTPSA) values were found in the patient group having the DD genotype (p = 0.017). PSA-AT levels were higher in homozygous mutant DD than homozygous II and the decrease in PSA-AT level was found to be statistically significant in each genotype (p = 0.000). Patients with the D allele showed a higher prevalence of late stage prostate carcinoma when compared to the patients with II genotype (p = 0.022) and the detrimental effects of the D allele, both in lymph node metastases and distant metastasis were observed. CONCLUSION: The risk of prostate cancer development, the PSA level and tumor metastasis may be associated with genetic variation in the ACE I/D genotypes which may be used as an important biomarker for further studies. |