Expression of Catechol O-Methyltransferase in Colorectal Adenoma Tissues and Colorectal Cancer Tissues_CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY

Authors：

 XIAOBo ¹ , XIONGGuang-bing ¹ , XIAOTi-xian ² , XIAOYi ¹

1. Department of General Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China;
2. Beijing No.5 Middle School, Beijing 100007, China;

Corresponding author：

XIAOBo, Email: 15911068781@163.com

Keywords：

Catechol-O-methyltransferase; Colorectal adenoma; Colorectal cancer

DOI：

10.7507/1007-9424.20150180

Video：

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Objective To investigate the expression of catechol O-methyltransferase (COMT) mRNA and its protein in colorectal adenoma tissues and corresponding adjacent tissues, colorectal cancer tissues and corresponding adjacent tissues. Methods Expressions of COMT mRNA and its protein were evaluated by real-time PCR and immunohistochemistry method in colorectal adenoma tissues and corresponding adjacent tissues, colorectal cancer tissues and corresponding adjacent tissues. Meanwhile, the relationship between the expression of COMT and clinic-pathological features of colorectal adenoma and colorectal cancer were analyzed. Results ①The expression of COMT mRNA in colorectal adenoma tissue/colorectal cancer tissue group was higher than that of corresponding adjacent tissue group (0.109 0 vs. 0.000 5, t=3.02, P=0.01; 0.041 8 vs. 0.013 5, t=2.71, P=0.02).②The rate of high-expression of COMT in colorectal adenoma tissue/colorectal cancer tissue group was higher than that of corresponding adjacent tissue group [72.34% (34/47) vs. 25.53% (12/47), χ²=28.72, P < 0.01; 66.67% (28/42) vs. 28.57% (12/42), χ²=4.97, P < 0.05].③High-expression of COMT was not related to age, gender, location of tumor, and pathological type in colorectal adenoma patients (P > 0.05). High-expression of COMT was not related to age, gender, location of tumor, and differentiation degree (P > 0.05), but was related to TNM staging, T staging, and N staging in colorectal cancer patients (P < 0.05), the patients of TNMⅠ+Ⅱstaging, T1+T2 staging, and N0 staging had higher rate of high-expression of COMT. Conclusion Compared with corresponding adjacent tissues, COMT expresses highly in colorectal adenoma tissues and colorectal cancer tissues, so it may play a partial role in the emergence and development of colorectal cancer.

Citation： XIAOBo, XIONGGuang-bing, XIAOTi-xian, XIAOYi. Expression of Catechol O-Methyltransferase in Colorectal Adenoma Tissues and Colorectal Cancer Tissues. CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY, 2015, 22(6): 705-709. doi: 10.7507/1007-9424.20150180 Copy

1.	Siegel R, Desantis C, Jemal A. Colorectal cancer statistics, 2014. CA Cancer J Clin, 2014, 64(2):104-117.
2.	Brenner H, Kloor M, Pox CP. Colorectal cancer. Lancet. 2014, 383 (9927):1490-1502.
3.	代珍, 郑荣寿, 邹小农, 等.中国结直肠癌发病趋势分析和预测.中华预防医学杂志, 2012, 46(7):598-603.
4.	Fearon ER, Vogelstein B. A genetic model for colorectal tumorigenesis. Cell, 1990, 61(5):759-767.
5.	Fearon ER. Molecular genetics of colorectal cancer. Annu Rev Pathol, 2011, 6:479-507.
6.	Dawling S, Roodi N, Mernaugh RL, et al. Catechol-O-methyltransferase (COMT)-mediated metabolism of catechol estrogens:comparison of wild-type and variant COMT isoforms. Cancer Res, 2001, 61(18):6716-6722.
7.	吴文铭, 赵玉沛, 廖泉, 等.儿茶酚氧位甲基转移酶基因在CRC组织中的表达.中华外科杂志, 2010, 48:535-538.
8.	Edge SB, Compton CC. The American Joint Committee on Cancer:the 7th edition of the AJCC cancer staging manual and the future of TNM. Ann Surg Oncol, 2010, 17(6):1471-1474.
9.	Männistö PT, Kaakkola S. Catechol-O-methyltransferase (COMT):biochemistry, molecular biology, pharmacology, and clinical efficacy of the new selective COMT inhibitors. Pharmacol Rev, 1999, 51(4):593-628.
10.	Fotsis T, Zhang Y, Pepper MS, et al. The endogenous oestrogen metabolite 2-methoxyoestradiol inhibits angiogenesis and suppresses tumour growth. Nature, 1994, 368(6468):237-239.
11.	Grossman MH, Emanuel BS, Budarf ML. Chromosomal mapping of the human catechol-O-methyltransferase gene to 22q11.1-q11.2. Genomics, 1992, 12(4):822-825.
12.	Huh MM, Friedhoff AJ. Multiple molecular forms of catechol-O-methyltransferase. Evidence for two distinct forms, and their purification and physical characterization. J Biol Chem, 1979, 254(2):299-308.
13.	Wan GX, Cao YW, Li WQ, et al. The catechol-O-methyltransferase val158Met polymorphism contributes to the risk of breast cancer in the Chinese population:an updated meta-analysis. J Breast Cancer, 2014, 17(2):149-156.
14.	Lin G, Zhao J, Wu J, et al. Contribution of catechol-O-methyltransferase Val158Met polymorphism to endometrial cancer risk in postmenopausal women:a meta-analysis. Genet Mol Res, 2013, 12(4):6442-6453.
15.	Holt SK, Rossing MA, Malone KE, et al. Ovarian cancer risk and polymorphisms involved in estrogen catabolism. Cancer Epidemiol Biomarkers Prev, 2007, 16(3):481-489.
16.	Udler MS, Azzato EM, Healey CS, et al. Common germline polymorphisms in COMT, CYP19A1, ESR1, PGR, SULT1E1 and STS and survival after a diagnosis of breast cancer. Int J Cancer, 2009, 125 (11):2687-2696.
17.	Hirata H, Hinoda Y, Okayama N, et al. COMT polymorphisms affecting protein expression are risk factors for endometrial cancer. Mol Carcinog, 2008, 47(10):768-774.
18.	Matsui A, Ikeda T, Enomoto K, et al. Progression of human breast cancers to the metastatic state is linked to genotypes of catechol-O-methyltransferase. Cancer Lett, 2000, 150(1):23-31.
19.	Huang J, Sun J, Chen Y, et al. Analysis of multiplex endogenous estrogen metabolites in human urine using ultra-fast liquid chromatography-tandem mass spectrometry:a case study for breast cancer. Anal Chim Acta, 2012, 711:60-68.
20.	Qasim BJ, Ali HH, Hussein AG. Immunohistochemical expression of estrogen and progesterone receptors in human colorectal adenoma and carcinoma using specified automated cellular image analysis system:a clinicopathological study. Oman Med Jv, 2011, 26(5):307-314.
21.	Barzi A, Lenz AM, Labonte MJ, et al. Molecular pathways:estrogen pathway in colorectal cancer. Clin Cancer Res, 2013, 19(21):5842-5848.
22.	Hartman J, Edvardsson K, Lindberg K, et al. Tumor repressive functions of estrogen receptor beta in SW480 colon cancer cells. Cancer Res, 2009, 69(15):6100-6106.
23.	Cleveland AG, Oikarinen SI, Bynoté KK, et al. Disruption of estrogen receptor signaling enhances intestinal neoplasia in Apc(Min/+) mice. Carcinogenesis, 2009, 30(9):1581-1590.
24.	Hogan AM, Collins D, Baird AW, et al. Estrogen and gastrointestinal malignancy. Mol Cell Endocrinol, 2009, 307(1-2):19-24.
25.	Green J, O'driscoll M, Barnes A, et al. Impact of gender and parent of origin on the phenotypic expression of hereditary nonpolyposis colorectal cancer in a large newfoundland kindred with a common MSH2 mutation. Dis Colon Rectum, 2002, 45(9):1223-1232.
26.	Solimando R, Bazzoli F, Ricciardiello L. Chemoprevention of colorectal cancer:a role for ursodeoxycholic acid, folate and hormone replacement treatment?. Best Pract Res Clin Gastroenterol, 2011, 25 (4-5):555-568.
27.	Zhao YN, Zhang W, Chen YC, et al. Relative imbalances in the expression of catechol-O-methyltransferase and cytochrome P450 in breast cancer tissue and their association with breast carcinoma. Maturitas, 2012, 72(2):139-145.
28.	Hevir N, Sinkovec J, Rižner TL. Disturbed expression of phaseⅠand phaseⅡestrogen-metabolizing enzymes in endometrial cancer:lower levels of CYP1B1 and increased expression of S-COMT. Mol Cell Endocrinol, 2011, 331(1):158-167.
29.	Wu W, Zhang J, Zhou L, et al. Increased COMT expression in pancreatic cancer and correlation with clinicopathologic parameters. Sci China Life Sci, 2012, 55(9):747-752.
30.	Rennert G, Rennert HS, Pinchev M, et al. Use of hormone replacement therapy and the risk of colorectal cancer. J Clin Oncol, 2009, 27(27):4542-4547.
31.	Passarelli MN, Newcomb PA, Makar KW, et al. No association between germline variation in catechol-O-methyltransferase and colorectal cancer survival in postmenopausal women. Menopause, 2014, 21(4):415-420.

1. Siegel R, Desantis C, Jemal A. Colorectal cancer statistics, 2014. CA Cancer J Clin, 2014, 64(2):104-117.
2. Brenner H, Kloor M, Pox CP. Colorectal cancer. Lancet. 2014, 383 (9927):1490-1502.
3. 代珍, 郑荣寿, 邹小农, 等.中国结直肠癌发病趋势分析和预测.中华预防医学杂志, 2012, 46(7):598-603.
4. Fearon ER, Vogelstein B. A genetic model for colorectal tumorigenesis. Cell, 1990, 61(5):759-767.
5. Fearon ER. Molecular genetics of colorectal cancer. Annu Rev Pathol, 2011, 6:479-507.
6. Dawling S, Roodi N, Mernaugh RL, et al. Catechol-O-methyltransferase (COMT)-mediated metabolism of catechol estrogens:comparison of wild-type and variant COMT isoforms. Cancer Res, 2001, 61(18):6716-6722.
7. 吴文铭, 赵玉沛, 廖泉, 等.儿茶酚氧位甲基转移酶基因在CRC组织中的表达.中华外科杂志, 2010, 48:535-538.
8. Edge SB, Compton CC. The American Joint Committee on Cancer:the 7th edition of the AJCC cancer staging manual and the future of TNM. Ann Surg Oncol, 2010, 17(6):1471-1474.
9. Männistö PT, Kaakkola S. Catechol-O-methyltransferase (COMT):biochemistry, molecular biology, pharmacology, and clinical efficacy of the new selective COMT inhibitors. Pharmacol Rev, 1999, 51(4):593-628.
10. Fotsis T, Zhang Y, Pepper MS, et al. The endogenous oestrogen metabolite 2-methoxyoestradiol inhibits angiogenesis and suppresses tumour growth. Nature, 1994, 368(6468):237-239.
11. Grossman MH, Emanuel BS, Budarf ML. Chromosomal mapping of the human catechol-O-methyltransferase gene to 22q11.1-q11.2. Genomics, 1992, 12(4):822-825.
12. Huh MM, Friedhoff AJ. Multiple molecular forms of catechol-O-methyltransferase. Evidence for two distinct forms, and their purification and physical characterization. J Biol Chem, 1979, 254(2):299-308.
13. Wan GX, Cao YW, Li WQ, et al. The catechol-O-methyltransferase val158Met polymorphism contributes to the risk of breast cancer in the Chinese population:an updated meta-analysis. J Breast Cancer, 2014, 17(2):149-156.
14. Lin G, Zhao J, Wu J, et al. Contribution of catechol-O-methyltransferase Val158Met polymorphism to endometrial cancer risk in postmenopausal women:a meta-analysis. Genet Mol Res, 2013, 12(4):6442-6453.
15. Holt SK, Rossing MA, Malone KE, et al. Ovarian cancer risk and polymorphisms involved in estrogen catabolism. Cancer Epidemiol Biomarkers Prev, 2007, 16(3):481-489.
16. Udler MS, Azzato EM, Healey CS, et al. Common germline polymorphisms in COMT, CYP19A1, ESR1, PGR, SULT1E1 and STS and survival after a diagnosis of breast cancer. Int J Cancer, 2009, 125 (11):2687-2696.
17. Hirata H, Hinoda Y, Okayama N, et al. COMT polymorphisms affecting protein expression are risk factors for endometrial cancer. Mol Carcinog, 2008, 47(10):768-774.
18. Matsui A, Ikeda T, Enomoto K, et al. Progression of human breast cancers to the metastatic state is linked to genotypes of catechol-O-methyltransferase. Cancer Lett, 2000, 150(1):23-31.
19. Huang J, Sun J, Chen Y, et al. Analysis of multiplex endogenous estrogen metabolites in human urine using ultra-fast liquid chromatography-tandem mass spectrometry:a case study for breast cancer. Anal Chim Acta, 2012, 711:60-68.
20. Qasim BJ, Ali HH, Hussein AG. Immunohistochemical expression of estrogen and progesterone receptors in human colorectal adenoma and carcinoma using specified automated cellular image analysis system:a clinicopathological study. Oman Med Jv, 2011, 26(5):307-314.
21. Barzi A, Lenz AM, Labonte MJ, et al. Molecular pathways:estrogen pathway in colorectal cancer. Clin Cancer Res, 2013, 19(21):5842-5848.
22. Hartman J, Edvardsson K, Lindberg K, et al. Tumor repressive functions of estrogen receptor beta in SW480 colon cancer cells. Cancer Res, 2009, 69(15):6100-6106.
23. Cleveland AG, Oikarinen SI, Bynoté KK, et al. Disruption of estrogen receptor signaling enhances intestinal neoplasia in Apc(Min/+) mice. Carcinogenesis, 2009, 30(9):1581-1590.
24. Hogan AM, Collins D, Baird AW, et al. Estrogen and gastrointestinal malignancy. Mol Cell Endocrinol, 2009, 307(1-2):19-24.
25. Green J, O'driscoll M, Barnes A, et al. Impact of gender and parent of origin on the phenotypic expression of hereditary nonpolyposis colorectal cancer in a large newfoundland kindred with a common MSH2 mutation. Dis Colon Rectum, 2002, 45(9):1223-1232.
26. Solimando R, Bazzoli F, Ricciardiello L. Chemoprevention of colorectal cancer:a role for ursodeoxycholic acid, folate and hormone replacement treatment?. Best Pract Res Clin Gastroenterol, 2011, 25 (4-5):555-568.
27. Zhao YN, Zhang W, Chen YC, et al. Relative imbalances in the expression of catechol-O-methyltransferase and cytochrome P450 in breast cancer tissue and their association with breast carcinoma. Maturitas, 2012, 72(2):139-145.
28. Hevir N, Sinkovec J, Rižner TL. Disturbed expression of phaseⅠand phaseⅡestrogen-metabolizing enzymes in endometrial cancer:lower levels of CYP1B1 and increased expression of S-COMT. Mol Cell Endocrinol, 2011, 331(1):158-167.
29. Wu W, Zhang J, Zhou L, et al. Increased COMT expression in pancreatic cancer and correlation with clinicopathologic parameters. Sci China Life Sci, 2012, 55(9):747-752.
30. Rennert G, Rennert HS, Pinchev M, et al. Use of hormone replacement therapy and the risk of colorectal cancer. J Clin Oncol, 2009, 27(27):4542-4547.
31. Passarelli MN, Newcomb PA, Makar KW, et al. No association between germline variation in catechol-O-methyltransferase and colorectal cancer survival in postmenopausal women. Menopause, 2014, 21(4):415-420.

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Expression of Catechol O-Methyltransferase in Colorectal Adenoma Tissues and Colorectal Cancer Tissues

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