Abstract
Background and aims
Elucidation of molecular basis of the adenomatous polyps (AP) and colorectal cancer (CRC) development is crucial for their prevention, early detection, and treatment. According to the recent discoveries, sulfatases are implied in extracellular matrix remodeling and degradation and also in the regulation of certain signaling pathways. However, their exact role in carcinogenesis remains unclear. Because the majority of CRCs arise from AP, the aim of our studies was the investigation of sulfatase activity in adenomas and adenocarcinomas and verification of possible usefulness of sulfatase activity determination as an indicator of the presence and discrimination between adenomas and carcinomas.
Patient–methods
One hundred twenty individuals were enrolled in the study. We assayed serum sulfatase activity in 79 patients with colorectal neoplasms (38 CRC and 41 AP) and 41 controls. Enzyme activity was determined colorimetrically.
Results
We found statistically higher serum sulfatase activity in patients with colonic neoplasms than in controls (124; 112–139 vs. 79.5; 73–87 U). The activity was more elevated in adenomas (149; 128–173 U) than in cancers (103; 90–112 U). Sulfatase activity exceeded the cutoff value in 71% of AP and 47% of CRC patients. It increased with number of adenomas and tended to decrease with tumor progression.
Conclusions
Sulfatases seem to be involved in the early stages of colonic neoplastic transformation which is reflected in their serum activity. The likelihood of elevated sulfatase activity is almost ten times higher in subjects with than without polyps. Sulfatase upregulation in majority of adenomas and their correlation tendencies warrants reconsideration of sulfatase determination as a possible diagnostic tool.
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References
WGO/OMGE Position Statement. (2004) Colorectal cancer screening and surveillance. World Gastroenterology News 9(Supplement 1–4)
Winawer S, Fletcher R, Rex D, Bond J, Burt R, Ferrucci J, Ganiats T, Levin T, Woolf S, Johnson D, Kirk L, Litin S, Simmang C, U.S. Multisociety Task Force on Colorectal Cancer (2003) Colorectal cancer screening and surveillance: clinical guidelines and rationale—update based on new evidence. Gastroenterology 124:544–560
Diez-Roux G, Ballabio A (2005) Sulfatases and human disease. Annu Rev Genomics Hum Genet 6:355–379
Sanderson RD, Yang Y, Kelly T, MacLeod V, Dai Y, Theus A (2005) Enzymatic remodeling of heparan sulfate proteoglycans within the tumor microenvironment: growth regulation and the prospect of new cancer therapies. J Cell Biochem 96:897–905
Doucas H, Garcea G, Neal CP, Manson MM, Berry DP (2005) Changes in the Wnt signaling pathway in gastrointestinal cancers and their prognostic significance. Eur J Cancer 41:365–379
Katoh M (2005) WNT/PCP signaling pathway and human cancer (review). Oncol Rep 14:1583–1588
Yi Y-F, Huang Y-R (1998) Arylsulfatase, b-galactosidase and lysozyme in gastric cancer cells and its relationship to invasion. World J Gastroenterol 4:52–54
Liu D, Shriver Z, Venataraman G, Shabrawi YE, Sasisekharan R (2002) Tumor cell surface heparan sulfate as cryptic promoters or inhibitors of tumor growth and metastasis. PNAS 99:568–573
Wang S, Ai X, Freeman SD, Pownall ME, Lu Q, Kessler DS, Emerson CP (2004) Qsulf1, a heparan sulfate 6-0-endosulfatase, inhibits fibroblast growth factor signaling in mesoderm induction and angiogenesis. Proc Natl Acad Sci U S A 101:4833–4838
Lai J, Chien J, Staub J, Avula R, Greene EL, Matthews TA, Smith DI, Kaufmann SH, Roberts LR, Shridhar V (2003) Loss of Hsulf-1 up-regulates heparin-binding growth factor signaling in cancer. J Biol Chem 278:23107–23117
Green FL, Page DL, Fleming ID, Fritz A, Balch ChM, Haller DG, Morrow M (2002) AJCC Cancer Staging Manual, 6th edn. Springer, New York
Singh J, Tavella D, Di Ferrante N (1975) Measurements of arylsulfatases A and B in human serum. J Pediatr 86:574–576
Li J, Kleeff J, Abiatari I, Kayed H, Giese NA, Felix K, Giese T, Büchler MW, Friess H (2005) Enhanced levels of Hsulf-I interfere with heparin-binding growth factor signaling in pancreatic cancer. Mol Cancer 4:14. DOI 10.1186/1476-4598-4-14
Morimoto-Tomita M, Uchimura K, Werb Z, Hemmerich S, Rosen SD (2002) Cloning and characterization of two extracellular heparin-degrading endosulfatases in mice and humans. J Biol Chem 277:49175–49185
Laidler P, Kowalski D, Silberring J (1991) Arylsulfatase A in serum from patients with cancer of various organ. Clin Chim Acta 204:69–78
Kocak H, Oner–Iyidogan Y, Kocak T, Oner P (2004) Determination of diagnostic and prognostic values of urinary interleukin-8, tumor necrosis factor-α, and leukocyte arylsulfatase-A activity in patients with bladder cancer. Clin Biochem 37:673–678
Woźniak A, Drewa T, Rozwodowska M, Drewa G, Lambrecht W, Wisniewska I (2002) Activity of some lysosomal enzymes in serum and in tumors of patients with squamous cell lung carcinoma. Neoplasma 49:10–15
Turkmen S, Oner P, Cinarv F, Kocak H, Guvenen G, Altun H, Eryavuz Y (2001) Evaluation of leukocyte arylsulfatase-A activity in patients with breast cancer and benign breast disease. Cancer Lett 166:95–101
Morgan LR, Samuels MS, Thomas W, Krementz ET, Meeker W (1975) Arylsulfatase B in colorectal cancer. Cancer 36:2337–2345
Rozwodowska M, Drewa T, Wozniak A, Mila-Kierzenkowska C, Drewa L, Makarewicz R, Maciak R, Musialkiewicz D (2004) Changes in arylsulphatase activity in blood serum in patients with breast cancer before and after treatment. Pol Merkur Lekarski 17:252–254
Wagenaar-Miller RA, Hanley G, Brandt-Shattuck R, DuBois RN, Bell RL, Matrisian LM, Morgan DW (2003) Cooperative effects of matrix metalloproteinase and cyclooxygenase-2 inhibition on intestinal adenoma reduction. Br J Cancer 88:1445–52
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Matusiewicz, M., Krzystek-Korpacka, M., Diakowska, D. et al. Serum sulfatase activity is more elevated in colonic adenomas than cancers. Int J Colorectal Dis 23, 383–387 (2008). https://doi.org/10.1007/s00384-007-0434-4
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DOI: https://doi.org/10.1007/s00384-007-0434-4