Increased histidine decarboxylase (HDC) activity in human colorectal cancer: Results of a study on ten patients

García-Caballero, M.; Neugebauer, E.; Campos, Rafael Paschoal de; Castro, Ignacio Núñez de; Vara-Thorbeck, C

doi:10.1007/bf02142587

Cited by 42 publications

(33 citation statements)

References 7 publications

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“…Accumulated evidence points to a direct relationship between up-regulation of histidine decarboxylase activity and growth of several types of human tumors (3 -7). As regards colorectal cancer, Garcia-Caballero et al (8) have shown a significantly higher histidine decarboxylase activity in 10 tumor specimens than in the corresponding normal colon mucosa. More recently, Boér et al (40) have shown a strong immunoreactivity for histidine decarboxylase in both adenomatous polyps and colorectal cancer specimens.…”

Section: Discussionmentioning

confidence: 97%

“…Therefore, histidine decarboxylase can serve as a specific marker for biosynthesis of histamine. It has been shown that levels of mRNA encoding histidine decarboxylase, histidine decarboxylase protein expression, and enzymatic activity are significantly increased in both experimental and human tumors, such as melanoma (3,4), small cell lung carcinoma (5), breast carcinoma (6), endometrial cancer (7), and colorectal carcinoma (8). These data suggest that histamine may be directly involved in tumor development and progression.…”

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confidence: 99%

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The Role of Cyclooxygenase-2 in Mediating the Effects of Histamine on Cell Proliferation and Vascular Endothelial Growth Factor Production in Colorectal Cancer

Cianchi

Cortesini

Schiavone³

et al. 2005

Clinical Cancer Research

104

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Purpose: Activity of histidine decarboxylase, the key enzyme in the synthesis of histamine, has been shown to be increased in several types of human tumors.We attempted to establish whether the possible involvement of histidine decarboxylase and histamine in colorectal carcinogenesis might be mediated by the activation of the cyclooxygenase-2 (COX-2) pathway. Experimental Design: Expression/activity of histidine decarboxylase, histamine content, and prostaglandin E 2 (PGE 2 ) production were analyzed in 33 colorectal cancer samples and in the HT29, Caco-2, and HCT116 colon cancer cell lines. The effects of histamine, celecoxib, and H 1 , H 2 , and H 4 receptor antagonists on COX-2 expression/activity, cell proliferation, and vascular endothelial growth factor (VEGF) production were assessed in the three colon cancer lines that showed different constitutive COX-2 expression. Results: We showed the up-regulation of histidine decarboxylase protein expression and activity in the tumor specimens when compared with normal colonic mucosa. Histidine decarboxylase activity and histamine content were also significantly higher in metastatic tumors than in nonmetastatic ones.These variables significantly correlated with tumor PGE 2 production.The administration of histamine increased COX-2 expression/activity, cell proliferation, and VEGF production in the COX-2-positive HT29 and Caco-2 cells. Treatment with either H 2 /H 4 receptor antagonists or celecoxib prevented these effects. Histamine had no effect on both the COX-2 pathway andVEGF production in the COX-2-negative HCT116 cells. Conclusions: Our data showed that histamine exerts both a proproliferative and a proangiogenic effect via H 2 /H 4 receptor activation. These effects are likely to be mediated by increasing COX-2-related PGE 2 production in COX-2-expressing colon cancer cells.

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Section: Discussionmentioning

confidence: 97%

mentioning

confidence: 99%

The Role of Cyclooxygenase-2 in Mediating the Effects of Histamine on Cell Proliferation and Vascular Endothelial Growth Factor Production in Colorectal Cancer

Cianchi

Cortesini

Schiavone³

et al. 2005

Clinical Cancer Research

104

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“…There is a large body of experimental evidence indicating the existence of massive up-regulation of L-histidine decarboxylase (HDC) activity along with the increase of several tumors such as colon (2) and pancreatic carcinomas (3), gastric (4) and breast cancers (5), and melanoma (6,7). HDC is the only enzyme responsible for the biosynthesis of the allergic mediator, histamine (8).…”

Section: Introductionmentioning

confidence: 99%

Phenotypic Profiling of Engineered Mouse Melanomas with Manipulated Histamine Production Identifies Histamine H2 Receptor and Rho-C as Histamine-Regulated Melanoma Progression Markers

Pós

Sáfrány

Müller³

et al. 2005

Cancer Research

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In the present study, the impact of acquired neoplastic L-histidine decarboxylase (HDC) expression, and its direct consequence, the release of histamine in the tumor environment, was assessed on melanoma tumor progression. B16-F10 mouse melanoma cells were manipulated via stable transfection, and nine novel transgenic variants were generated in triplicates, constitutively expressing the full-length sense mouse HDC mRNA, a mock control, and an antisense HDC RNA segment, respectively. Establishing both primary skin tumors and lung metastases in C57BL/6 mice, the nine variants with different histamine-releasing capacities were subjected to a comprehensive comparative progression profiling in vivo. Our analyses showed trends of markedly accelerated tumor growth (P < 0.001), and moderately increased metastatic colony-forming potential (P = 0.010) along with rising levels of local histamine production. Using RNase protection assay for screening of the melanoma progression profile, and Western blotting for subsequent result validation, we looked for molecular progression markers affected by melanoma histamine secretion. Investigation of 21 functionally clustered markers associated with tumor proliferation, angiogenesis, invasivity, metastasis formation, local or systemic immunomodulation, and histamine signaling revealed positive correlations between histamine production, tumor histamine H2 receptor and rho-C expression (P < 0.001, P = 0.002, respectively). These observations confirm the involvement of histamine in the molecular machinery of melanoma progression. (Cancer Res 2005; 65(10): 4458-66)

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“…Expression of histidine decarboxylase (HDC), the key enzyme in the synthesis of histamine, has been shown to be increased in colorectal carcinoma [1] and other types of human tumors, suggesting that histamine may be directly involved in tumor development and progression. Histamine has been shown to stimulate the in vitro and in vivo growth of gastrointestinal cancer cells while treatment with cimetidine, an H 2 receptor antagonist, can reverse this effect [2].…”

Section: Introductionmentioning

confidence: 99%

Prostaglandin E2 correlates with histamine production in human colorectal cancer

et al. 2006

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Increased histidine decarboxylase (HDC) activity in human colorectal cancer: Results of a study on ten patients

Cited by 42 publications

References 7 publications

The Role of Cyclooxygenase-2 in Mediating the Effects of Histamine on Cell Proliferation and Vascular Endothelial Growth Factor Production in Colorectal Cancer

The Role of Cyclooxygenase-2 in Mediating the Effects of Histamine on Cell Proliferation and Vascular Endothelial Growth Factor Production in Colorectal Cancer

Phenotypic Profiling of Engineered Mouse Melanomas with Manipulated Histamine Production Identifies Histamine H2 Receptor and Rho-C as Histamine-Regulated Melanoma Progression Markers

Prostaglandin E2 correlates with histamine production in human colorectal cancer

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