Localization of mucin (MUC2 and MUC3) messenger RNA and peptide expression in human normal intestine and colon cancer

Chang, Sae-Kyung; Dohrman, Austin F.; Basbaum, Carol; Ho, Samuel B.; Tsuda, Tohru; Toribara, Neil W.; Gum, James R.; Kim, Young S.

doi:10.1016/0016-5085(94)90057-4

Cited by 263 publications

(189 citation statements)

References 19 publications

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“…MUC5/6 apomucin was frequently expressed in CC alone MUC2 apomucin is expressed in goblet cells of the small intestine and colon, 14 and, to a lesser degree, in the bron-(71%), and in CC with hepatolithiasis (71%), while it was significantly infrequent in CC of HC-CC (21%). In CC alone, chus.…”

Section: Apomucin Expression In Nonneoplastic Andmentioning

confidence: 98%

“…In this study, we examined to the biological behavior of carcinoma, are under evaluathe expression of MUC1, MUC2, MUC3, and MUC5/6 apotion. [10][11][12][13][14][15][16][17][18] Some carcinoma cells retain the cell-or tissue-spemucins in cholangiocarcinoma (CC) and biliary epithecific apomucin expression of their source, whereas others exlial dysplasia. We used 14 liver samples from patients press aberrant apomucin or lose the original pattern.…”

mentioning

confidence: 99%

“…[9][10][11][12][13][14][15][16][17][18] Changes in apomucin expression in carcinoma tisand their expression in malignant and premalignant lesues and their precursor lesions, as well as their relationship sions is under evaluation. In this study, we examined to the biological behavior of carcinoma, are under evaluathe expression of MUC1, MUC2, MUC3, and MUC5/6 apotion.…”

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confidence: 99%

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Characterization of apomucin expression in intrahepatic cholangiocarcinomas and their precursor lesions: An immunohistochemical study

1996

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of their genes suggest that they have unique roles and distriTo date, seven apomucins have been characterized bution. [9][10][11][12][13][14][15][16][17][18] Changes in apomucin expression in carcinoma tisand their expression in malignant and premalignant lesues and their precursor lesions, as well as their relationship sions is under evaluation. In this study, we examined to the biological behavior of carcinoma, are under evaluathe expression of MUC1, MUC2, MUC3, and MUC5/6 apotion. [10][11][12][13][14][15][16][17][18] Some carcinoma cells retain the cell-or tissue-spemucins in cholangiocarcinoma (CC) and biliary epithecific apomucin expression of their source, whereas others exlial dysplasia. We used 14 liver samples from patients press aberrant apomucin or lose the original pattern. 10 with hepatolithiasis and CC, 11 with hepatolithiasisThere are a few reports describing the expression of aposhowing biliary epithelial dysplasia, 31 with CC alone mucins in normal and pathological livers. [11][12][13] We showed that (19 hilar, 10 peripheral, and 2 unclassifiable), and 14 with MUC1 apomucin is frequently expressed both in the develcombined hepatocellular-cholangiocellular carcinoma oping intrahepatic bile ducts in fetal liver 13 and in cholangio-(HC-CC) and immunohistochemically characterized the carcinoma (CC) but is absent in the normal adult intrahepatic expression profiles of apomucins. Nondysplastic biliary biliary tree. 11,12 Therefore, we proposed that MUC1 apomucin epithelial cells in the intrahepatic large bile ducts conis an ''oncofetal'' antigen in the intrahepatic biliary tree. 13 stantly expressed MUC3 apomucin. MUC5/6 and MUC3CC occurs at any segment of the intrahepatic biliary tree, apomucin expression was widespread in dysplastic biliwhereas the cell origin and the precursor lesions remain ary epithelial cells in hepatolithiasis, although the latter largely uncharted. Biliary epithelial dysplasia is considered was reduced or absent in dysplastic foci. CC extensively to be a precursor lesion of CC as a complication of hepatolithiexpressed MUC1 apomucin and focally expressed MUC2 asis and primary sclerosing cholangitis. [19][20][21][22] However, little apomucin. In addition, CC of the hilar type, including is known about the distribution of apomucins other than those with hepatolithiasis, frequently expressed MUC3MUC1 in CC and their precursor lesions. Furthermore, it apomucin (68% and 57%, respectively), whereas those of remains unclear whether and to what degree the apomucin the peripheral type infrequently expressed MUC3 apoprofiles of biliary epithelial cells are retained in CC. mucin (10%) (P õ .01). MUC5/6 apomucin was more freIn this study, we immunohistochemically examined the exquently expressed in well-differentiated (89%), compression of MUC1, MUC2, MUC3, and MUC5/6 apomucins pared with poorly differentiated CC (42%) (P õ .01).in CC, combined hepatocellular-cholangiocellular carcinoma Cholangiocellular elements of combined HC-CC fre-(HC-CC), and biliary epithelial dysplasia in hepatolith...

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Section: Apomucin Expression In Nonneoplastic Andmentioning

confidence: 98%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Characterization of apomucin expression in intrahepatic cholangiocarcinomas and their precursor lesions: An immunohistochemical study

1996

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“…1 To date, eight apomucins (MUC 1-7 and MUC5B) have been identified 2-8 and the tissue-and cell-specific expression of these mucin genes is now emerging, suggesting that each has a distinct role. [9][10][11][12][13][14][15][16][17][18][19] …”

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confidence: 99%

Expression of apomucins in the intrahepatic biliary tree in hepatolithiasis differs from that in normal liver and extrahepatic biliary obstruction

1998

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Mucin plays an important role in the development of hepatoliths, which are formed within the intrahepatic large bile ducts. To date, eight apomucins, components of mucin, have been identified. The purpose of this study is to characterize the expression of MUC1, MUC2, MUC3, MUC5, and MUC6 apomucins at both the protein and messenger RNA (mRNA) levels in the intrahepatic large bile ducts and peribiliary glands in 36 livers from patients with hepatolithiasis, in 25 livers from the patients with extrahepatic biliary obstruction, and in 23 histologically-normal livers. MUC3 and MUC6 were constantly and focally expressed, respectively, in the biliary epithelial cells in the intrahepatic large bile ducts in normal livers, extrahepatic biliary obstruction, and, also, hepatolithiasis. In hepatolithiasis, MUC1, MUC2, and MUC5 apomucins were also focally expressed in 33%, 64%, and 89%, respectively, of the large intrahepatic bile ducts examined, whereas such expression was infrequent in normal livers and in extrahepatic biliary obstruction. The markedly proliferated intramural and extramural peribiliary glands in hepatolithiasis frequently expressed MUC3 and MUC6 apomucins and focally expressed MUC2 and MUC5 apomucins. All of the apomucins mRNA expression, except that of MUC1, resembled each protein expression. In conclusion, the characteristics of apomucins in the intrahepatic biliary tree in hepatolithiasis differs from those in normal livers and extrahepatic biliary obstructrion. Increased expression of gel-forming mucins, such as MUC5 and MUC2, could be involved in the formation and development of hepatolithiasis. (HEPATOLOGY 1998;27:46-53.)Epithelial mucins and their alterations are involved in the pathogenesis of neoplastic and non-neoplastic diseases. These mucins have in common a protein backbone which is generally called apomucin or mucin core protein. 1 To date, eight apomucins (MUC 1-7 and MUC5B) have been identified 2-8 and the tissue-and cell-specific expression of these mucin genes is now emerging, suggesting that each has a distinct role. [9][10][11][12][13][14][15][16][17][18][19]

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“…Our previous work has utilized HT29 cells to study the regulation and structure of a human gastrointestinal mucin gene, MUC2 (Velcich and Augenlicht, 1993;Velcich et al, 1997), which encodes the major form of intestinal mucins and is expressed predominantly in goblet cells (Chang et al, 1994;Gum et al, 1994;Gendler and Spicer, 1995). We have shown that in HT29 cells MUC2 gene expression can be induced (Velcich and Augenlicht, 1993), however, the cells do not acquire a fully di erentiated goblet phenotype, as they fail to polarize and secrete a mucus gel (Velcich et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

Altered phenotype of HT29 colonic adenocarcinoma cells following expression of the DCC gene

et al. 1999

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On 18q, frequently deleted in late stage colorectal cancers, a gene, Deleted in Colon Cancer (DCC), has been identi®ed and postulated to play a role as a tumor suppressor gene. DCC is retained in the majority of mucinous tumors, which produce high levels of mucins, and seems to be preferentially expressed in intestinal goblet cells. To investigate whether DCC is related to mucin expression and can modulate the transformed phenotype, we introduced a full-length DCC cDNA into HT29 cells, which can be induced in vitro to express MUC2, the gene that encodes the major colonic mucin. Expression of DCC did not modulate constitutive or induced expression of MUC2, nor did DCC induce a mature goblet cell phenotype. However, HT29 clones expressing high and low levels of DCC protein showed a signi®cant decrease in cell proliferation and tumorigenicity. Furthermore, increased shedding and an elevated rate of spontaneous apoptosis were associated with higher levels of expression of DCC. In summary, while restoration of DCC expression in a human colon carcinoma cell line did not in¯uence expression of di erentiation markers, DCC expression did a ect the growth and tumorigenic properties of the cells suggesting that DCC can modulate the malignant phenotype of colon cancer.

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Localization of mucin (MUC2 and MUC3) messenger RNA and peptide expression in human normal intestine and colon cancer

Cited by 263 publications

References 19 publications

Characterization of apomucin expression in intrahepatic cholangiocarcinomas and their precursor lesions: An immunohistochemical study

Characterization of apomucin expression in intrahepatic cholangiocarcinomas and their precursor lesions: An immunohistochemical study

Expression of apomucins in the intrahepatic biliary tree in hepatolithiasis differs from that in normal liver and extrahepatic biliary obstruction

Altered phenotype of HT29 colonic adenocarcinoma cells following expression of the DCC gene

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