Expression of prostasin and its inhibitors during colorectal cancer carcinogenesis

Publication: Research - peer-reviewJournal article – Annual report year: 2009

Standard

Expression of prostasin and its inhibitors during colorectal cancer carcinogenesis. / Selzer-Plon, J.; Bornholdt, J.; Friis, S.; Bisgaard, H. C.; Lothe, I. M. B.; Tveit, K. M.; Kure, E. H.; Vogel, Ulla Birgitte; Vogel, L. K.

In: B M C Cancer, Vol. 9, 2009, p. 201.

Publication: Research - peer-reviewJournal article – Annual report year: 2009

Harvard

Selzer-Plon, J, Bornholdt, J, Friis, S, Bisgaard, HC, Lothe, IMB, Tveit, KM, Kure, EH, Vogel, UB & Vogel, LK 2009, 'Expression of prostasin and its inhibitors during colorectal cancer carcinogenesis' B M C Cancer, vol 9, pp. 201., 10.1186/1471-2407-9-201

APA

Selzer-Plon, J., Bornholdt, J., Friis, S., Bisgaard, H. C., Lothe, I. M. B., Tveit, K. M., ... Vogel, L. K. (2009). Expression of prostasin and its inhibitors during colorectal cancer carcinogenesis. B M C Cancer, 9, 201. 10.1186/1471-2407-9-201

CBE

Selzer-Plon J, Bornholdt J, Friis S, Bisgaard HC, Lothe IMB, Tveit KM, Kure EH, Vogel UB, Vogel LK. 2009. Expression of prostasin and its inhibitors during colorectal cancer carcinogenesis. B M C Cancer. 9:201. Available from: 10.1186/1471-2407-9-201

MLA

Vancouver

Selzer-Plon J, Bornholdt J, Friis S, Bisgaard HC, Lothe IMB, Tveit KM et al. Expression of prostasin and its inhibitors during colorectal cancer carcinogenesis. B M C Cancer. 2009;9:201. Available from: 10.1186/1471-2407-9-201

Author

Selzer-Plon, J.; Bornholdt, J.; Friis, S.; Bisgaard, H. C.; Lothe, I. M. B.; Tveit, K. M.; Kure, E. H.; Vogel, Ulla Birgitte; Vogel, L. K. / Expression of prostasin and its inhibitors during colorectal cancer carcinogenesis.

In: B M C Cancer, Vol. 9, 2009, p. 201.

Publication: Research - peer-reviewJournal article – Annual report year: 2009

Bibtex

@article{16d7b7e4ba5a45eba85f9cdbb76647e3,
title = "Expression of prostasin and its inhibitors during colorectal cancer carcinogenesis",
publisher = "BioMed Central Ltd.",
author = "J. Selzer-Plon and J. Bornholdt and S. Friis and Bisgaard, {H. C.} and Lothe, {I. M. B.} and Tveit, {K. M.} and Kure, {E. H.} and Vogel, {Ulla Birgitte} and Vogel, {L. K.}",
year = "2009",
doi = "10.1186/1471-2407-9-201",
volume = "9",
pages = "201",
journal = "B M C Cancer",
issn = "1471-2407",

}

RIS

TY - JOUR

T1 - Expression of prostasin and its inhibitors during colorectal cancer carcinogenesis

A1 - Selzer-Plon,J.

A1 - Bornholdt,J.

A1 - Friis,S.

A1 - Bisgaard,H. C.

A1 - Lothe,I. M. B.

A1 - Tveit,K. M.

A1 - Kure,E. H.

A1 - Vogel,Ulla Birgitte

A1 - Vogel,L. K.

AU - Selzer-Plon,J.

AU - Bornholdt,J.

AU - Friis,S.

AU - Bisgaard,H. C.

AU - Lothe,I. M. B.

AU - Tveit,K. M.

AU - Kure,E. H.

AU - Vogel,Ulla Birgitte

AU - Vogel,L. K.

PB - BioMed Central Ltd.

PY - 2009

Y1 - 2009

N2 - Background: Clinical trials where cancer patients were treated with protease inhibitors have suggested that the serine protease, prostasin, may act as a tumour suppressor. Prostasin is proteolytically activated by the serine protease, matriptase, which has a very high oncogenic potential. Prostasin is inhibited by protease nexin-1 (PN-1) and the two isoforms encoded by the mRNA splice variants of hepatocyte growth factor activator inhibitor-1 (HAI-1), HAI-1A, and HAI-1B. Methods: Using quantitative RT-PCR, we have determined the mRNA levels for prostasin and PN-1 in colorectal cancer tissue (n = 116), severe dysplasia (n = 13), mild/moderate dysplasia (n = 93), and in normal tissue from the same individuals. In addition, corresponding tissues were examined from healthy volunteers (n = 23). A part of the cohort was further analysed for the mRNA levels of the two variants of HAI-1, here denoted HAI-1A and HAI-1B. mRNA levels were normalised to beta-actin. Immunohistochemical analysis of prostasin and HAI-1 was performed on normal and cancer tissue. Results: The mRNA level of prostasin was slightly but significantly decreased in both mild/moderate dysplasia (p <0.001) and severe dysplasia (p <0.01) and in carcinomas (p <0.05) compared to normal tissue from the same individual. The mRNA level of PN-1 was more that two-fold elevated in colorectal cancer tissue as compared to healthy individuals (p <0.001) and elevated in both mild/moderate dysplasia (p <0.01), severe dysplasia (p <0.05) and in colorectal cancer tissue (p <0.001) as compared to normal tissue from the same individual. The mRNA levels of HAI-1A and HAI-1B mRNAs showed the same patterns of expression. Immunohistochemistry showed that prostasin is located mainly on the apical plasma membrane in normal colorectal tissue. A large variation was found in the degree of polarization of prostasin in colorectal cancer tissue. Conclusion: These results show that the mRNA level of PN-1 is significantly elevated in colorectal cancer tissue. Future studies are required to clarify whether down-regulation of prostasin activity via up regulation of PN-1 is causing the malignant progression or if it is a consequence of it.

AB - Background: Clinical trials where cancer patients were treated with protease inhibitors have suggested that the serine protease, prostasin, may act as a tumour suppressor. Prostasin is proteolytically activated by the serine protease, matriptase, which has a very high oncogenic potential. Prostasin is inhibited by protease nexin-1 (PN-1) and the two isoforms encoded by the mRNA splice variants of hepatocyte growth factor activator inhibitor-1 (HAI-1), HAI-1A, and HAI-1B. Methods: Using quantitative RT-PCR, we have determined the mRNA levels for prostasin and PN-1 in colorectal cancer tissue (n = 116), severe dysplasia (n = 13), mild/moderate dysplasia (n = 93), and in normal tissue from the same individuals. In addition, corresponding tissues were examined from healthy volunteers (n = 23). A part of the cohort was further analysed for the mRNA levels of the two variants of HAI-1, here denoted HAI-1A and HAI-1B. mRNA levels were normalised to beta-actin. Immunohistochemical analysis of prostasin and HAI-1 was performed on normal and cancer tissue. Results: The mRNA level of prostasin was slightly but significantly decreased in both mild/moderate dysplasia (p <0.001) and severe dysplasia (p <0.01) and in carcinomas (p <0.05) compared to normal tissue from the same individual. The mRNA level of PN-1 was more that two-fold elevated in colorectal cancer tissue as compared to healthy individuals (p <0.001) and elevated in both mild/moderate dysplasia (p <0.01), severe dysplasia (p <0.05) and in colorectal cancer tissue (p <0.001) as compared to normal tissue from the same individual. The mRNA levels of HAI-1A and HAI-1B mRNAs showed the same patterns of expression. Immunohistochemistry showed that prostasin is located mainly on the apical plasma membrane in normal colorectal tissue. A large variation was found in the degree of polarization of prostasin in colorectal cancer tissue. Conclusion: These results show that the mRNA level of PN-1 is significantly elevated in colorectal cancer tissue. Future studies are required to clarify whether down-regulation of prostasin activity via up regulation of PN-1 is causing the malignant progression or if it is a consequence of it.

UR - http://www.biomedcentral.com/1471-2407/9/201

U2 - 10.1186/1471-2407-9-201

DO - 10.1186/1471-2407-9-201

JO - B M C Cancer

JF - B M C Cancer

SN - 1471-2407

VL - 9

SP - 201

ER -