An Antioxidant Response Phenotype Shared between Hereditary and Sporadic Type 2 Papillary Renal Cell Carcinoma

Aikseng Ooi; Jing Chii Wong; David Petillo; Douglas Roossien; Victoria Perrier-Trudova; Douglas Whitten; Bernice Wong Hui Min; Min Han Tan; Zhongfa Zhang; Ximing J. Yang; Ming Zhou; Betty Gardie; Vincent Molinié; Stéphane Richard; Puay Hoon Tan; Bin Tean Teh; Kyle A. Furge

doi:10.1016/j.ccr.2011.08.024

An Antioxidant Response Phenotype Shared between Hereditary and Sporadic Type 2 Papillary Renal Cell Carcinoma

Aikseng Ooi
, Jing Chii Wong
, David Petillo
, Douglas Roossien
, Victoria Perrier-Trudova
, Douglas Whitten
, Bernice Wong Hui Min
, Min Han Tan
, Zhongfa Zhang
, Ximing J. Yang
, Ming Zhou
, Betty Gardie
, Vincent Molinié
, Stéphane Richard
, Puay Hoon Tan
, Bin Tean Teh
, Kyle A. Furge

Research output: Contribution to journal › Article › peer-review

357 Scopus citations

Abstract

Fumarate hydratase (FH) mutation causes hereditary type 2 papillary renal cell carcinoma (PRCC2). The main effect of FH mutation is fumarate accumulation. The current paradigm posits that the main consequence of fumarate accumulation is HIF-α stabilization. Paradoxically, FH mutation differs from other HIF-α stabilizing mutations, such as VHL and SDH mutations, in its associated tumor types. We identified that fumarate can directly up-regulate antioxidant response element (ARE)-controlled genes. We demonstrated that aldo-keto reductase family 1 member B10 (AKR1B10) is an ARE-controlled gene and is up-regulated upon FH knockdown as well as in FH null cell lines. AKR1B10 overexpression is also a prominent feature in both hereditary and sporadic PRCC2. This phenotype better explains the similarities between hereditary and sporadic PRCC2.

Original language	English (US)
Pages (from-to)	511-523
Number of pages	13
Journal	Cancer Cell
Volume	20
Issue number	4
DOIs	https://doi.org/10.1016/j.ccr.2011.08.024
State	Published - Oct 18 2011
Externally published	Yes

ASJC Scopus subject areas

Oncology
Cancer Research

Access to Document

10.1016/j.ccr.2011.08.024

Cite this

Ooi, A., Wong, J. C., Petillo, D., Roossien, D., Perrier-Trudova, V., Whitten, D., Min, B. W. H., Tan, M. H., Zhang, Z., Yang, X. J., Zhou, M., Gardie, B., Molinié, V., Richard, S., Tan, P. H., Teh, B. T., & Furge, K. A. (2011). An Antioxidant Response Phenotype Shared between Hereditary and Sporadic Type 2 Papillary Renal Cell Carcinoma. Cancer Cell, 20(4), 511-523. https://doi.org/10.1016/j.ccr.2011.08.024

Ooi, A, Wong, JC, Petillo, D, Roossien, D, Perrier-Trudova, V, Whitten, D, Min, BWH, Tan, MH, Zhang, Z, Yang, XJ, Zhou, M, Gardie, B, Molinié, V, Richard, S, Tan, PH, Teh, BT & Furge, KA 2011, 'An Antioxidant Response Phenotype Shared between Hereditary and Sporadic Type 2 Papillary Renal Cell Carcinoma', Cancer Cell, vol. 20, no. 4, pp. 511-523. https://doi.org/10.1016/j.ccr.2011.08.024

@article{26356db72a9e4ed19266e4ace4d1b24f,

title = "An Antioxidant Response Phenotype Shared between Hereditary and Sporadic Type 2 Papillary Renal Cell Carcinoma",

abstract = "Fumarate hydratase (FH) mutation causes hereditary type 2 papillary renal cell carcinoma (PRCC2). The main effect of FH mutation is fumarate accumulation. The current paradigm posits that the main consequence of fumarate accumulation is HIF-α stabilization. Paradoxically, FH mutation differs from other HIF-α stabilizing mutations, such as VHL and SDH mutations, in its associated tumor types. We identified that fumarate can directly up-regulate antioxidant response element (ARE)-controlled genes. We demonstrated that aldo-keto reductase family 1 member B10 (AKR1B10) is an ARE-controlled gene and is up-regulated upon FH knockdown as well as in FH null cell lines. AKR1B10 overexpression is also a prominent feature in both hereditary and sporadic PRCC2. This phenotype better explains the similarities between hereditary and sporadic PRCC2.",

author = "Aikseng Ooi and Wong, \{Jing Chii\} and David Petillo and Douglas Roossien and Victoria Perrier-Trudova and Douglas Whitten and Min, \{Bernice Wong Hui\} and Tan, \{Min Han\} and Zhongfa Zhang and Yang, \{Ximing J.\} and Ming Zhou and Betty Gardie and Vincent Molini{\'e} and St{\'e}phane Richard and Tan, \{Puay Hoon\} and Teh, \{Bin Tean\} and Furge, \{Kyle A.\}",

note = "Funding Information: We thank Sabrina Noyes for administrative support and David Nadziejka for technical editing. We acknowledge the Van Andel Research Foundation, the Singapore Millennium Foundation, and Fondation IGR \& INCa (PNES Rein and Centre Expert National Cancers Rares PREDIR) for funding. A.O., K.F., and B.T. designed the study; A.O. performed all experiments, bioinformatics, and data analysis; J.C.W. and D.R. performed IHC staining; D.P. performed microarray experiments; D.W. performed tandem mass spectrometry; and X.J.Y. and M.Z. performed histological evaluation. B.T., Z.Z., M.Z., M.H.T., B.H.W., V.P.T., P.H.T., B.G., V.M., and S.R. provided samples and clinical data. A.O. and K.F. prepared the manuscript. Mass spectrometry and data analysis were performed in the Michigan State University, Proteomic Core Facility. ",

year = "2011",

month = oct,

day = "18",

doi = "10.1016/j.ccr.2011.08.024",

language = "English (US)",

volume = "20",

pages = "511--523",

journal = "Cancer Cell",

issn = "1535-6108",

publisher = "Cell Press",

number = "4",

}

TY - JOUR

T1 - An Antioxidant Response Phenotype Shared between Hereditary and Sporadic Type 2 Papillary Renal Cell Carcinoma

AU - Ooi, Aikseng

AU - Wong, Jing Chii

AU - Petillo, David

AU - Roossien, Douglas

AU - Perrier-Trudova, Victoria

AU - Whitten, Douglas

AU - Min, Bernice Wong Hui

AU - Tan, Min Han

AU - Zhang, Zhongfa

AU - Yang, Ximing J.

AU - Zhou, Ming

AU - Gardie, Betty

AU - Molinié, Vincent

AU - Richard, Stéphane

AU - Tan, Puay Hoon

AU - Teh, Bin Tean

AU - Furge, Kyle A.

N1 - Funding Information: We thank Sabrina Noyes for administrative support and David Nadziejka for technical editing. We acknowledge the Van Andel Research Foundation, the Singapore Millennium Foundation, and Fondation IGR & INCa (PNES Rein and Centre Expert National Cancers Rares PREDIR) for funding. A.O., K.F., and B.T. designed the study; A.O. performed all experiments, bioinformatics, and data analysis; J.C.W. and D.R. performed IHC staining; D.P. performed microarray experiments; D.W. performed tandem mass spectrometry; and X.J.Y. and M.Z. performed histological evaluation. B.T., Z.Z., M.Z., M.H.T., B.H.W., V.P.T., P.H.T., B.G., V.M., and S.R. provided samples and clinical data. A.O. and K.F. prepared the manuscript. Mass spectrometry and data analysis were performed in the Michigan State University, Proteomic Core Facility.

PY - 2011/10/18

Y1 - 2011/10/18

N2 - Fumarate hydratase (FH) mutation causes hereditary type 2 papillary renal cell carcinoma (PRCC2). The main effect of FH mutation is fumarate accumulation. The current paradigm posits that the main consequence of fumarate accumulation is HIF-α stabilization. Paradoxically, FH mutation differs from other HIF-α stabilizing mutations, such as VHL and SDH mutations, in its associated tumor types. We identified that fumarate can directly up-regulate antioxidant response element (ARE)-controlled genes. We demonstrated that aldo-keto reductase family 1 member B10 (AKR1B10) is an ARE-controlled gene and is up-regulated upon FH knockdown as well as in FH null cell lines. AKR1B10 overexpression is also a prominent feature in both hereditary and sporadic PRCC2. This phenotype better explains the similarities between hereditary and sporadic PRCC2.

AB - Fumarate hydratase (FH) mutation causes hereditary type 2 papillary renal cell carcinoma (PRCC2). The main effect of FH mutation is fumarate accumulation. The current paradigm posits that the main consequence of fumarate accumulation is HIF-α stabilization. Paradoxically, FH mutation differs from other HIF-α stabilizing mutations, such as VHL and SDH mutations, in its associated tumor types. We identified that fumarate can directly up-regulate antioxidant response element (ARE)-controlled genes. We demonstrated that aldo-keto reductase family 1 member B10 (AKR1B10) is an ARE-controlled gene and is up-regulated upon FH knockdown as well as in FH null cell lines. AKR1B10 overexpression is also a prominent feature in both hereditary and sporadic PRCC2. This phenotype better explains the similarities between hereditary and sporadic PRCC2.

UR - https://www.scopus.com/pages/publications/80054772589

UR - https://www.scopus.com/pages/publications/80054772589#tab=citedBy

U2 - 10.1016/j.ccr.2011.08.024

DO - 10.1016/j.ccr.2011.08.024

M3 - Article

C2 - 22014576

AN - SCOPUS:80054772589

SN - 1535-6108

VL - 20

SP - 511

EP - 523

JO - Cancer Cell

JF - Cancer Cell

IS - 4

ER -

An Antioxidant Response Phenotype Shared between Hereditary and Sporadic Type 2 Papillary Renal Cell Carcinoma

Abstract

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this