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2. Supplementary Table 1 from FBXW7/hCDC4 Is a General Tumor Suppressor in Human Cancer

Author

Akhoondi, Shahab, primary, Sun, Dahui, primary, von der Lehr, Natalie, primary, Apostolidou, Sophia, primary, Klotz, Kathleen, primary, Maljukova, Alena, primary, Cepeda, Diana, primary, Fiegl, Heidi, primary, Dofou, Dimitra, primary, Marth, Christian, primary, Mueller-Holzner, Elisabeth, primary, Corcoran, Martin, primary, Dagnell, Markus, primary, Nejad, Sepideh Zabihi, primary, Nayer, Babak Noori, primary, Zali, Mohammad Reza, primary, Hansson, Johan, primary, Egyhazi, Susanne, primary, Petersson, Fredrik, primary, Sangfelt, Per, primary, Nordgren, Hans, primary, Grander, Dan, primary, Reed, Steven I., primary, Widschwendter, Martin, primary, Sangfelt, Olle, primary, and Spruck, Charles, primary

Published
2023
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4. Data from FBXW7/hCDC4 Is a General Tumor Suppressor in Human Cancer

Author

Akhoondi, Shahab, primary, Sun, Dahui, primary, von der Lehr, Natalie, primary, Apostolidou, Sophia, primary, Klotz, Kathleen, primary, Maljukova, Alena, primary, Cepeda, Diana, primary, Fiegl, Heidi, primary, Dofou, Dimitra, primary, Marth, Christian, primary, Mueller-Holzner, Elisabeth, primary, Corcoran, Martin, primary, Dagnell, Markus, primary, Nejad, Sepideh Zabihi, primary, Nayer, Babak Noori, primary, Zali, Mohammad Reza, primary, Hansson, Johan, primary, Egyhazi, Susanne, primary, Petersson, Fredrik, primary, Sangfelt, Per, primary, Nordgren, Hans, primary, Grander, Dan, primary, Reed, Steven I., primary, Widschwendter, Martin, primary, Sangfelt, Olle, primary, and Spruck, Charles, primary

Published
2023
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10. Interferon-γ-induced p27KIP1 binds to and targets MYC for proteasome-mediated degradation

Author

Bahram, Fuad, primary, Hydbring, Per, additional, Tronnersjö, Susanna, additional, Zakaria, Siti Mariam, additional, Frings, Oliver, additional, Fahlén, Sara, additional, Nilsson, Helén, additional, Goodwin, Jacob, additional, von der Lehr, Natalie, additional, Su, Yingtao, additional, Lüscher, Bernhard, additional, Castell, Alina, additional, and Larsson, Lars-Gunnar, additional

Published
2015
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11. FBXW7/hCDC4 is a general tumor suppressor in human cancer

Author

Akhoondi, Shahab, Sun, Dahui, von der Lehr, Natalie, Apostolidou, Sophia, Klotz, Kathleen, Maljukova, Alena, Cepeda, Diana, Fiegl, Heidi, Dofou, Dimitra, Marth, Christian, Mueller-Holzner, Elisabeth, Corcoran, Martin, Dagnell, Markus, Nejad, Sepideh Zabihi, Nayer, Babak Noori, Zali, Mohammad Reza, Hansson, Johan, Egyhazi, Susanne, Petersson, Fredrik, Sangfelt, Per, Nordgren, Hans, Grander, Dan, Reed, Steven I, Widschwendter, Martin, Sangfelt, Olle, Spruck, Charles, Akhoondi, Shahab, Sun, Dahui, von der Lehr, Natalie, Apostolidou, Sophia, Klotz, Kathleen, Maljukova, Alena, Cepeda, Diana, Fiegl, Heidi, Dofou, Dimitra, Marth, Christian, Mueller-Holzner, Elisabeth, Corcoran, Martin, Dagnell, Markus, Nejad, Sepideh Zabihi, Nayer, Babak Noori, Zali, Mohammad Reza, Hansson, Johan, Egyhazi, Susanne, Petersson, Fredrik, Sangfelt, Per, Nordgren, Hans, Grander, Dan, Reed, Steven I, Widschwendter, Martin, Sangfelt, Olle, and Spruck, Charles

Abstract

The ubiquitin-proteasome system is a major regulatory pathway of protein degradation and plays an important role in cellular division. Fbxw7 (or hCdc4), a member of the F-box family of proteins, which are substrate recognition components of the multisubunit ubiquitin ligase SCF (Skpl-Cdc53/ Cullin-F-box-protein), has been shown to mediate the ubiquitin-dependent proteolysis of several oncoproteins including cyclin El, c-Myc, c-Jun, and Notch. The oncogenic potential of Fbxw7 substrates, frequent allelic loss in human cancers, and demonstration that mutation of FBXW7 cooperates with p53 in mouse tumorigenesis have suggested that Fbxw7 could function as a tumor suppressor in human cancer. Here, we carry out an extensive genetic screen of primary tumors to evaluate the role of FBXW7 as a tumor suppressor in human tumorigenesis. Our results indicate that FBXW7 is inactivated by mutation in diverse human cancer types with an overall mutation frequency of ∼ 6%. The highest mutation frequencies were found in tumors of the bile duct (cholangio-carcinomas, 35%), blood (T-cell acute lymphocytic leukemia, 31%), endometrium (9%), colon (9%), and stomach (6%). Approximately 43% of all mutations occur at two mutational "hotspots," which alter Arg residues (Arg465 and Arg479) that are critical for substrate recognition. Furthermore, we show that Fbxw7Arg465 hotspot mutant can abrogate wild-type Fbxw7 function through a dominant negative mechanism. Our study is the first comprehensive screen of FBXW7 mutations in various human malignancies and shows that FBXW7 is a general tumor suppressor in human cancer.

Published
2007
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12. Phosphorylation by Cdk2 is required for Myc to repress Ras-induced senescence in cotransformation

Author

Hydbring, Per, primary, Bahram, Fuad, additional, Su, Yingtao, additional, Tronnersjö, Susanna, additional, Högstrand, Kari, additional, von der Lehr, Natalie, additional, Sharifi, Hamid Reza, additional, Lilischkis, Richard, additional, Hein, Nadine, additional, Wu, Siqin, additional, Vervoorts, Jörg, additional, Henriksson, Marie, additional, Grandien, Alf, additional, Lüscher, Bernhard, additional, and Larsson, Lars-Gunnar, additional

Published
2009
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13. FBXW7/hCDC4 Is a General Tumor Suppressor in Human Cancer

Author

Akhoondi, Shahab, primary, Sun, Dahui, additional, von der Lehr, Natalie, additional, Apostolidou, Sophia, additional, Klotz, Kathleen, additional, Maljukova, Alena, additional, Cepeda, Diana, additional, Fiegl, Heidi, additional, Dofou, Dimitra, additional, Marth, Christian, additional, Mueller-Holzner, Elisabeth, additional, Corcoran, Martin, additional, Dagnell, Markus, additional, Nejad, Sepideh Zabihi, additional, Nayer, Babak Noori, additional, Zali, Mohammad Reza, additional, Hansson, Johan, additional, Egyhazi, Susanne, additional, Petersson, Fredrik, additional, Sangfelt, Per, additional, Nordgren, Hans, additional, Grander, Dan, additional, Reed, Steven I., additional, Widschwendter, Martin, additional, Sangfelt, Olle, additional, and Spruck, Charles, additional

Published
2007
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16. Interferon-γ-induced p27KIP1 binds to and targets MYC for proteasome-mediated degradation.

Author

Bahram F, Hydbring P, Tronnersjö S, Zakaria SM, Frings O, Fahlén S, Nilsson H, Goodwin J, von der Lehr N, Su Y, Lüscher B, Castell A, and Larsson LG

Subjects
Animals, COS Cells, Cell Line, Tumor, Cell Nucleus metabolism, Cellular Senescence physiology, Chlorocebus aethiops, Cyclin-Dependent Kinase 2 metabolism, Gene Expression Regulation, Neoplastic, HeLa Cells, Humans, Phosphorylation, Protein Binding, Cyclin-Dependent Kinase Inhibitor p27 metabolism, Interferon-gamma metabolism, Proteasome Endopeptidase Complex metabolism, Proto-Oncogene Proteins c-myc metabolism
Abstract

The Myc oncoprotein is tightly regulated at multiple levels including ubiquitin-mediated protein turnover. We recently demonstrated that inhibition of Cdk2-mediated phosphorylation of Myc at Ser-62 pharmacologically or through interferon (IFN)-γ-induced expression of p27(Kip1) (p27) repressed Myc's activity to suppress cellular senescence and differentiation. In this study we identified an additional activity of p27 to interfere with Myc independent of Ser-62 phosphorylation. p27 is required and sufficient for IFN-γ-induced turnover of Myc. p27 interacted with Myc in the nucleus involving the C-termini of the two proteins, including Myc box 4 of Myc. The C-terminus but not the Cdk2 binding fragment of p27 was sufficient for inducing Myc degradation. Protein expression data of The Cancer Genome Atlas breast invasive carcinoma set revealed significantly lower Myc protein levels in tumors with highly expressed p27 lacking phosphorylation at Thr-157--a marker for active p27 localized in the nucleus. Further, these conditions correlated with favorable tumor stage and patient outcome. This novel regulation of Myc by IFN-γ/p27(KIP1) potentially offers new possibilities for therapeutic intervention in tumors with deregulated Myc.

Published
2016
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