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2. GREM1 is required to maintain cellular heterogeneity in pancreatic cancer

Author

Lan, Linxiang, Evan, Theodore, Li, Huafu, Hussain, Aasia, Ruiz, E. Josue, Zaw Thin, May, Ferreira, Rute M. M., Ps, Hari, Riising, Eva M., Zen, Yoh, Almagro, Jorge, Ng, Kevin W., Soro-Barrio, Pablo, Nelson, Jessica, Koifman, Gabriela, Carvalho, Joana, Nye, Emma L., He, Yulong, Zhang, Changhua, Sadanandam, Anguraj, and Behrens, Axel

Published
2022
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6. Supplementary Information and Figure Legends from YAP and β-Catenin Cooperate to Drive Oncogenesis in Basal Breast Cancer

Author

Quinn, Hazel M., primary, Vogel, Regina, primary, Popp, Oliver, primary, Mertins, Philipp, primary, Lan, Linxiang, primary, Messerschmidt, Clemens, primary, Landshammer, Alexandro, primary, Lisek, Kamil, primary, Château-Joubert, Sophie, primary, Marangoni, Elisabetta, primary, Koren, Elle, primary, Fuchs, Yaron, primary, and Birchmeier, Walter, primary

Published
2023
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7. Supplementary Figure 2 from YAP and β-Catenin Cooperate to Drive Oncogenesis in Basal Breast Cancer

Author

Quinn, Hazel M., primary, Vogel, Regina, primary, Popp, Oliver, primary, Mertins, Philipp, primary, Lan, Linxiang, primary, Messerschmidt, Clemens, primary, Landshammer, Alexandro, primary, Lisek, Kamil, primary, Château-Joubert, Sophie, primary, Marangoni, Elisabetta, primary, Koren, Elle, primary, Fuchs, Yaron, primary, and Birchmeier, Walter, primary

Published
2023
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10. Source File 1 from YAP and β-Catenin Cooperate to Drive Oncogenesis in Basal Breast Cancer

Author

Quinn, Hazel M., primary, Vogel, Regina, primary, Popp, Oliver, primary, Mertins, Philipp, primary, Lan, Linxiang, primary, Messerschmidt, Clemens, primary, Landshammer, Alexandro, primary, Lisek, Kamil, primary, Château-Joubert, Sophie, primary, Marangoni, Elisabetta, primary, Koren, Elle, primary, Fuchs, Yaron, primary, and Birchmeier, Walter, primary

Published
2023
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11. Supplementary Figure 4 from YAP and β-Catenin Cooperate to Drive Oncogenesis in Basal Breast Cancer

Author

Quinn, Hazel M., primary, Vogel, Regina, primary, Popp, Oliver, primary, Mertins, Philipp, primary, Lan, Linxiang, primary, Messerschmidt, Clemens, primary, Landshammer, Alexandro, primary, Lisek, Kamil, primary, Château-Joubert, Sophie, primary, Marangoni, Elisabetta, primary, Koren, Elle, primary, Fuchs, Yaron, primary, and Birchmeier, Walter, primary

Published
2023
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13. Supplementary Figure 6 from YAP and β-Catenin Cooperate to Drive Oncogenesis in Basal Breast Cancer

Author

Quinn, Hazel M., primary, Vogel, Regina, primary, Popp, Oliver, primary, Mertins, Philipp, primary, Lan, Linxiang, primary, Messerschmidt, Clemens, primary, Landshammer, Alexandro, primary, Lisek, Kamil, primary, Château-Joubert, Sophie, primary, Marangoni, Elisabetta, primary, Koren, Elle, primary, Fuchs, Yaron, primary, and Birchmeier, Walter, primary

Published
2023
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14. Supplementary Figure 7 from YAP and β-Catenin Cooperate to Drive Oncogenesis in Basal Breast Cancer

Author

Quinn, Hazel M., primary, Vogel, Regina, primary, Popp, Oliver, primary, Mertins, Philipp, primary, Lan, Linxiang, primary, Messerschmidt, Clemens, primary, Landshammer, Alexandro, primary, Lisek, Kamil, primary, Château-Joubert, Sophie, primary, Marangoni, Elisabetta, primary, Koren, Elle, primary, Fuchs, Yaron, primary, and Birchmeier, Walter, primary

Published
2023
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16. Supplementary Figure 5 from YAP and β-Catenin Cooperate to Drive Oncogenesis in Basal Breast Cancer

Author

Quinn, Hazel M., primary, Vogel, Regina, primary, Popp, Oliver, primary, Mertins, Philipp, primary, Lan, Linxiang, primary, Messerschmidt, Clemens, primary, Landshammer, Alexandro, primary, Lisek, Kamil, primary, Château-Joubert, Sophie, primary, Marangoni, Elisabetta, primary, Koren, Elle, primary, Fuchs, Yaron, primary, and Birchmeier, Walter, primary

Published
2023
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19. GREM1 is required to maintain cellular heterogeneity in pancreatic cancer

Author

Lan, Linxiang, Evan, Theodore, Li, Huafu, Hussain, Aasia, Ruiz, E. Josue, Zaw Thin, May, Ferreira, Rute M. M., Ps, Hari, Riising, Eva M., Zen, Yoh, Almagro, Jorge, Ng, Kevin W., Soro-Barrio, Pablo, Nelson, Jessica, Koifman, Gabriela, Carvalho, Joana, Nye, Emma L., He, Yulong, Zhang, Changhua, Sadanandam, Anguraj, and Behrens, Axel

Abstract

Pancreatic ductal adenocarcinoma (PDAC) shows pronounced epithelial and mesenchymal cancer cell populations1–4. Cellular heterogeneity in PDAC is an important feature in disease subtype specification3–5, but how distinct PDAC subpopulations interact, and the molecular mechanisms that underlie PDAC cell fate decisions, are incompletely understood. Here we identify the BMP inhibitor GREM16,7as a key regulator of cellular heterogeneity in pancreatic cancer in human and mouse. Grem1inactivation in established PDAC in mice resulted in a direct conversion of epithelial into mesenchymal PDAC cells within days, suggesting that persistent GREM1 activity is required to maintain the epithelial PDAC subpopulations. By contrast, Grem1overexpression caused an almost complete ‘epithelialization’ of highly mesenchymal PDAC, indicating that high GREM1 activity is sufficient to revert the mesenchymal fate of PDAC cells. Mechanistically, Grem1was highly expressed in mesenchymal PDAC cells and inhibited the expression of the epithelial–mesenchymal transition transcription factors Snai1(also known as Snail) and Snai2(also known as Slug) in the epithelial cell compartment, therefore restricting epithelial–mesenchymal plasticity. Thus, constant suppression of BMP activity is essential to maintain epithelial PDAC cells, indicating that the maintenance of the cellular heterogeneity of pancreatic cancer requires continuous paracrine signalling elicited by a single soluble factor.

Published
2024
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21. USP28 deletion and small-molecule inhibition destabilizes c-MYC and elicits regression of squamous cell lung carcinoma

Author

Ruiz, E Josue, primary, Pinto-Fernandez, Adan, additional, Turnbull, Andrew P, additional, Lan, Linxiang, additional, Charlton, Thomas M, additional, Scott, Hannah C, additional, Damianou, Andreas, additional, Vere, George, additional, Riising, Eva M, additional, Da Costa, Clive, additional, Krajewski, Wojciech W, additional, Guerin, David, additional, Kearns, Jeffrey D, additional, Ioannidis, Stephanos, additional, Katz, Marie, additional, McKinnon, Crystal, additional, O'Connell, Jonathan, additional, Moncaut, Natalia, additional, Rosewell, Ian, additional, Nye, Emma, additional, Jones, Neil, additional, Heride, Claire, additional, Gersch, Malte, additional, Wu, Min, additional, Dinsmore, Christopher J, additional, Hammonds, Tim R, additional, Kim, Sunkyu, additional, Komander, David, additional, Urbe, Sylvie, additional, Clague, Michael J, additional, Kessler, Benedikt M, additional, and Behrens, Axel, additional

Published
2021
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22. Author response: USP28 deletion and small-molecule inhibition destabilizes c-MYC and elicits regression of squamous cell lung carcinoma

Author

Ruiz, E Josue, primary, Pinto-Fernandez, Adan, additional, Turnbull, Andrew P, additional, Lan, Linxiang, additional, Charlton, Thomas M, additional, Scott, Hannah C, additional, Damianou, Andreas, additional, Vere, George, additional, Riising, Eva M, additional, Da Costa, Clive, additional, Krajewski, Wojciech W, additional, Guerin, David, additional, Kearns, Jeffrey D, additional, Ioannidis, Stephanos, additional, Katz, Marie, additional, McKinnon, Crystal, additional, O'Connell, Jonathan, additional, Moncaut, Natalia, additional, Rosewell, Ian, additional, Nye, Emma, additional, Jones, Neil, additional, Heride, Claire, additional, Gersch, Malte, additional, Wu, Min, additional, Dinsmore, Christopher J, additional, Hammonds, Tim R, additional, Kim, Sunkyu, additional, Komander, David, additional, Urbe, Sylvie, additional, Clague, Michael J, additional, Kessler, Benedikt M, additional, and Behrens, Axel, additional

Published
2021
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23. PARP1 Inhibitor Combined With Oxaliplatin Efficiently Suppresses Oxaliplatin Resistance in Gastric Cancer-Derived Organoids via Homologous Recombination and the Base Excision Repair Pathway

Author

Li, Huafu, primary, Wang, Chunming, additional, Lan, Linxiang, additional, Wu, Wenhui, additional, Evans, Ian, additional, Ruiz, E. Josue, additional, Yan, Leping, additional, Zhou, Zhijun, additional, Oliveira, Joaquim M., additional, Reis, Rui L., additional, Hu, Zhenran, additional, Chen, Wei, additional, Behrens, Axel, additional, He, Yulong, additional, and Zhang, Changhua, additional

Published
2021
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24. JunD, not c-Jun, is the AP-1 transcription factor required for Ras-induced lung cancer

Author

Ruiz, E. Josue, primary, Lan, Linxiang, additional, Diefenbacher, Markus Elmar, additional, Riising, Eva Madi, additional, Da Costa, Clive, additional, Chakraborty, Atanu, additional, Hoeck, Joerg D., additional, Spencer-Dene, Bradley, additional, Kelly, Gavin, additional, David, Jean-Pierre, additional, Nye, Emma, additional, Downward, Julian, additional, and Behrens, Axel, additional

Published
2021
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26. Oxaliplatin Compromised CDK1 Activity Sensitizes BRCA-Proficient Cancers to PARP Inhibition in Oxaliplatin Resistance Gastric Cancer

Author

Li, Huafu, primary, Wang, Chunming, additional, Lan, Linxiang, additional, Wu, Wenhui, additional, Evans, Ian, additional, Ruiz, E Josue, additional, Yan, Leping, additional, Zhang, Haiyong, additional, Zhou, Zhijun, additional, Hu, Zhenran, additional, Chen, Wei, additional, Behrens, Axel, additional, He, Yulong, additional, and Zhang, Changhua, additional

Published
2021
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28. YAP and β-Catenin Cooperate to Drive Oncogenesis in Basal Breast Cancer

Author

Quinn, Hazel M., primary, Vogel, Regina, additional, Popp, Oliver, additional, Mertins, Philipp, additional, Lan, Linxiang, additional, Messerschmidt, Clemens, additional, Landshammer, Alexandro, additional, Lisek, Kamil, additional, Château-Joubert, Sophie, additional, Marangoni, Elisabetta, additional, Koren, Elle, additional, Fuchs, Yaron, additional, and Birchmeier, Walter, additional

Published
2021
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29. High expression of vinculin predicts poor prognosis and distant metastasis and associates with influencing tumor-associated NK cell infiltration and epithelial-mesenchymal transition in gastric cancer

Author

Li, Huafu, primary, Wang, Chunming, additional, Lan, Linxiang, additional, Behrens, Axel, additional, Tomaschko, Mona, additional, Ruiz, Josue, additional, Su, Qiao, additional, Zhao, Guangying, additional, Yuan, Cheng, additional, Xiao, Xing, additional, Li, Bo, additional, Yan, Leping, additional, Wu, Wang, additional, Li, Wuguo, additional, Chen, Junzong, additional, He, Yulong, additional, and Zhang, Changhua, additional

Published
2021
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30. USP28 deletion and small molecule inhibition destabilises c-Myc and elicits regression of squamous cell lung carcinoma

Author

Ruiz, E. Josue, primary, Pinto-Fernandez, Adan, additional, Turnbull, Andrew P., additional, Lan, Linxiang, additional, Charlton, Thomas M., additional, Scott, Hannah Claire, additional, Damianou, Andreas, additional, Vere, George, additional, Riising, Eva M., additional, Da Costa, Clive, additional, Krajewski, Wojciech W., additional, Guerin, David, additional, Kearns, Jeffrey, additional, Ioannidis, Stephanos, additional, Katz, Marie, additional, McKinnon, Crystal, additional, O’Connell, Jonathan C., additional, Moncaut, Natalia, additional, Rosewell, Ian, additional, Nye, Emma, additional, Jones, Neil, additional, Heride, Claire, additional, Gersch, Malte, additional, Wu, Min, additional, Dinsmore, Christopher J., additional, Hammonds, Tim R., additional, Kim, Sunkyu, additional, Komander, David, additional, Urbé, Sylvie, additional, Clague, Michael J., additional, Kessler, Benedikt M., additional, and Behrens, Axel, additional

Published
2020
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35. Gab1 and Mapk Signaling Are Essential in the Hair Cycle and Hair Follicle Stem Cell Quiescence.

Author

80323004, Akilli Öztürk, Özlem, Pakula, Hubert, Chmielowiec, Jolanta, Qi, Jingjing, Stein, Simone, Lan, Linxiang, Sasaki, Yoshiteru, Rajewsky, Klaus, Birchmeier, Walter, 80323004, Akilli Öztürk, Özlem, Pakula, Hubert, Chmielowiec, Jolanta, Qi, Jingjing, Stein, Simone, Lan, Linxiang, Sasaki, Yoshiteru, Rajewsky, Klaus, and Birchmeier, Walter

Abstract

Gab1 is a scaffold protein that acts downstream of receptor tyrosine kinases. Here, we produced conditional Gab1 mutant mice (by K14- and Krox20-cre) and show that Gab1 mediates crucial signals in the control of both the hair cycle and the self-renewal of hair follicle stem cells. Remarkably, mutant hair follicles do not enter catagen, the destructive phase of the hair cycle. Instead, hair follicle stem cells lose quiescence and become exhausted, and thus no stem cell niches are established in the bulges. Moreover, conditional sustained activation of Mapk signaling by expression of a gain-of-function Mek1DD allele (by Krox20-cre) rescues hair cycle deficits and restores quiescence of the stem cells. Our data thus demonstrate an essential role of Gab1 downstream of receptor tyrosine kinases and upstream of Shp2 and Mapk in the regulation of the hair cycle and the self-renewal of hair follicle stem cells.

Published
2015

38. PARP1 inhibitor combined with oxaliplatin efficiently suppresses oxaliplatin resistance in gastric cancer-derived organoids via homologous recombination and the base excision repair pathway

Author

Li, Huafu, Wang, Chunming, Lan, Linxiang, Wu, Wenhui, Evans, Ian, Ruiz, E Josue, Yan, Leping, Zhou, Zhijun, Oliveira, Joaquim M, Reis, Rui L, Hu, Zhenran, Chen, Wei, Behrens, Axel, He, Yulong, and Zhang, Changhua

Subjects
Model organisms, integumentary system, Stem Cells, Genome Integrity & Repair, polycyclic compounds, bacteria, Gene Expression, biochemical phenomena, metabolism, and nutrition, Tumour Biology, Genetics & Genomics, 3. Good health
Abstract

Oxaliplatin (OXA) resistance in the treatment of different types of cancer is an important and complex problem. The culture of tumor organoids derived from gastric cancer can help us to provide a deeper understanding of the underlying mechanisms that lead to OXA resistance. In this study, our purpose was to understand the mechanisms that lead to OXA resistance, and to provide survival benefits to patients with OXA through targeted combination therapies. Using sequence analysis of OXA-resistant and non-OXA-resistant organoids, we found that PARP1 is an important gene that mediates OXA resistance. Through the patients' follow-up data, it was observed that the expression level of PARP1 was significantly correlated with OXA resistance. This was confirmed by genetic manipulation of PARP1 expression in OXA-resistant organoids used in subcutaneous tumor formation. Results further showed that PARP1 mediated OXA resistance by inhibiting the base excision repair pathway. OXA also inhibited homologous recombination by CDK1 activity and importantly made cancers with normal BRCA1 function sensitive to PARP inhibition. As a result, combination of OXA and Olaparib (PARP-1/2/3 inhibitor), inhibited in vivo and in vitro OXA resistant organoid growth and viability.

39. PARP1 inhibitor combined with oxaliplatin efficiently suppresses oxaliplatin resistance in gastric cancer-derived organoids via homologous recombination and the base excision repair pathway

Author

Li, Huafu, Wang, Chunming, Lan, Linxiang, Wu, Wenhui, Evans, Ian, Ruiz, E Josue, Yan, Leping, Zhou, Zhijun, Oliveira, Joaquim M, Reis, Rui L, Hu, Zhenran, Chen, Wei, Behrens, Axel, He, Yulong, and Zhang, Changhua

Subjects
Model organisms, integumentary system, Stem Cells, Genome Integrity & Repair, polycyclic compounds, bacteria, Gene Expression, biochemical phenomena, metabolism, and nutrition, Tumour Biology, Genetics & Genomics, 3. Good health
Abstract

Oxaliplatin (OXA) resistance in the treatment of different types of cancer is an important and complex problem. The culture of tumor organoids derived from gastric cancer can help us to provide a deeper understanding of the underlying mechanisms that lead to OXA resistance. In this study, our purpose was to understand the mechanisms that lead to OXA resistance, and to provide survival benefits to patients with OXA through targeted combination therapies. Using sequence analysis of OXA-resistant and non-OXA-resistant organoids, we found that PARP1 is an important gene that mediates OXA resistance. Through the patients' follow-up data, it was observed that the expression level of PARP1 was significantly correlated with OXA resistance. This was confirmed by genetic manipulation of PARP1 expression in OXA-resistant organoids used in subcutaneous tumor formation. Results further showed that PARP1 mediated OXA resistance by inhibiting the base excision repair pathway. OXA also inhibited homologous recombination by CDK1 activity and importantly made cancers with normal BRCA1 function sensitive to PARP inhibition. As a result, combination of OXA and Olaparib (PARP-1/2/3 inhibitor), inhibited in vivo and in vitro OXA resistant organoid growth and viability.

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