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2. PTEN Is a Potent Suppressor of Small Cell Lung Cancer

Author

Cui, Min, Augert, Arnaud, Rongione, Michael, Conkrite, Karina, Parazzoli, Susan, Nikitin, Alexander Yu, Ingolia, Nicholas, and MacPherson, David

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Rare Diseases, Lung, Human Genome, Cancer, Genetics, Lung Cancer, Development of treatments and therapeutic interventions, 5.1 Pharmaceuticals, Animals, Disease Models, Animal, Female, Genes, Tumor Suppressor, Humans, Lung Neoplasms, Male, Mice, PTEN Phosphohydrolase, Small Cell Lung Carcinoma, Developmental Biology, Oncology & Carcinogenesis, Biochemistry and cell biology, Oncology and carcinogenesis
Abstract

UnlabelledSmall cell lung carcinoma (SCLC) is a highly metastatic tumor type with neuroendocrine features and a dismal prognosis. PTEN mutations and PIK3CA activating mutations have been reported in SCLC but the functional relevance of this pathway is unknown. The PTEN/PIK3CA pathway was interrogated using an AdenoCre-driven mouse model of SCLC harboring inactivated Rb and p53. Inactivation of one allele of PTEN in Rb/p53-deleted mice led to accelerated SCLC with frequent metastasis to the liver. In contrast with the high mutation burden reported in human SCLC, exome analyses revealed a low number of protein-altering mutations in mouse SCLC. Inactivation of both alleles of PTEN in the Rb/p53-deleted system led to nonmetastatic adenocarcinoma with neuroendocrine differentiation. This study reveals a critical role for the PTEN/PI3K pathway in both SCLC and lung adenocarcinoma and provides an ideal system to test the phosphoinositide 3-kinase (PI3K) pathway inhibitors as targeted therapy for subsets of patients with SCLC.ImplicationsThe ability of PTEN inactivation to accelerate SCLC in a genetic mouse model suggests that targeting the PTEN pathway is a therapeutic option for a subset of human patients with SCLC. VISUAL OVERVIEW: http://mcr.aacrjournals.org/content/early/2014/04/28/1541-7786.MCR-13-0554/F1.large.jpg. more...

Published
2014

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8. Figures S1-S16 from Crebbp Loss Drives Small Cell Lung Cancer and Increases Sensitivity to HDAC Inhibition

Author

Jia, Deshui, primary, Augert, Arnaud, primary, Kim, Dong-Wook, primary, Eastwood, Emily, primary, Wu, Nan, primary, Ibrahim, Ali H., primary, Kim, Kee-Beom, primary, Dunn, Colin T., primary, Pillai, Smitha P.S., primary, Gazdar, Adi F., primary, Bolouri, Hamid, primary, Park, Kwon-Sik, primary, and MacPherson, David, primary more...

Published
2023
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9. Tables S1-S5 from Crebbp Loss Drives Small Cell Lung Cancer and Increases Sensitivity to HDAC Inhibition

Author

Jia, Deshui, primary, Augert, Arnaud, primary, Kim, Dong-Wook, primary, Eastwood, Emily, primary, Wu, Nan, primary, Ibrahim, Ali H., primary, Kim, Kee-Beom, primary, Dunn, Colin T., primary, Pillai, Smitha P.S., primary, Gazdar, Adi F., primary, Bolouri, Hamid, primary, Park, Kwon-Sik, primary, and MacPherson, David, primary more...

Published
2023
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13. Supplementary Figures 1 - 4 from PTEN Is a Potent Suppressor of Small Cell Lung Cancer

Author

David MacPherson, Nicholas Ingolia, Alexander Yu. Nikitin, Susan Parazzoli, Karina Conkrite, Michael Rongione, Arnaud Augert, and Min Cui

Abstract

PDF file - 1172KB, S1. Neuroendocrine lung tumors in Rb/p53 AdCre model. S2. Neuroendocrine lung tumors in Rb/p53/Ptenlox/+AdCre model. S3. Analyses of Rb, p53 and Pten recombination in lung tumors. S4. Comparison of Rb/p53/Ptenlox/+ vs. Rb/p53/Ptenlox/lox lung tumors for expression of neuroendocrine and other lung cancer markers. more...

Published
2023
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27. Supplementary Table 1, Figures 1 - 8 from PLA2R1 Mediates Tumor Suppression by Activating JAK2

Author

David Bernard, Gérard Lambeau, Hélène Simonnet, Michael Gelb, Michael Perrais, Sébastien Aubert, Alain Puisieux, Xavier Leroy, Yvan de Launoit, Stéphanie Verbeke, Mylène Ferrand, Baptiste Gras, Benjamin Le Calvé, Clotilde Wiel, Helene Lallet-Daher, Delphine Gitenay, Christophe A. Girard, Arnaud Augert, and David Vindrieux more...

Abstract

PDF file - 326K, Supplementary Figure 1: The knockdown of PLA2R1 favors OIS escape. Supplementary Figure 2: The knockdown of PLA2R1 favors transformation. Supplementary Figure 3: The knockdown of PLA2R1 favors OIS escape in human normal keratinocytes. Supplementary Figure 4: DMBA/TPA treatment induces senescence and its escape correlates with papillomas formation. Supplementary Figure 5: Validation of H-Ras mutation in papilloma. Supplementary Figure 6: JAK2 is involved in PLA2R1-mediated cell growth regulation. Supplementary Figure 7: PLA2R1 regulates JAK2 activity. -Supplementary Figure 8: JAK2 mediates PLA2R1 tumor suppressive effects. more...

Published
2023
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30. Data from Potassium Channel KCNA1 Modulates Oncogene-Induced Senescence and Transformation

Author

David Bernard, David Vindrieux, Sébastien Aubert, David Carling, Stéphanie Verbeke, Benjamin Le Calvé, Arnaud Augert, Naveenan Navaratnam, Delphine Gitenay, Clotilde Wiel, and Hélène Lallet-Daher

Abstract

Oncogene-induced senescence (OIS) constitutes a failsafe program that restricts tumor development. However, the mechanisms that link oncogenesis to senescence are not completely understood. We carried out a loss-of-function genetic screen that identified the potassium channel KCNA1 as a determinant of OIS escape that can license tumor growth. Oncogenic stress triggers an increase in KCNA1 expression and its relocation from the cytoplasm to the membrane. Mechanistically, this relocation is due to a loss of protein kinase A (PKA)-induced phosphorylation at residue S446 of KCNA1. Accordingly, sustaining PKA activity or expressing a KCNA1 phosphomimetic mutant maintained KCNA1 in the cytoplasm and caused escape from OIS. KCNA1 relocation to the membrane induced a change in membrane potential that invariably resulted in cellular senescence. Restoring KCNA1 expression in transformation-competent cells triggered variation in membrane potential and blocked RAS-induced transformation, and PKA activation suppressed both effects. Furthermore, KCNA1 expression was reduced in human cancers, and this decrease correlated with an increase in breast cancer aggressiveness. Taken together, our results identify a novel pathway that restricts oncogenesis through a potassium channel-dependent senescence pathway. Cancer Res; 73(16); 5253–65. ©2013 AACR. more...

Published
2023
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39. Data from PLA2R1 Mediates Tumor Suppression by Activating JAK2

Author

Vindrieux, David, primary, Augert, Arnaud, primary, Girard, Christophe A., primary, Gitenay, Delphine, primary, Lallet-Daher, Helene, primary, Wiel, Clotilde, primary, Le Calvé, Benjamin, primary, Gras, Baptiste, primary, Ferrand, Mylène, primary, Verbeke, Stéphanie, primary, de Launoit, Yvan, primary, Leroy, Xavier, primary, Puisieux, Alain, primary, Aubert, Sébastien, primary, Perrais, Michael, primary, Gelb, Michael, primary, Simonnet, Hélène, primary, Lambeau, Gérard, primary, and Bernard, David, primary more...

Published
2023
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43. Supplementary Materials and Methods from Potassium Channel KCNA1 Modulates Oncogene-Induced Senescence and Transformation

Author

Lallet-Daher, Hélène, primary, Wiel, Clotilde, primary, Gitenay, Delphine, primary, Navaratnam, Naveenan, primary, Augert, Arnaud, primary, Le Calvé, Benjamin, primary, Verbeke, Stéphanie, primary, Carling, David, primary, Aubert, Sébastien, primary, Vindrieux, David, primary, and Bernard, David, primary more...

Published
2023
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45. Supplementary Table 1, Figures 1 - 8 from PLA2R1 Mediates Tumor Suppression by Activating JAK2

Author

Vindrieux, David, primary, Augert, Arnaud, primary, Girard, Christophe A., primary, Gitenay, Delphine, primary, Lallet-Daher, Helene, primary, Wiel, Clotilde, primary, Le Calvé, Benjamin, primary, Gras, Baptiste, primary, Ferrand, Mylène, primary, Verbeke, Stéphanie, primary, de Launoit, Yvan, primary, Leroy, Xavier, primary, Puisieux, Alain, primary, Aubert, Sébastien, primary, Perrais, Michael, primary, Gelb, Michael, primary, Simonnet, Hélène, primary, Lambeau, Gérard, primary, and Bernard, David, primary more...

Published
2023
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