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Your search keyword '"Chatterjee, Aditi"' showing total 15 results
Start Over Author "Chatterjee, Aditi" Journal cancer research
15 results on '"Chatterjee, Aditi"'

5. Abstract 4512: Doublecortin-like kinase 1 (DCLK1) correlates with Notch pathway signaling, controls metastatic characteristics in head and neck cancer

Author

Broner, Esther Channah, primary, Subbannayya, Tejaswini, additional, Advani, Jayshree, additional, Zhavoronkov, Alex, additional, Artemov, Artem, additional, Ozerov, Ivan, additional, Sloma, Ido, additional, Gowda, Harsha, additional, Sidransky, David, additional, Izumchenko, Eugene, additional, and Chatterjee, Aditi, additional

Published
2018
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8. Abstract 4891: GULP1, a potential tumor suppressor gene in ovarian tumors and its utility as a biomarker

Author

Maldonado, Leonel, primary, Brait, Mariana, additional, Begum, Shahnaz, additional, Chatterjee, Aditi, additional, Loyo, Myriam, additional, Barbosa, Alvaro, additional, Poeta, M Luana, additional, Fazio, Vito M., additional, Roberto, Angioli, additional, Tarquini, Elisabetta, additional, Criekinge, Wim Van, additional, Ongenaert, Mate, additional, Wisman, G Bea A, additional, de Graeff, Pauline, additional, Van der Zee, Ate, additional, Sidransky, David, additional, and Hoque, Mohammad O., additional

Published
2010
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9. Abstract 2703: Loss of dependence on EGFR signaling by upregulation of Mig6 confers drug resistance to erlotinib

Author

Chang, Xiaofei, primary, Chatterjee, Aditi, additional, Huang, Shyhmin, additional, Kim, Myoung Sook, additional, Shao, Chunbo, additional, Monitto, Constance L., additional, Ha, Patrick K., additional, Hidalgo, Manuel, additional, Harari, Paul M., additional, Berman, David M., additional, Bedi, Atul, additional, and Sidransky, David, additional

Published
2010
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12. Overexpression of Glycosylphosphatidylinositol (GPI) Transamidase Subunits Phosphatidylinositol Glycan Class T and/or GPI Anchor Attachment 1 Induces Tumorigenesis and Contributes to Invasion in Human Breast Cancer

Author

Wu, Guojun, primary, Guo, Zhongmin, additional, Chatterjee, Aditi, additional, Huang, Xin, additional, Rubin, Ethel, additional, Wu, Feng, additional, Mambo, Elizabeth, additional, Chang, Xiaofei, additional, Osada, Motonobu, additional, Sook Kim, Myoung, additional, Moon, Chulso, additional, Califano, Joseph A., additional, Ratovitski, Edward A., additional, Gollin, Susanne M., additional, Sukumar, Saraswati, additional, Sidransky, David, additional, and Trink, Barry, additional

Published
2006
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14. DeltaNp63alpha confers tumor cell resistance to cisplatin through the AKT1 transcriptional regulation.

Author

Sen T, Sen N, Brait M, Begum S, Chatterjee A, Hoque MO, Ratovitski E, and Sidransky D

Subjects
Carcinoma, Non-Small-Cell Lung drug therapy, Carcinoma, Non-Small-Cell Lung genetics, Carcinoma, Non-Small-Cell Lung metabolism, Carcinoma, Non-Small-Cell Lung pathology, Cell Line, Tumor, Cell Survival physiology, Drug Resistance, Neoplasm, Gene Expression Regulation, Neoplastic drug effects, Gene Knockdown Techniques, Head and Neck Neoplasms drug therapy, Head and Neck Neoplasms genetics, Head and Neck Neoplasms metabolism, Head and Neck Neoplasms pathology, Humans, Lung Neoplasms drug therapy, Lung Neoplasms genetics, Lung Neoplasms metabolism, Lung Neoplasms pathology, Neoplasms metabolism, Neoplasms pathology, Phosphorylation, Proto-Oncogene Proteins c-akt genetics, Trans-Activators genetics, Trans-Activators metabolism, Transcription Factors, Transcription, Genetic drug effects, Tumor Suppressor Proteins genetics, Tumor Suppressor Proteins metabolism, Antineoplastic Agents pharmacology, Cisplatin pharmacology, Neoplasms drug therapy, Neoplasms genetics, Proto-Oncogene Proteins c-akt biosynthesis, Trans-Activators biosynthesis, Tumor Suppressor Proteins biosynthesis
Abstract

Strategies to address resistance to platin drugs are greatly needed in human epithelial cancers (e.g., ovarian, head/neck, and lung) where platins are used widely and resistance occurs commonly. We found that upon ΔNp63α overexpression, AKT1 and phospho-AKT1 levels are upregulated in cancer cells. Investigations using gel-shift, chromatin immunoprecipitation and functional reporter assays implicated ΔNp63α in positive regulation of AKT1 transcription. Importantly, we found that ΔNp63α, AKT1, and phospho-AKT levels are greater in 2008CI3 CDDP-resistant ovarian cancer cells than in 2008 CDDP-sensitive cells. siRNA-mediated knockdown of ΔNp63α expression dramatically decreased AKT1 expression, whereas knockdown of either ΔNp63α or AKT1 decreased cell proliferation and increased death of ovarian and head/neck cancer cells. Conversely, enforced expression of ΔNp63α increased cancer cell proliferation and reduced apoptosis. Together, our findings define a novel ΔNp63α-dependent regulatory mechanism for AKT1 expression and its role in chemotherapeutic resistance of ovarian and head/neck cancer cells.

Published
2011
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15. Regulation of p53 family member isoform DeltaNp63alpha by the nuclear factor-kappaB targeting kinase IkappaB kinase beta.

Author

Chatterjee A, Chang X, Sen T, Ravi R, Bedi A, and Sidransky D

Subjects
Cell Death drug effects, Cell Death genetics, Cisplatin pharmacology, DNA Damage drug effects, DNA Damage genetics, Enzyme Activation drug effects, Enzyme Activation physiology, Gene Expression Regulation, Neoplastic drug effects, Humans, I-kappa B Kinase metabolism, NF-kappa B metabolism, Proteasome Endopeptidase Complex metabolism, Protein Binding drug effects, Protein Isoforms genetics, Protein Isoforms metabolism, Protein Processing, Post-Translational drug effects, Transcription Factors, Transcriptional Activation drug effects, Transcriptional Activation physiology, Tumor Cells, Cultured, Tumor Necrosis Factor-alpha pharmacology, Tumor Suppressor Protein p53 genetics, Tumor Suppressor Protein p53 metabolism, Ubiquitin metabolism, I-kappa B Kinase physiology, Trans-Activators genetics, Trans-Activators metabolism, Tumor Suppressor Proteins genetics, Tumor Suppressor Proteins metabolism
Abstract

The p53 family gene p63 plays an instrumental role in cellular stress responses including responses to DNA damage. In addition to encoding a full-length transcriptional activator, p63 also encodes several dominant inhibitory isoforms including the isoform DeltaNp63alpha, the function of which is not fully understood. DeltaNp63alpha is degraded in response to DNA damage, thereby enabling an effective cellular response to genotoxic agents. Here, we identify a key molecular mechanism underlying regulation of DeltaNp63alpha expression in response to chemotherapeutic agents or tumor necrosis factor-alpha. We found that DeltaNp63alpha interacts with IkappaB kinase (IKK), a multisubunit protein kinase that consists of two catalytic subunits, IKKalpha and IKKbeta, and a regulatory subunit, IKKgamma. The IKKbeta kinase promotes ubiquitin-mediated proteasomal degradation of DeltaNp63alpha, whereas a kinase-deficient mutant IKKbeta-K44A fails to do so. Cytokine- or chemotherapy-induced stimulation of IKKbeta caused degradation of DeltaNp63alpha and augmented transactivation of p53 family-induced genes involved in the cellular response to DNA damage. Conversely, IKKbeta inhibition attenuated cytokine- or chemotherapy-induced degradation of DeltaNp63alpha. Our findings show that IKKbeta plays an essential role in regulating DeltaNp63alpha in response to extrinsic stimuli. IKK activation represents one mechanism by which levels of DeltaNp63alpha can be reduced, thereby rendering cells susceptible to cell death in the face of cellular stress or DNA damage.

Published
2010
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