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Your search keyword '"Krichevsky, Anna M."' showing total 28 results
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28 results on '"Krichevsky, Anna M."'

7. Supplementary Methods, Figure Legends 1-5 from miRNA-7 Attenuation in Schwannoma Tumors Stimulates Growth by Upregulating Three Oncogenic Signaling Pathways

Author

Saydam, Okay, primary, Senol, Ozlem, primary, Würdinger, Thomas, primary, Mizrak, Arda, primary, Ozdener, Gokhan Baris, primary, Stemmer-Rachamimov, Anat O., primary, Yi, Ming, primary, Stephens, Robert M., primary, Krichevsky, Anna M., primary, Saydam, Nurten, primary, Brenner, Gary J., primary, and Breakefield, Xandra O., primary

Published
2023
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12. Data from miRNA-7 Attenuation in Schwannoma Tumors Stimulates Growth by Upregulating Three Oncogenic Signaling Pathways

Author

Saydam, Okay, primary, Senol, Ozlem, primary, Würdinger, Thomas, primary, Mizrak, Arda, primary, Ozdener, Gokhan Baris, primary, Stemmer-Rachamimov, Anat O., primary, Yi, Ming, primary, Stephens, Robert M., primary, Krichevsky, Anna M., primary, Saydam, Nurten, primary, Brenner, Gary J., primary, and Breakefield, Xandra O., primary

Published
2023
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13. Supplementary Table 1 from miRNA-7 Attenuation in Schwannoma Tumors Stimulates Growth by Upregulating Three Oncogenic Signaling Pathways

Author

Saydam, Okay, primary, Senol, Ozlem, primary, Würdinger, Thomas, primary, Mizrak, Arda, primary, Ozdener, Gokhan Baris, primary, Stemmer-Rachamimov, Anat O., primary, Yi, Ming, primary, Stephens, Robert M., primary, Krichevsky, Anna M., primary, Saydam, Nurten, primary, Brenner, Gary J., primary, and Breakefield, Xandra O., primary

Published
2023
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16. Supplementary Figures 1-5 from miRNA-7 Attenuation in Schwannoma Tumors Stimulates Growth by Upregulating Three Oncogenic Signaling Pathways

Author

Saydam, Okay, primary, Senol, Ozlem, primary, Würdinger, Thomas, primary, Mizrak, Arda, primary, Ozdener, Gokhan Baris, primary, Stemmer-Rachamimov, Anat O., primary, Yi, Ming, primary, Stephens, Robert M., primary, Krichevsky, Anna M., primary, Saydam, Nurten, primary, Brenner, Gary J., primary, and Breakefield, Xandra O., primary

Published
2023
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17. Data from Human Glioma Growth Is Controlled by MicroRNA-10b

Author

Gabriely, Galina, primary, Yi, Ming, primary, Narayan, Ravi S., primary, Niers, Johanna M., primary, Wurdinger, Thomas, primary, Imitola, Jaime, primary, Ligon, Keith L., primary, Kesari, Santosh, primary, Esau, Christine, primary, Stephens, Robert M., primary, Tannous, Bakhos A., primary, and Krichevsky, Anna M., primary

Published
2023
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20. Small Molecule Inducers of Neuroprotective miR-132 Identified by HTS-HTS in Human iPSC-derived Neurons

Author

Nguyen, Lien D., primary, Wei, Zhiyun, additional, Silva, M. Catarina, additional, Barberán-Soler, Sergio, additional, Rabinovsky, Rosalia, additional, Muratore, Christina R., additional, Stricker, Jonathan M. S., additional, Hortman, Colin, additional, Young-Pearse, Tracy L., additional, Haggarty, Stephen J., additional, and Krichevsky, Anna M., additional

Published
2022
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21. Correction to: Tumor-Derived Cell Culture Model for the Investigation of Meningioma Biology

Author

Uhlmann, Erik J, primary, Rabinovsky, Rosalia, additional, Varma, Hemant, additional, El Fatimy, Rachid, additional, Kasper, Ekkehard M, additional, Moore, Justin M, additional, Vega, Rafael A, additional, Thomas, Ajith J, additional, Alterman, Ronald L, additional, Stippler, Martina, additional, Anderson, Matthew P, additional, Uhlmann, Erik N, additional, Kipper, Franciela C, additional, and Krichevsky, Anna M, additional

Published
2022
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22. Promoter and enhancer RNAs regulate chromatin reorganization and activation of miR-10b/HOXD locus, and neoplastic transformation in glioma

Author

Deforzh, Evgeny, primary, Uhlmann, Erik J., additional, Das, Eashita, additional, Galitsyna, Aleksandra, additional, Arora, Ramil, additional, Saravanan, Harini, additional, Rabinovsky, Rosalia, additional, Wirawan, Aditya D., additional, Teplyuk, Nadiya M., additional, El Fatimy, Rachid, additional, Perumalla, Sucika, additional, Jairam, Anirudh, additional, Wei, Zhiyun, additional, Mirny, Leonid, additional, and Krichevsky, Anna M., additional

Published
2022
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25. Tumor-Derived Cell Culture Model for the Investigation of Meningioma Biology

Author

Uhlmann, Erik J, primary, Rabinovsky, Rosalia, additional, Varma, Hemant, additional, El Fatimy, Rachid, additional, Kasper, Ekkehard M, additional, Moore, Justin M, additional, Vega, Rafael A, additional, Thomas, Ajith J, additional, Alterman, Ronald L, additional, Stippler, Martina, additional, Anderson, Matthew P, additional, Uhlmann, Erik N, additional, Kipper, Franciele C, additional, and Krichevsky, Anna M, additional

Published
2021
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26. Novel miRNA-inducing drugs enable differentiation of retinoic acid-resistant neuroblastoma cells.

Author

Nguyen LD, Sengupta S, Cho K, Floru A, George RE, and Krichevsky AM

Abstract

Tumor cell heterogeneity in neuroblastoma, a pediatric cancer arising from neural crest-derived progenitor cells, poses a significant clinical challenge. In particular, unlike adrenergic (ADRN) neuroblastoma cells, mesenchymal (MES) cells are resistant to chemotherapy and retinoid therapy and thereby significantly contribute to relapses and treatment failures. Previous research suggested that overexpression or activation of miR-124, a neurogenic microRNA with tumor suppressor activity, can induce the differentiation of retinoic acid-resistant neuroblastoma cells. Leveraging our established screen for miRNA-modulatory small molecules, we validated PP121, a dual inhibitor of tyrosine and phosphoinositide kinases, as a robust inducer of miR-124. A combination of PP121 and BDNF-activating bufalin synergistically arrests proliferation, induces differentiation, and maintains the differentiated state of MES SK-N-AS cells for 8 weeks. RNA-seq and deconvolution analyses revealed a collapse of the ADRN core regulatory circuitry (CRC) and the emergence of novel CRCs associated with chromaffin cells and Schwann cell precursors. Using a similar protocol, we differentiated and maintained MES neuroblastoma GI-ME-N and SH-EP cell lines, as well as glioblastoma LN-229 and U-251 cell lines, for over 16 weeks. In conclusion, our novel protocol suggests a promising treatment for therapy-resistant cancers of the nervous system. Moreover, these long-lived, differentiated cells provide valuable models for studying mechanisms underlying differentiation, maturation, and senescence.

Published
2024
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27. HOXDeRNA activates a cancerous transcription program and super-enhancers genome-wide.

Author

Deforzh E, Kharel P, Karelin A, Ivanov P, and Krichevsky AM

Abstract

Background: The origin and genesis of highly malignant and heterogenous glioblastoma brain tumors remain unknown. We previously identified an enhancer-associated long non-coding RNA, LINC01116 (named HOXDeRNA here), that is absent in the normal brain but is commonly expressed in malignant glioma. HOXDeRNA has a unique capacity to transform human astrocytes into glioma-like cells. This work aimed to investigate molecular events underlying the genome-wide function of this lncRNA in glial cell fate and transformation., Results: Using a combination of RNA-Seq, ChIRP-Seq, and ChIP-Seq, we now demonstrate that HOXDeRNA binds in trans to the promoters of genes encoding 44 glioma-specific transcription factors distributed throughout the genome and derepresses them by removing the Polycomb repressive complex 2 (PRC2). Among the activated transcription factors are the core neurodevelopmental regulators SOX2, OLIG2, POU3F2, and SALL2. This process requires an RNA quadruplex structure of HOXDeRNA that interacts with EZH2. Moreover, HOXDeRNA-induced astrocyte transformation is accompanied by the activation of multiple oncogenes such as EGFR, PDGFR, BRAF, and miR-21, and glioma-specific super-enhancers enriched for binding sites of glioma master transcription factors SOX2 and OLIG2., Conclusions: Our results demonstrate that HOXDeRNA overrides PRC2 repression of glioma core regulatory circuitry with RNA quadruplex structure. These findings help reconstruct the sequence of events underlying the process of astrocyte transformation and suggest a driving role for HOXDeRNA and a unifying RNA-dependent mechanism of gliomagenesis., Competing Interests: COMPETING FINANCIAL INTERESTS All other authors declare no competing financial interests.

Published
2023
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28. Secreted PGK1 and IGFBP2 contribute to the bystander effect of miR-10b gene editing in glioma.

Author

Zhang Y, Rabinovsky R, Wei Z, El Fatimy R, Deforzh E, Luan B, Peshkin L, Uhlmann EJ, and Krichevsky AM

Abstract

MicroRNA-10b (miR-10b) is an essential glioma driver and one of the top candidates for targeted therapies for glioblastoma and other cancers. This unique miRNA controls glioma cell cycle and viability via an array of established conventional and unconventional mechanisms. Previously reported CRISPR-Cas9-mediated miR-10b gene editing of glioma cells in vitro and established orthotopic glioblastoma in mouse models demonstrated the efficacy of this approach and its promise for therapy development. However, therapeutic gene editing in patients' brain tumors may be hampered, among other factors, by the imperfect delivery and distribution of targeting vectors. Here, we demonstrate that miR-10b gene editing in glioma cells triggers a potent bystander effect that leads to the selective cell death of the unedited glioma cells without affecting the normal neuroglial cells. The effect is mediated by the secreted miR-10b targets phosphoglycerate kinase 1 (PGK1) and insulin-like growth factor binding protein 2 (IGFBP2) that block cell-cycle progression and induce glioma cell death. These findings further support the feasibility of therapeutic miR-10b editing without the need to target every cell of the tumor., Competing Interests: The authors declare no competing interests., (© 2023 The Authors.)

Published
2023
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