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2. CDKL3 is a targetable regulator of cell cycle progression in cancers

Author

Zhang, Haijiao, Lin, Jiahui, Zheng, Shaoqin, Ma, Lanjing, Pang, Zhongqiu, Yin, Hongyi, Meng, Chengcheng, Wang, Yinuo, Han, Qing, Zhang, Xi, Li, Zexu, Cao, Liu, Liu, Lijun, Fei, Teng, Gao, Daming, Yang, Liang, Peng, Xueqiang, Ding, Chen, Wang, Shixue, and Sheng, Ren

Subjects
Cell cycle -- Health aspects -- Genetic aspects, Tumor suppressor genes -- Health aspects, Phosphotransferases -- Health aspects, Enzyme inhibitors -- Testing
Abstract

Cell cycle regulation is largely abnormal in cancers. Molecular understanding and therapeutic targeting of the aberrant cell cycle are essential. Here, we identified that an underappreciated serine/threonine kinase, cyclin-dependent kinase-like 3 (CDKL3), crucially drives rapid cell cycle progression and cell growth in cancers. With regard to mechanism, CDKL3 localizes in the nucleus and associates with specific cyclin to directly phosphorylate retinoblastoma (Rb) for quiescence exit. In parallel, CDKL3 prevents the ubiquitin-proteasomal degradation of cyclin-dependent kinase 4 (CDK4) by direct phosphorylation on T172 to sustain [G.sub.1] phase advancement. The crucial function of CDKL3 in cancers was demonstrated both in vitro and in vivo. We also designed, synthesized, and characterized a first-in-class CDKL3-specific inhibitor, HZ1. HZ1 exhibits greater potency than CDK4/6 inhibitor in pan-cancer treatment by causing cell cycle arrest and overcomes acquired resistance to CDK4/6 inhibitor. In particular, CDKL3 has significant clinical relevance in colon cancer, and the effectiveness of HZ1 was demonstrated by murine and patient-derived cancer models. Collectively, this work presents an integrated paradigm of cancer cell cycle regulation and suggests CDKL3 targeting as a feasible approach in cancer treatment., Introduction The cell cycle consists of multiple modules and machineries to regulate cell division in a precise manner (1, 2). A complete cell cycle is composed of [G.sub.1], S, [G.sub.2], [...]

Published
2024
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16. Correction: Activation of RAS/MAPK pathway confers MCL-1 mediated acquired resistance to BCL-2 inhibitor venetoclax in acute myeloid leukemia

Author

Zhang, Qi, Riley-Gillis, Bridget, Han, Lina, Jia, Yannan, Lodi, Alessia, Zhang, Haijiao, Ganesan, Saravanan, Pan, Rongqing, Konoplev, Sergej N., Sweeney, Shannon R., Ryan, Jeremy A., Jitkova, Yulia, Dunner, Jr, Kenneth, Grosskurth, Shaun E., Vijay, Priyanka, Ghosh, Sujana, Lu, Charles, Ma, Wencai, Kurtz, Stephen, Ruvolo, Vivian R., Ma, Helen, Weng, Connie C., Ramage, Cassandra L., Baran, Natalia, Shi, Ce, Cai, Tianyu, Davis, Richard Eric, Battula, Venkata L., Mi, Yingchang, Wang, Jing, DiNardo, Courtney D., Andreeff, Michael, Tyner, Jeffery W., Schimmer, Aaron, Letai, Anthony, Padua, Rose Ann, Bueso-Ramos, Carlos E., Tiziani, Stefano, Leverson, Joel, Popovic, Relja, and Konopleva, Marina

Published
2022
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17. Activation of RAS/MAPK pathway confers MCL-1 mediated acquired resistance to BCL-2 inhibitor venetoclax in acute myeloid leukemia

Author

Zhang, Qi, Riley-Gillis, Bridget, Han, Lina, Jia, Yannan, Lodi, Alessia, Zhang, Haijiao, Ganesan, Saravanan, Pan, Rongqing, Konoplev, Sergej N., Sweeney, Shannon R., Ryan, Jeremy A., Jitkova, Yulia, Dunner, Jr, Kenneth, Grosskurth, Shaun E., Vijay, Priyanka, Ghosh, Sujana, Lu, Charles, Ma, Wencai, Kurtz, Stephen, Ruvolo, Vivian R., Ma, Helen, Weng, Connie C., Ramage, Cassandra L., Baran, Natalia, Shi, Ce, Cai, Tianyu, Davis, Richard Eric, Battula, Venkata L., Mi, Yingchang, Wang, Jing, DiNardo, Courtney D., Andreeff, Michael, Tyner, Jeffery W., Schimmer, Aaron, Letai, Anthony, Padua, Rose Ann, Bueso-Ramos, Carlos E., Tiziani, Stefano, Leverson, Joel, Popovic, Relja, and Konopleva, Marina

Published
2022
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31. Upregulation of HOXA3 by isoform‐specific Wilms tumour 1 drives chemotherapy resistance in acute myeloid leukaemia.

Author

Allen, Basil, Savoy, Lindsey, Ryabinin, Peter, Bottomly, Daniel, Chen, Reid, Goff, Bonnie, Wang, Anthony, McWeeney, Shannon K., and Zhang, Haijiao

Subjects
ACUTE myeloid leukemia, GENE expression, ALTERNATIVE RNA splicing, CANCER chemotherapy, BIOMARKERS
Abstract

Summary: Upregulation of the Wilms' tumour 1 (WT1) gene is common in acute myeloid leukaemia (AML) and is associated with poor prognosis. WT1 generates 12 primary transcripts through different translation initiation sites and alternative splicing. The short WT1 transcripts express abundantly in primary leukaemia samples. We observed that overexpression of short WT1 transcripts lacking exon 5 with and without the KTS motif (sWT1+/− and sWT1−/−) led to reduced cell growth. However, only sWT1+/− overexpression resulted in decreased CD71 expression, G1 arrest, and cytarabine resistance. Primary AML patient cells with low CD71 expression exhibit resistance to cytarabine, suggesting that CD71 may serve as a potential biomarker for chemotherapy. RNAseq differential expressed gene analysis identified two transcription factors, HOXA3 and GATA2, that are specifically upregulated in sWT1+/− cells, whereas CDKN1A is upregulated in sWT1−/− cells. Overexpression of either HOXA3 or GATA2 reproduced the effects of sWT1+/−, including decreased cell growth, G1 arrest, reduced CD71 expression and cytarabine resistance. HOXA3 expression correlates with chemotherapy response and overall survival in NPM1 mutation‐negative leukaemia specimens. Overexpression of HOXA3 leads to drug resistance against a broad spectrum of chemotherapeutic agents. Our results suggest that WT1 regulates cell proliferation and drug sensitivity in an isoform‐specific manner. [ABSTRACT FROM AUTHOR]

Published
2024
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40. Genomic landscape of neutrophilic leukemias of ambiguous diagnosis

Author

Zhang, Haijiao, Wilmot, Beth, Bottomly, Daniel, Dao, Kim-Hien T., Stevens, Emily, Eide, Christopher A., Khanna, Vishesh, Rofelty, Angela, Savage, Samantha, Reister Schultz, Anna, Long, Nicola, White, Libbey, Carlos, Amy, Henson, Rachel, Lin, Chenwei, Searles, Robert, Collins, Robert H., DeAngelo, Daniel J., Deininger, Michael W., Dunn, Tamara, Hein, Than, Luskin, Marlise R., Medeiros, Bruno C., Oh, Stephen T., Pollyea, Daniel A., Steensma, David P., Stone, Richard M., Druker, Brian J., McWeeney, Shannon K., Maxson, Julia E., Gotlib, Jason R., and Tyner, Jeffrey W.

Published
2019
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46. A 3 µm‐Ultrathin Hybrid Electrolyte Membrane with Integrative Architecture for All‐Solid‐State Lithium Metal Batteries.

Author

Liu, Kexin, Cheng, Hui, Wang, Zhuyi, Zhao, Yin, Lv, Yingying, Shi, Liyi, Cai, Xuesong, Cheng, Zhongling, Zhang, Haijiao, and Yuan, Shuai

Abstract

Ultrathin all‐solid‐state electrolytes with an excellent Li+ transport behavior are highly desirable for developing high‐energy‐density solid‐state lithium metal batteries. However, how to balance the electrochemical performance and their mechanical properties remains a huge challenge. Herein, an ultrathin solid electrolyte membrane with a thickness of only 3 µm and a weight of 11.7 g m−2 is well constructed by integrating individual functionalized organic with inorganic modules. Impressively, the optimized hybrid electrolyte membrane shows a set of merits including a high room‐temperature ionic conductivity of 1.77 × 10−4 S cm−1, large Li+ transference number of 0.65, and strong mechanical strength (strength of 29 MPa, elongation of 95%), as well as negligible thermal shrink at 180 °C. The analysis results reveal that the lithium sulfonate‐functionalized mesoporous silica nanoparticles in the membrane play a crucial role in the selective transport of Li+ through anion trapping and cation exchange. The pouch full cell is further assembled with a high‐voltage NCM cathode and thin lithium anode, which exhibits excellent long‐term cycling stability, outstanding rate performance at room temperature, and high safety against abused conditions. The current work provides an innovative strategy for achieving lithium metal batteries with ultrathin all‐solid‐state electrolytes. [ABSTRACT FROM AUTHOR]

Published
2024
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