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175 results on '"Qin, Fujun"'

3. Molecular Imaging of Prostate Cancer Targeting CD46 Using ImmunoPET

Author

Wang, Sinan, Li, Jun, Hua, Jun, Su, Yang, Beckford-Vera, Denis R, Zhao, Walter, Jayaraman, Mayuri, Huynh, Tony L, Zhao, Ning, Wang, Yung-hua, Huang, Yangjie, Qin, Fujun, Shen, Sui, Gioeli, Daniel, Dreicer, Robert, Sriram, Renuka, Egusa, Emily A, Chou, Jonathan, Feng, Felix Y, Aggarwal, Rahul, Evans, Michael J, Seo, Youngho, Liu, Bin, Flavell, Robert R, and He, Jiang

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Oncology and Carcinogenesis, Prostate Cancer, Biotechnology, Urologic Diseases, Biomedical Imaging, Cancer, Adenocarcinoma, Animals, Apoptosis, Cell Proliferation, Humans, Immunoconjugates, Male, Membrane Cofactor Protein, Mice, Mice, Inbred NOD, Mice, Nude, Mice, SCID, Molecular Imaging, Neuroendocrine Tumors, Positron-Emission Tomography, Prostatic Neoplasms, Radiopharmaceuticals, Tissue Distribution, Tumor Cells, Cultured, Xenograft Model Antitumor Assays, Zirconium, Oncology & Carcinogenesis, Clinical sciences, Oncology and carcinogenesis
Abstract

PurposeWe recently identified CD46 as a novel therapeutic target in prostate cancer. In this study, we developed a CD46-targeted PET radiopharmaceutical, [89Zr]DFO-YS5, and evaluated its performance for immunoPET imaging in murine prostate cancer models.Experimental design[89Zr]DFO-YS5 was prepared and its in vitro binding affinity for CD46 was measured. ImmunoPET imaging was conducted in male athymic nu/nu mice bearing DU145 [AR-, CD46+, prostate-specific membrane antigen-negative (PSMA-)] or 22Rv1 (AR+, CD46+, PSMA+) tumors, and in NOD/SCID gamma mice bearing patient-derived adenocarcinoma xenograft, LTL-331, and neuroendocrine prostate cancers, LTL-331R and LTL-545.Results[89Zr]DFO-YS5 binds specifically to the CD46-positive human prostate cancer DU145 and 22Rv1 xenografts. In biodistribution studies, the tumor uptake of [89Zr]DFO-YS5 was 13.3 ± 3.9 and 11.2 ± 2.5 %ID/g, respectively, in DU145 and 22Rv1 xenografts, 4 days postinjection. Notably, [89Zr]DFO-YS5 demonstrated specific uptake in the PSMA- and AR-negative DU145 model. [89Zr]DFO-YS5 also showed uptake in the patient-derived LTL-331 and -331R models, with particularly high uptake in the LTL-545 neuroendocrine prostate cancer tumors (18.8 ± 5.3, 12.5 ± 1.8, and 32 ± 5.3 %ID/g in LTL-331, LTL-331R, and LTL-545, respectively, at 4 days postinjection).Conclusions[89Zr]DFO-YS5 is an excellent PET imaging agent across a panel of prostate cancer models, including in both adenocarcinoma and neuroendocrine prostate cancer, both cell line- and patient-derived xenografts, and both PSMA-positive and -negative tumors. It demonstrates potential for clinical translation as an imaging agent, theranostic platform, and companion biomarker in prostate cancer.

Published
2021

7. UBA1-CDK16: A Sex-Specific Chimeric RNA and Its Role in Immune Sexual Dimorphism

Author

Shi, Xinrui, primary, Facemire, Loryn, additional, Singh, Sandeep, additional, Kumar, Shailesh, additional, Cornelison, Robert, additional, Liang, Chen, additional, Qin, Fujun, additional, Liu, Aiqun, additional, Lin, Shitong, additional, Tang, Yue, additional, Elfman, Justin, additional, Manley, Thomas, additional, Bullock, Timothy, additional, Haverstick, Doris M., additional, Wu, Peng, additional, and Li, Hui, additional

Published
2024
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9. Relieving DYRK1A repression of MKL1 confers an adult-like phenotype to human infantile megakaryocytes

Author

Elagib, Kamaleldin E., Brock, Ashton, Clementelli, Cara M., Mosoyan, Goar, Delehanty, Lorrie L., Sahu, Ranjit K., Pacheco-Benichou, Alexandra, Fruit, Corinne, Besson, Thierry, Morris, Stephan W., Eto, Koji, Jobaliya, Chintan, French, Deborah L., Gadue, Paul, Singh, Sandeep, Shi, Xinrui, Qin, Fujun, Cornelison, Robert, Li, Hui, Iancu-Rubin, Camelia, and Goldfarb, Adam N.

Subjects
Bone marrow cells -- Analysis, Morphogenesis -- Health aspects, Hematopoietic stem cells -- Transplantation, Infants (Newborn) -- Health aspects, Thrombocytopenia -- Risk factors -- Prevention, Health care industry
Abstract

Infantile (fetal and neonatal) megakaryocytes (Mks) have a distinct phenotype consisting of hyperproliferation, limited morphogenesis, and low platelet production capacity. These properties contribute to clinical problems that include thrombocytopenia in neonates, delayed platelet engraftment in recipients of cord blood stem cell transplants, and inefficient ex vivo platelet production from pluripotent stem cell-derived Mks. The infantile phenotype results from deficiency of the actin-regulated coactivator, MKL1, which programs cytoskeletal changes driving morphogenesis. As a strategy to complement this molecular defect, we screened pathways with the potential to affect MKL1 function and found that DYRK1A inhibition dramatically enhanced Mk morphogenesis in vitro and in vivo. Dyrk1 inhibitors rescued enlargement, polyploidization, and thrombopoiesis in human neonatal Mks. Mks derived from induced pluripotent stem cells responded in a similar manner. Progenitors undergoing Dyrk1 inhibition demonstrated filamentous actin assembly, MKL1 nuclear translocation, and modulation of MKL1 target genes. Loss-of-function studies confirmed MKL1 involvement in this morphogenetic pathway. Expression of Ablim2, a stabilizer of filamentous actin, increased with Dyrk1 inhibition, and Ablim2 knockdown abrogated the actin, MKL1, and morphogenetic responses to Dyrk1 inhibition. These results delineate a pharmacologically tractable morphogenetic pathway whose manipulation may alleviate clinical problems associated with the limited thrombopoietic capacity of infantile Mks., Introduction Human megakaryocytes (Mks) undergo dramatic changes during ontogenic progression from fetal through adult stages. These changes include diminishing proliferation and a concomitant increase in adult-type morphogenesis (1-3). Adult-type morphogenesis [...]

Published
2022
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38. Molecular characterization of an MLL1 fusion and its role in chromosomal instability

Author

Parameswaran, Sreejit, primary, Vizeacoumar, Frederick S., additional, Kalyanasundaram Bhanumathy, Kalpana, additional, Qin, Fujun, additional, Islam, Md. Fahmid, additional, Toosi, Behzad M., additional, Cunningham, Chelsea E., additional, Mousseau, Darrell D., additional, Uppalapati, Maruti C., additional, Stirling, Peter C., additional, Wu, Yuliang, additional, Bonham, Keith, additional, Freywald, Andrew, additional, Li, Hui, additional, and Vizeacoumar, Franco J., additional

Published
2018
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42. Linc00210 drives Wnt/β-catenin signaling activation and liver tumor progression through CTNNBIP1-dependent manner

Author

Fu, Xiaomin, Zhu, Xiaoyan, Qin, Fujun, Zhang, Yong, Lin, Jizhen, Ding, Yuechao, Yang, Zihe, Shang, Yiman, Wang, Li, Zhang, Qinxian, and Gao, Quanli

Subjects
Wnt/β-catenin, DNA Copy Number Variations, Research, Liver TICs, Liver Neoplasms, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, CTNNBIP1, lcsh:RC254-282, Xenograft Model Antitumor Assays, Linc00210, Gene Expression Regulation, Neoplastic, Disease Models, Animal, Cell Line, Tumor, Copy number alterations, Neoplastic Stem Cells, Animals, Humans, RNA, Long Noncoding, Wnt Signaling Pathway, beta Catenin, Cell Proliferation, Protein Binding
Abstract

Background Liver tumor initiating cells (TICs) have self-renewal and differentiation properties, accounting for tumor initiation, metastasis and drug resistance. Long noncoding RNAs are involved in many physiological and pathological processes, including tumorigenesis. DNA copy number alterations (CNA) participate in tumor formation and progression, while the CNA of lncRNAs and their roles are largely unknown. Methods LncRNA CNA was determined by microarray analyses, realtime PCR and DNA FISH. Liver TICs were enriched by surface marker CD133 and oncosphere formation. TIC self-renewal was analyzed by oncosphere formation, tumor initiation and propagation. CRISPRi and ASO were used for lncRNA loss of function. RNA pulldown, western blot and double FISH were used to identify the interaction between lncRNA and CTNNBIP1. Results Using transcriptome microarray analysis, we identified a frequently amplified long noncoding RNA in liver cancer termed linc00210, which was highly expressed in liver cancer and liver TICs. Linc00210 copy number gain is associated with its high expression in liver cancer and liver TICs. Linc00210 promoted self-renewal and tumor initiating capacity of liver TICs through Wnt/β-catenin signaling. Linc00210 interacted with CTNNBIP1 and blocked its inhibitory role in Wnt/β-catenin activation. Linc00210 silencing cells showed enhanced interaction of β-catenin and CTNNBIP1, and impaired interaction of β-catenin and TCF/LEF components. We also confirmed linc00210 copy number gain using primary hepatocellular carcinoma (HCC) samples, and found the correlation between linc00210 CNA and Wnt/β-catenin activation. Of interest, linc00210, CTNNBIP1 and Wnt/β-catenin signaling targeting can efficiently inhibit tumor growth and progression, and liver TIC propagation. Conclusion With copy-number gain in liver TICs, linc00210 is highly expressed along with liver tumorigenesis. Linc00210 drives the self-renewal and propagation of liver TICs through activating Wnt/β-catenin signaling. Linc00210 interacts with CTNNBIP1 and blocks the combination between CTNNBIP1 and β-catenin, driving the activation of Wnt/β-catenin signaling. Linc00210-CTNNBIP1-Wnt/β-catenin axis can be targeted for liver TIC elimination.

Published
2017

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