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38. The RARS–MAD1L1 Fusion Gene Induces Cancer Stem Cell–like Properties and Therapeutic Resistance in Nasopharyngeal Carcinoma

Author

Zhong, Qian, Liu, Zhi-Hua, Lin, Zhi-Rui, Hu, Ze-Dong, Yuan, Li, Liu, Yan-min, Zhou, Ai-Jun, Xu, Li-Hua, Hu, Li-Juan, Wang, Zi-Feng, Guan, Xin-Yuan, Hao, Jia-Jie, Lui, Vivian WY, Guo, Ling, Mai, Hai-Qiang, Chen, Ming-Yuan, Han, Fei, Xia, Yun-Fei, Grandis, Jennifer R, Zhang, Xing, and Zeng, Mu-Sheng

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Dental/Oral and Craniofacial Disease, Stem Cell Research, Genetics, Cancer, Aetiology, 2.1 Biological and endogenous factors, Animals, Arginine-tRNA Ligase, Biomarkers, Tumor, Cell Cycle Proteins, Cell Line, Tumor, Disease Models, Animal, Drug Resistance, Neoplasm, Gene Knockdown Techniques, Gene Rearrangement, Humans, In Situ Hybridization, Fluorescence, Mice, Nasopharyngeal Carcinoma, Neoplastic Stem Cells, Nuclear Proteins, Oncogene Proteins, Fusion, Promoter Regions, Genetic, Protein Binding, Proto-Oncogene Proteins c-myc, Oncology & Carcinogenesis, Clinical sciences, Oncology and carcinogenesis
Abstract

Purpose: Nasopharyngeal carcinoma (NPC) is the most common head and neck cancer in Southeast Asia. Because local recurrence and distant metastasis are still the main causes of NPC treatment failure, it is urgent to identify new tumor markers and therapeutic targets for advanced NPC.Experimental Design: RNA sequencing (RNA-seq) was applied to look for interchromosome translocation in NPC. PCR, FISH, and immunoprecipitation were used to examine the fusion gene expression at RNA, DNA, and protein levels in NPC biopsies. MTT assay, colony formation assay, sphere formation assay, co-immunoprecipitation, chromatin immunoprecipitation assay, and in vivo chemoresistance assay were applied to explore the function of RARS-MAD1L1 in NPC.Results: We demonstrated that RARS-MAD1L1 was present in 10.03% (35/349) primary NPC biopsies and 10.7% (9/84) in head and neck cancer (HNC) samples. RARS-MAD1L1 overexpression increased cell proliferation, colony formation, and tumorigenicity in vitro, and the silencing of endogenous RARS-MAD1L1 reduced cancer cell growth and colony formation in vitro In addition, RARS-MAD1L1 increased the side population (SP) ratio and induced chemo- and radioresistance. Furthermore RARS-MAD1L1 interacted with AIMP2, which resulted in activation of FUBP1/c-Myc pathway. The silencing of FUBP1 or the administration of a c-Myc inhibitor abrogated the cancer stem cell (CSC)-like characteristics induced by RARS-MAD1L1. The expression of c-Myc and ABCG2 was higher in RARS-MAD1L1-positive HNC samples than in negative samples.Conclusions: Our findings indicate that RARS-MAD1L1 might contribute to tumorigenesis, CSC-like properties, and therapeutic resistance, at least in part, through the FUBP1/c-Myc axis, implying that RARS-MAD1L1 might serve as an attractive target for therapeutic intervention for NPC. Clin Cancer Res; 24(3); 659-73. ©2017 AACR.

Published
2018

42. Fat body‐derived juvenile hormone acid methyltransferase functions to maintain iron homeostasis in Drosophila melanogaster.

Author

Ye, Yun‐Yan, Liu, Zhi‐Hua, and Wang, Hui‐Li

Abstract

Iron homeostasis is of critical importance to living organisms. Drosophila melanogaster has emerged as an excellent model to study iron homeostasis, while the regulatory mechanism of iron metabolism remains poorly understood. Herein, we accidently found that knockdown of juvenile hormone (JH) acid methyltransferase (Jhamt) specifically in the fat body, a key rate‐limiting enzyme for JH synthesis, led to iron accumulation locally, resulting in serious loss and dysfunction of fat body. Jhamt knockdown‐induced phenotypes were mitigated by iron deprivation, antioxidant and Ferrostatin‐1, a well‐known inhibitor of ferroptosis, suggesting ferroptosis was involved in Jhamt knockdown‐induced defects in the fat body. Further study demonstrated that upregulation of Tsf1 and Malvolio (Mvl, homolog of mammalian DMT1), two iron importers, accounted for Jhamt knockdown‐induced iron accumulation and dysfunction of the fat body. Mechanistically, Kr‐h1, a key transcription factor of JH, acts downstream of Jhamt inhibiting Tsf1 and Mvl transcriptionally. In summary, the findings indicated that fat body‐derived Jhamt is required for the development of Drosophila by maintaining iron homeostasis in the fat body, providing unique insight into the regulatory mechanisms of iron metabolism in Drosophila. [ABSTRACT FROM AUTHOR]

Published
2024
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