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4. CSNK2A1-mediated MAX phosphorylation upregulates HMGB1 and IL-6 expression in cholangiocarcinoma progression.

Author

Yang, Bing, Zhang, Jing, Wang, Jiaohong, Fan, Wei, Barbier-Torres, Lucía, Yang, Xi, Justo, Monica Anne R, Liu, Ting, Chen, Yongheng, Steggerda, Justin, Ramani, Komal, Lu, Shelly C, and Yang, Heping

Subjects
Bile Ducts, Intrahepatic, Animals, Humans, Mice, Cholangiocarcinoma, Bile Duct Neoplasms, Hyperplasia, Casein Kinase II, HMGB1 Protein, Interleukin-6, Phosphorylation, beta Catenin, Liver Cancer, Digestive Diseases, Chronic Liver Disease and Cirrhosis, Cancer, Digestive Diseases - (Gallbladder), Rare Diseases, Liver Disease, 2.1 Biological and endogenous factors, Aetiology
Abstract

BackgroundWe established a novel diethylnitrosamine (DEN) -induced mouse model that reflected the progression of cholangiocarcinoma (CCA) from atypical cystic hyperplasia.MethodsBALB/c mice were administered DEN by oral gavage. Cells isolated from livers were analyzed for expression of CSNK2A1, MAX and MAX-interacting proteins. Human CCA cell lines (MzChA-1, HuCCT1), normal human cholangiocyte (H69), human hepatic stellate cells (LX-2), macrophages (RAW 264.7), and primary hepatic cells were used for cellular and molecular biology assays.ResultsExpression of MAX, CSNK2A1, C-MYC, β-catenin, HMGB1, and IL-6 was upregulated in hepatic cells from CCA liver tissue. The half-life of MAX is higher in CCA cells, and this favors their proliferation. Overexpression of MAX increased growth, migration, and invasion of MzChA-1, whereas silencing of MAX had the opposite effect. MAX positively regulated IL-6 and HMGB1 through paracrine signaling in HepG2, LX2, and RAW cells and autocrine signaling in MzChA-1 cells. CSNK2A1-mediated MAX phosphorylation shifts MAX-MAX homodimer to C-MYC-MAX and β-catenin-MAX heterodimers and increases the HMGB1 and IL-6 promoter activities. Increase of MAX phosphorylation promotes cell proliferation, migration, invasion, and cholangiocarcinogenesis. The casein kinase 2 inhibitor CX-4945 induces cell cycle arrest and inhibits cell proliferation, migration, invasion, and carcinogenesis in MzChA-1 cells through the downregulation of CSNK2A1, MAX, and MAX-interaction proteins.ConclusionC-MYC-MAX and β-catenin-MAX binding to E-box site or β-catenin-MAX bound to TCFs/LEF1 enhanced HMGB1 or IL-6 promoter activities, respectively. IL-6 and HMGB1 secreted by hepatocytes, HSCs, and KCs exert paracrine effects on cholangiocytes to promote cell growth, migration, and invasion and lead to the progression of cholangiocarcinogenesis. CX-4945 provides perspectives on therapeutic strategies to attenuate progression from atypical cystic hyperplasia to cholangiocarcinogenesis.

Published
2023

18. SQUIRREL: Testing Database Management Systems with Language Validity and Coverage Feedback

Author

Zhong, Rui, Chen, Yongheng, Hu, Hong, Zhang, Hangfan, Lee, Wenke, and Wu, Dinghao

Subjects
Computer Science - Cryptography and Security
Abstract

Fuzzing is an increasingly popular technique for verifying software functionalities and finding security vulnerabilities. However, current mutation-based fuzzers cannot effectively test database management systems (DBMSs), which strictly check inputs for valid syntax and semantics. Generation-based testing can guarantee the syntax correctness of the inputs, but it does not utilize any feedback, like code coverage, to guide the path exploration. In this paper, we develop Squirrel, a novel fuzzing framework that considers both language validity and coverage feedback to test DBMSs. We design an intermediate representation (IR) to maintain SQL queries in a structural and informative manner. To generate syntactically correct queries, we perform type-based mutations on IR, including statement insertion, deletion and replacement. To mitigate semantic errors, we analyze each IR to identify the logical dependencies between arguments, and generate queries that satisfy these dependencies. We evaluated Squirrel on four popular DBMSs: SQLite, MySQL, PostgreSQL and MariaDB. Squirrel found 51 bugs in SQLite, 7 in MySQL and 5 in MariaDB. 52 of the bugs are fixed with 12 CVEs assigned. In our experiment, Squirrel achieves 2.4x-243.9x higher semantic correctness than state-of-the-art fuzzers, and explores 2.0x-10.9x more new edges than mutation-based tools. These results show that Squirrel is effective in finding memory errors of database management systems., Comment: In Proceedings of the 27th ACM Conference on Computer and Communications Security (CCS 2020)

Published
2020

21. Reciprocal Regulation Between Forkhead Box M1/NF‐κB and Methionine Adenosyltransferase 1A Drives Liver Cancer

Author

Li, Yuan, Lu, Liqing, Tu, Jian, Zhang, Jing, Xiong, Ting, Fan, Wei, Wang, Jiaohong, Li, Meng, Chen, Yibu, Steggerda, Justin, Peng, Hui, Chen, Yongheng, Li, Tony WH, Zhou, Zhi‐Gang, Mato, José M, Seki, Ekihiro, Liu, Ting, Yang, Heping, and Lu, Shelly C

Subjects
Chronic Liver Disease and Cirrhosis, Rare Diseases, Liver Disease, Cancer, Digestive Diseases, Liver Cancer, Genetics, Animals, Carcinogenesis, Cell Line, Tumor, Datasets as Topic, Feedback, Physiological, Forkhead Box Protein M1, Gene Expression Regulation, Neoplastic, Hepatocytes, Humans, Hydrocarbons, Fluorinated, Liver, Liver Neoplasms, Male, Methionine Adenosyltransferase, Mice, Mice, Knockout, NF-kappa B, Primary Cell Culture, Promoter Regions, Genetic, Pyridines, S-Adenosylmethionine, Sulfonamides, Thiophenes, Tumor Suppressor Proteins, Xenograft Model Antitumor Assays, Medical Biochemistry and Metabolomics, Clinical Sciences, Immunology, Gastroenterology & Hepatology
Abstract

Background and aimsForkhead box M1 (FOXM1) and nuclear factor kappa B (NF-ĸB) are oncogenic drivers in liver cancer that positively regulate each other. We showed that methionine adenosyltransferase 1A (MAT1A) is a tumor suppressor in the liver and inhibits NF-ĸB activity. Here, we examined the interplay between FOXM1/NF-κB and MAT1A in liver cancer.Approach and resultsWe examined gene and protein expression, effects on promoter activities and binding of proteins to promoter regions, as well as effects of FOXM1 inhibitors T0901317 (T0) and forkhead domain inhibitory-6 (FDI-6) in vitro and in xenograft and syngeneic models of liver cancer. We found, in both hepatocellular carcinoma and cholangiocarcinoma, that an induction in FOXM1 and NF-κB expression is accompanied by a fall in MATα1 (protein encoded by MAT1A). The Cancer Genome Atlas data set confirmed the inverse correlation between FOXM1 and MAT1A. Interestingly, FOXM1 directly interacts with MATα1 and they negatively regulate each other. In contrast, FOXM1 positively regulates p50 and p65 expression through MATα1, given that the effect is lost in its absence. FOXM1, MATα1, and NF-κB all bind to the FOX binding sites in the FOXM1 and MAT1A promoters. However, binding of FOXM1 and NF-κB repressed MAT1A promoter activity, but activated the FOXM1 promoter. In contrast, binding of MATα1 repressed the FOXM1 promoter. MATα1 also binds and represses the NF-κB element in the presence of p65 or p50. Inhibiting FOXM1 with either T0 or FDI-6 inhibited liver cancer cell growth in vitro and in vivo. However, inhibiting FOXM1 had minimal effects in liver cancer cells that do not express MAT1A.ConclusionsWe have found a crosstalk between FOXM1/NF-κB and MAT1A. Up-regulation in FOXM1 lowers MAT1A, but raises NF-κB, expression, and this is a feed-forward loop that enhances tumorigenesis.

Published
2020

33. Supplementary Figure 6 from Targeting the Epigenetic Reader ENL Inhibits Super-Enhancer–Driven Oncogenic Transcription and Synergizes with BET Inhibition to Suppress Tumor Progression

Author

Chen, Yongheng, primary, Ying, Ying, primary, Ma, Wenlong, primary, Ma, Hongchao, primary, Shi, Liang, primary, Gao, Xuefeng, primary, Jia, Min, primary, Li, Meiqi, primary, Song, Xiaoman, primary, Kong, Weixiao, primary, Chen, Wei, primary, Zheng, Xiangyi, primary, Muluh, Tobias Achu, primary, Wang, Xiaobin, primary, Wang, Maolin, primary, and Shu, Xing-sheng, primary

Published
2024
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34. Supplementary Figure 4 from Targeting the Epigenetic Reader ENL Inhibits Super-Enhancer–Driven Oncogenic Transcription and Synergizes with BET Inhibition to Suppress Tumor Progression

Author

Chen, Yongheng, primary, Ying, Ying, primary, Ma, Wenlong, primary, Ma, Hongchao, primary, Shi, Liang, primary, Gao, Xuefeng, primary, Jia, Min, primary, Li, Meiqi, primary, Song, Xiaoman, primary, Kong, Weixiao, primary, Chen, Wei, primary, Zheng, Xiangyi, primary, Muluh, Tobias Achu, primary, Wang, Xiaobin, primary, Wang, Maolin, primary, and Shu, Xing-sheng, primary

Published
2024
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35. Supplementary Figure 1 from Targeting the Epigenetic Reader ENL Inhibits Super-Enhancer–Driven Oncogenic Transcription and Synergizes with BET Inhibition to Suppress Tumor Progression

Author

Chen, Yongheng, primary, Ying, Ying, primary, Ma, Wenlong, primary, Ma, Hongchao, primary, Shi, Liang, primary, Gao, Xuefeng, primary, Jia, Min, primary, Li, Meiqi, primary, Song, Xiaoman, primary, Kong, Weixiao, primary, Chen, Wei, primary, Zheng, Xiangyi, primary, Muluh, Tobias Achu, primary, Wang, Xiaobin, primary, Wang, Maolin, primary, and Shu, Xing-sheng, primary

Published
2024
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36. Supplementary Figure 2 from Targeting the Epigenetic Reader ENL Inhibits Super-Enhancer–Driven Oncogenic Transcription and Synergizes with BET Inhibition to Suppress Tumor Progression

Author

Chen, Yongheng, primary, Ying, Ying, primary, Ma, Wenlong, primary, Ma, Hongchao, primary, Shi, Liang, primary, Gao, Xuefeng, primary, Jia, Min, primary, Li, Meiqi, primary, Song, Xiaoman, primary, Kong, Weixiao, primary, Chen, Wei, primary, Zheng, Xiangyi, primary, Muluh, Tobias Achu, primary, Wang, Xiaobin, primary, Wang, Maolin, primary, and Shu, Xing-sheng, primary

Published
2024
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37. Supplementary Figure 5 from Targeting the Epigenetic Reader ENL Inhibits Super-Enhancer–Driven Oncogenic Transcription and Synergizes with BET Inhibition to Suppress Tumor Progression

Author

Chen, Yongheng, primary, Ying, Ying, primary, Ma, Wenlong, primary, Ma, Hongchao, primary, Shi, Liang, primary, Gao, Xuefeng, primary, Jia, Min, primary, Li, Meiqi, primary, Song, Xiaoman, primary, Kong, Weixiao, primary, Chen, Wei, primary, Zheng, Xiangyi, primary, Muluh, Tobias Achu, primary, Wang, Xiaobin, primary, Wang, Maolin, primary, and Shu, Xing-sheng, primary

Published
2024
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38. Supplementary Figure 7 from Targeting the Epigenetic Reader ENL Inhibits Super-Enhancer–Driven Oncogenic Transcription and Synergizes with BET Inhibition to Suppress Tumor Progression

Author

Chen, Yongheng, primary, Ying, Ying, primary, Ma, Wenlong, primary, Ma, Hongchao, primary, Shi, Liang, primary, Gao, Xuefeng, primary, Jia, Min, primary, Li, Meiqi, primary, Song, Xiaoman, primary, Kong, Weixiao, primary, Chen, Wei, primary, Zheng, Xiangyi, primary, Muluh, Tobias Achu, primary, Wang, Xiaobin, primary, Wang, Maolin, primary, and Shu, Xing-sheng, primary

Published
2024
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39. Supplementary Table 5 from Targeting the Epigenetic Reader ENL Inhibits Super-Enhancer–Driven Oncogenic Transcription and Synergizes with BET Inhibition to Suppress Tumor Progression

Author

Chen, Yongheng, primary, Ying, Ying, primary, Ma, Wenlong, primary, Ma, Hongchao, primary, Shi, Liang, primary, Gao, Xuefeng, primary, Jia, Min, primary, Li, Meiqi, primary, Song, Xiaoman, primary, Kong, Weixiao, primary, Chen, Wei, primary, Zheng, Xiangyi, primary, Muluh, Tobias Achu, primary, Wang, Xiaobin, primary, Wang, Maolin, primary, and Shu, Xing-sheng, primary

Published
2024
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40. Supplementary Table 2 from Targeting the Epigenetic Reader ENL Inhibits Super-Enhancer–Driven Oncogenic Transcription and Synergizes with BET Inhibition to Suppress Tumor Progression

Author

Chen, Yongheng, primary, Ying, Ying, primary, Ma, Wenlong, primary, Ma, Hongchao, primary, Shi, Liang, primary, Gao, Xuefeng, primary, Jia, Min, primary, Li, Meiqi, primary, Song, Xiaoman, primary, Kong, Weixiao, primary, Chen, Wei, primary, Zheng, Xiangyi, primary, Muluh, Tobias Achu, primary, Wang, Xiaobin, primary, Wang, Maolin, primary, and Shu, Xing-sheng, primary

Published
2024
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41. Supplementary Table 1 from Targeting the Epigenetic Reader ENL Inhibits Super-Enhancer–Driven Oncogenic Transcription and Synergizes with BET Inhibition to Suppress Tumor Progression

Author

Chen, Yongheng, primary, Ying, Ying, primary, Ma, Wenlong, primary, Ma, Hongchao, primary, Shi, Liang, primary, Gao, Xuefeng, primary, Jia, Min, primary, Li, Meiqi, primary, Song, Xiaoman, primary, Kong, Weixiao, primary, Chen, Wei, primary, Zheng, Xiangyi, primary, Muluh, Tobias Achu, primary, Wang, Xiaobin, primary, Wang, Maolin, primary, and Shu, Xing-sheng, primary

Published
2024
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42. Supplementary Figure 3 from Targeting the Epigenetic Reader ENL Inhibits Super-Enhancer–Driven Oncogenic Transcription and Synergizes with BET Inhibition to Suppress Tumor Progression

Author

Chen, Yongheng, primary, Ying, Ying, primary, Ma, Wenlong, primary, Ma, Hongchao, primary, Shi, Liang, primary, Gao, Xuefeng, primary, Jia, Min, primary, Li, Meiqi, primary, Song, Xiaoman, primary, Kong, Weixiao, primary, Chen, Wei, primary, Zheng, Xiangyi, primary, Muluh, Tobias Achu, primary, Wang, Xiaobin, primary, Wang, Maolin, primary, and Shu, Xing-sheng, primary

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2024
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43. Supplementary Materials and Methods from Targeting the Epigenetic Reader ENL Inhibits Super-Enhancer–Driven Oncogenic Transcription and Synergizes with BET Inhibition to Suppress Tumor Progression

Author

Chen, Yongheng, primary, Ying, Ying, primary, Ma, Wenlong, primary, Ma, Hongchao, primary, Shi, Liang, primary, Gao, Xuefeng, primary, Jia, Min, primary, Li, Meiqi, primary, Song, Xiaoman, primary, Kong, Weixiao, primary, Chen, Wei, primary, Zheng, Xiangyi, primary, Muluh, Tobias Achu, primary, Wang, Xiaobin, primary, Wang, Maolin, primary, and Shu, Xing-sheng, primary

Published
2024
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44. Supplementary Figure 8 from Targeting the Epigenetic Reader ENL Inhibits Super-Enhancer–Driven Oncogenic Transcription and Synergizes with BET Inhibition to Suppress Tumor Progression

Author

Chen, Yongheng, primary, Ying, Ying, primary, Ma, Wenlong, primary, Ma, Hongchao, primary, Shi, Liang, primary, Gao, Xuefeng, primary, Jia, Min, primary, Li, Meiqi, primary, Song, Xiaoman, primary, Kong, Weixiao, primary, Chen, Wei, primary, Zheng, Xiangyi, primary, Muluh, Tobias Achu, primary, Wang, Xiaobin, primary, Wang, Maolin, primary, and Shu, Xing-sheng, primary

Published
2024
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45. Supplementary Table 4 from Targeting the Epigenetic Reader ENL Inhibits Super-Enhancer–Driven Oncogenic Transcription and Synergizes with BET Inhibition to Suppress Tumor Progression

Author

Chen, Yongheng, primary, Ying, Ying, primary, Ma, Wenlong, primary, Ma, Hongchao, primary, Shi, Liang, primary, Gao, Xuefeng, primary, Jia, Min, primary, Li, Meiqi, primary, Song, Xiaoman, primary, Kong, Weixiao, primary, Chen, Wei, primary, Zheng, Xiangyi, primary, Muluh, Tobias Achu, primary, Wang, Xiaobin, primary, Wang, Maolin, primary, and Shu, Xing-sheng, primary

Published
2024
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46. Supplementary Table 3 from Targeting the Epigenetic Reader ENL Inhibits Super-Enhancer–Driven Oncogenic Transcription and Synergizes with BET Inhibition to Suppress Tumor Progression

Author

Chen, Yongheng, primary, Ying, Ying, primary, Ma, Wenlong, primary, Ma, Hongchao, primary, Shi, Liang, primary, Gao, Xuefeng, primary, Jia, Min, primary, Li, Meiqi, primary, Song, Xiaoman, primary, Kong, Weixiao, primary, Chen, Wei, primary, Zheng, Xiangyi, primary, Muluh, Tobias Achu, primary, Wang, Xiaobin, primary, Wang, Maolin, primary, and Shu, Xing-sheng, primary

Published
2024
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47. Data from Targeting the Epigenetic Reader ENL Inhibits Super-Enhancer–Driven Oncogenic Transcription and Synergizes with BET Inhibition to Suppress Tumor Progression

Author

Chen, Yongheng, primary, Ying, Ying, primary, Ma, Wenlong, primary, Ma, Hongchao, primary, Shi, Liang, primary, Gao, Xuefeng, primary, Jia, Min, primary, Li, Meiqi, primary, Song, Xiaoman, primary, Kong, Weixiao, primary, Chen, Wei, primary, Zheng, Xiangyi, primary, Muluh, Tobias Achu, primary, Wang, Xiaobin, primary, Wang, Maolin, primary, and Shu, Xing-sheng, primary

Published
2024
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48. Structure-Based Optimization of Pyrazinamide-Containing Macrocyclic Derivatives as Fms-like Tyrosine Kinase 3 (FLT3) Inhibitors to Overcome Clinical Mutations

Author

Zheng, Xuan, primary, Chen, Zhiwen, additional, Guo, Ming, additional, Liang, Hong, additional, Song, Xiaojuan, additional, Liu, Yiling, additional, Liao, Zhenling, additional, Zhang, Yan, additional, Guo, Jing, additional, Zhou, Yang, additional, Zhang, Zhi-min, additional, Tu, Zhengchao, additional, Zhang, Ye, additional, Chen, Yongheng, additional, Zhang, Zhang, additional, and Lu, Xiaoyun, additional

Published
2024
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