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6. Dehydroabietylamine exerts antitumor effects by affecting nucleotide metabolism in gastric cancer.

Author

Ma, Jingsong, Zhao, Jiabao, Wu, Zhengxin, Tan, Jinshui, Xu, Meijuan, Ye, Wenjie, Zhong, Mengya, Xiong, Yubo, Pan, Guangchao, Zhou, Huiwen, Zhou, Shengyi, and Hong, Xuehui

Subjects
CELL metabolism, GENETIC transcription, NUCLEIC acids, TRANSGENIC mice, ANTINEOPLASTIC agents
Abstract

Nucleotide metabolism is the ultimate and most critical link in the self-replication process of tumors, including gastric cancer (GC). However, in clinical treatment, classic antitumor drugs such as 5-fluorouracil (5-FU) are mostly metabolic analogs of purines or pyrimidines, which lack specificity for tumor cells and therefore have significant side effects. It is unclear whether there are other drugs that can target nucleotide metabolism, except for nucleic acid analogs. Here, we found that a natural compound, dehydroabietylamine (DHAA), significantly reduced the viability and proliferation of GC cells and organoids. DHAA disrupts the purine and pyrimidine metabolism of GC cells, causing DNA damage and further inducing apoptosis. DHAA treatment decreased transcription and protein levels of key enzymes involved in the nucleotide metabolism pathway, with significant reductions in the expression of pyrimidine metabolism key enzymes CAD, DHODH, and purine metabolism key enzymes PAICS. We also found that DHAA directly binds to and reduces the expression of Forkhead box K2 (FOXK2), a common transcription factor for these metabolic enzymes. Ultimately, DHAA was shown to delay tumorigenesis in K19-Wnt1/C2mE transgenic mice model and reduce levels of CAD, DHODH, and PAICS in vivo. We demonstrate that DHAA exerts an anticancer effect on GC by targeting transcription factor FOXK2, reducing transcription of key genes for nucleotide metabolism and impairing nucleotide biosynthesis, thus DHAA is a promising candidate for GC therapy. [ABSTRACT FROM AUTHOR]

Published
2024
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15. High-Throughput Drug Screen for Potential Combinations With Venetoclax Guides the Treatment of Transformed Follicular Lymphoma.

Author

Li, Zhifeng, Pan, Guangchao, Zhong, Mengya, Zhang, Li, Yu, Xingxing, Zha, Jie, and Xu, Bing

Subjects
FOLLICULAR lymphoma, HIGH throughput screening (Drug development), CHEMICAL libraries, VENETOCLAX, CELL lines, FRACTIONS
Abstract

Transformed follicular lymphoma (t-FL) is an aggressive malignancy that is refractory and rapidly progressing with poor prognosis. There is currently no effective treatment. High-throughput screening (HTS) platforms are used to profile the sensitivity or toxicity of hundreds of drug molecules, and this approach is applied to identify potential effective treatments for t-FL. We randomly selected a compound panel from the School of Pharmaceutical Sciences Xiamen University, tested the effects of the panel on the activity of t-FL cell lines using HTS and the CCK-8 assay, and identified compounds showing synergistic anti-proliferative activity with the Bcl-2 inhibitor venetoclax (ABT-199). Bioinformatics tools were used to analyze the potential synergistic mechanisms. The single-concentration compound library demonstrated varying degrees of activity across the t-FL cell lines evaluated, of which the Karpas422 cells were the most sensitive, but it was the cell line with the least synergy with ABT-199. We computationally identified 30 drugs with synergistic effects in all cell lines. Molecularly, we found that the targets of these 30 drugs didn't directly regulate Bcl-2 and identified 13 medications with high evidence value above.9 of coordination with ABT-199, further confirming TP53 may play the largest role in the synergistic effect. Collectively, these findings identified the combined regimens of ABT-199 and further suggested that the mechanism is far from directly targeting Bcl-2, but rather through the regulation and synergistic action of p53 and Bcl-2. This study intended to reveal the best synergistic scheme of ABT-199 through HTS to more quickly inform the treatment of t-FL. [ABSTRACT FROM AUTHOR]

Published
2023
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16. MSI2 deficiency in ILC3s attenuates DSS-induced colitis by affecting the intestinal microbiota

Author

Li, Nengneng, primary, Xu, Shiquan, additional, Zhang, Shuaishuai, additional, Zhu, Qiang, additional, Meng, Xiaole, additional, An, Wenbin, additional, Fu, Baoqing, additional, Zhong, Mengya, additional, Yang, Yan, additional, Lin, Zeyang, additional, Liu, Xueni, additional, Xia, Junjie, additional, Wang, Jie, additional, You, Tingting, additional, Yan, Changxiu, additional, Tang, Huamei, additional, Zhuang, Guohong, additional, and Peng, Zhihai, additional

Published
2023
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17. Preclinical Studies of Chiauranib Show It Inhibits Transformed Follicular Lymphoma through the VEGFR2/ERK/STAT3 Signaling Pathway

Author

Tang, Yuanfang, primary, Zhong, Mengya, additional, Pan, Guangchao, additional, Tan, Jinshui, additional, Xie, Chendi, additional, Jiang, Yuelong, additional, Yao, Jingwei, additional, Shan, Weihang, additional, Lin, Jiaqi, additional, Huang, Jiewen, additional, Liu, Yating, additional, Li, Zhifeng, additional, Xu, Bing, additional, and Zha, Jie, additional

Published
2022
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18. Orelabrutinib and venetoclax synergistically induce cell death in double-hit lymphoma by interfering with the crosstalk between the PI3K/AKT and p38/MAPK signaling

Author

Pan, Guangchao, primary, Zhong, Mengya, additional, Yao, Jingwei, additional, Tan, Jinshui, additional, Zheng, Huijian, additional, Jiang, Yuelong, additional, Tang, Yuanfang, additional, Zhou, Hui, additional, Qin, Dongmei, additional, Yu, Xingxing, additional, Liu, Long, additional, Li, Zhifeng, additional, Lin, Zhijuan, additional, Jiang, Yirong, additional, Xu, Bing, additional, and Zha, Jie, additional

Published
2022
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19. Supplemental Material - High-Throughput Drug Screen for Potential Combinations With Venetoclax Guides the Treatment of Transformed Follicular Lymphoma

Author

Li, Zhifeng, Pan, Guangchao, Zhong, Mengya, Zhang, Li, Yu, Xingxing, Zha, Jie, and Xu, Bing

Subjects
FOS: Clinical medicine, 111599 Pharmacology and Pharmaceutical Sciences not elsewhere classified
Abstract

Supplemental Material for High-Throughput Drug Screen for Potential Combinations With Venetoclax Guides the Treatment of Transformed Follicular Lymphoma by Zhifeng Li, Guangchao Pan, Mengya Zhong, Li Zhang, Xingxing Yu, Jie Zha, and Bing Xu in International Journal of Toxicology.

Published
2023
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20. Novel Therapeutic Combining CS055 with Chiglitazar Targets Leukemia Stem and Progenitor Cells in Acute Myeloid Leukemia

Author

Zhou, Hui, primary, Qin, Dongmei, additional, Xie, Chendi, additional, Zhou, Jie, additional, Li, Wenjuan, additional, Zhong, Mengya, additional, Jiang, Yuelong, additional, Deng, Manman, additional, Zhao, Haijun, additional, Zhou, Yong, additional, Lai, Qian, additional, Fang, Zhihong, additional, Luo, Yiming, additional, Xu, Bing, additional, and Zha, Jie, additional

Published
2022
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22. Preclinical Studies and Phase II Trial of Venetoclax in Combination with Chidamide and Azacitidine in Relapsed/Refractory Acute Myeloid Leukemia

Author

Zha, Jie, primary, Zhou, Hui, additional, Zhong, Mengya, additional, Wang, Ying, additional, Du, Xin, additional, Gong, Tiejun, additional, Lin, Zhijuan, additional, Cai, Yun, additional, Xie, Siting, additional, Xie, Chendi, additional, Feng, XianQi, additional, Huang, ZhenQi, additional, Su, Liping, additional, Luo, Jianmin, additional, Yang, Lin, additional, Li, Zhenling, additional, Chen, Bi-yun, additional, Xie, Ying, additional, Zhu, Yu, additional, Shi, Pengcheng, additional, Li, Zhifeng, additional, Jiang, Yirong, additional, and Xu, Bing, additional

Published
2022
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26. sj-pdf-2-ccx-10.1177_10732748221081369 ��� Supplemental Material for Period 2 suppresses the malignant cellular behaviors of colorectal cancer through the EMT process

Author

Xiong, Yubo, Zhuang, Yifan, Zhong, Mengya, Qin, Wenjuan, Huang, Boyi, Zhao, Jiabao, Gao, Zhi, Ma, Jingsong, Wu, Zhengxin, Hong, Xuehui, Yue, Zhicao, and Lu, Haijie

Subjects
FOS: Clinical medicine, 111299 Oncology and Carcinogenesis not elsewhere classified
Abstract

Supplemental Material, sj-pdf-2-ccx-10.1177_10732748221081369 for period 2 suppresses the malignant cellular behaviors of colorectal cancer through the EMT process by Yubo Xiong, Yifan Zhuang, Mengya Zhong, Wenjuan Qin, Boyi Huang, Jiabao Zhao, Zhi Gao, Jingsong Ma, Zhengxin Wu, Xuehui Hong, Zhicao Yue, and Haijie Lu in cancer control

Published
2022
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27. sj-pdf-1-ccx-10.1177_10732748221081369 ��� Supplemental Material for Period 2 Suppresses the Malignant Cellular Behaviors of Colorectal Cancer Through the Epithelial-Mesenchymal Transformation Process

Author

Xiong, Yubo, Zhuang, Yifan, Zhong, Mengya, Qin, Wenjuan, Huang, Boyi, Zhao, Jiabao, Gao, Zhi, Ma, Jingsong, Wu, Zhengxin, Hong, Xuehui, Yue, Zhicao, and Lu, Haijie

Subjects
FOS: Clinical medicine, 111299 Oncology and Carcinogenesis not elsewhere classified
Abstract

Supplemental Material, sj-pdf-1-ccx-10.1177_10732748221081369 for Period 2 Suppresses the Malignant Cellular Behaviors of Colorectal Cancer Through the Epithelial-Mesenchymal Transformation Process by Yubo Xiong, Yifan Zhuang, Mengya Zhong, Wenjuan Qin, Boyi Huang, Jiabao Zhao, Zhi Gao, Jingsong Ma, Zhengxin Wu, Xuehui Hong, Zhicao Yue, and Haijie Lu in cancer control

Published
2022
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28. Additional file 1 of Therapeutic synergy of Triptolide and MDM2 inhibitor against acute myeloid leukemia through modulation of p53-dependent and -independent pathways

Author

Chen, Qinwei, Deng, Suqi, Deng, Manman, Shi, Yuanfei, Zhong, Mengya, Ding, Lihong, Jiang, Yuelong, Zhou, Yong, Carter, Bing Z., and Xu, Bing

Abstract

Additional file 1: Fig. S1 The synergistic interaction of LD Triptolide and MDM2 inhibitor in p53 wt AML cells. (A) The representative flow plots of cell apoptosis. (B) Fluorescence analysis of DAPI staining of OCI-AML3 cells treated with TPL and Nutlin-3a alone or in combination. (C) Immunoblotting examination of caspase 3 and PARP in OCI-AML3 and MV4-11 cell lines treated with Nutlin-3a (10 uM for AML3, 2uM for MV4-11), TPL (20 nM) alone or in combination for 24 h. (D) Analysis of Annexin-V + cells of OCI-AML3 cells treated as indicated with or without a v-ZAD-FMK pretreatment. (E) Analysis of apoptotic cells in health donors (n = 4). Fig. S2. The synergistic interaction of LD Triptolide and MDM2 inhibitor in p53 wt AML cells. (A) The representative flow plots of JC-1 fluorescence signal. Red fluorescence: aggregates; green fluorescence: means monomers. (B) Bar plot shows the reduction of MMP (MFI (red channel)/ MFI (green channel) *100%) after 48 h drug treatment. (C) Body weight analysis of AML xenografts treated with different treatment groups. (D) Tumors sections were prepared and stained by H.E. for histological examination. Data were presented as mean ± S.D. ns indicates not significant, * p

Published
2022
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35. Preclinical Studies of Chiauranib Show It Inhibits Transformed Follicular Lymphoma through the VEGFR2/ERK/STAT3 Signaling Pathway.

Author

Tang, Yuanfang, Zhong, Mengya, Pan, Guangchao, Tan, Jinshui, Xie, Chendi, Jiang, Yuelong, Yao, Jingwei, Shan, Weihang, Lin, Jiaqi, Huang, Jiewen, Liu, Yating, Li, Zhifeng, Xu, Bing, and Zha, Jie

Subjects
*FOLLICULAR lymphoma, *CELLULAR signal transduction, *CELL growth, *THERAPEUTICS, *WESTERN immunoblotting, *CELL cycle
Abstract

Transformed follicular lymphoma (t-FL), for which there is no efficient treatment strategy, has a rapid progression, treatment resistance, and poor prognosis, which are the main reasons for FL treatment failure. In this study, we identified a promising therapeutic approach with chiauranib, a novel orally developed multitarget inhibitor targeting VEGFR/Aurora B/CSF-1R. We first determined the cytotoxicity of chiauranib in t-FL cell lines through CCK-8, EdU staining, flow cytometry, and transwell assays. We also determined the killing effect of chiauranib in a xenograft model. More importantly, we identified the underlying mechanism of chiauranib in t-FL tumorigenesis by immunofluorescence and Western blotting. Treatment with chiauranib significantly inhibited cell growth and migration, promoted apoptosis, induced cell cycle arrest in G2/M phase, and resulted in significant killing in vivo. Mechanistically, chiauranib suppresses the phosphorylation level of VEGFR2, which has an anti-t-FL effect by inhibiting the downstream MEK/ERK/STAT3 signaling cascade. In conclusion, chiauranib may be a potential therapy to treat t-FL, since it inhibits tumor growth and migration and induces apoptosis by altering the VEGFR2/ERK/STAT3 signaling pathway. [ABSTRACT FROM AUTHOR]

Published
2023
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37. Identification of Crucial Genes of Pyrimidine Metabolism as Biomarkers for Gastric Cancer Prognosis

Author

Wu, Zhengxin, primary, Tan, Jinshui, additional, Zhuang, Yifan, additional, Zhong, Mengya, additional, Xiong, Yubo, additional, Ma, Jingsong, additional, Yang, Yan, additional, Gao, Zhi, additional, Zhao, Jiabao, additional, Ye, Zhijian, additional, Zhou, Huiwen, additional, Zhu, Yuekun, additional, Lu, Haijie, additional, and Hong, Xuehui, additional

Published
2021
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38. Combination of mesenchymal stem cells and FK506 prolongs heart allograft survival by inhibiting TBK1/IRF3-regulated-IFN-γ production

Author

Chen, Yingyu, primary, Yan, Guoliang, additional, Ma, Yunhan, additional, Zhong, Mengya, additional, Yang, Yan, additional, Guo, Junjun, additional, Wang, Chenxi, additional, Han, Weimin, additional, Zhang, Liyi, additional, Xu, Shuangyue, additional, Huang, Jinjin, additional, Dai, Helong, additional, and Qi, Zhongquan, additional

Published
2021
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39. Therapeutic Interaction of Apatinib and Chidamide in T-Cell Acute Lymphoblastic Leukemia through Interference with Mitochondria Associated Biogenesis and Intrinsic Apoptosis

Author

Zhong, Mengya, primary, Lin, Fusheng, additional, Jiang, Yuelong, additional, Pan, Guangchao, additional, Tan, Jinshui, additional, Zhou, Hui, additional, Lai, Qian, additional, Chen, Qinwei, additional, Deng, Manman, additional, Zha, Jie, additional, and Xu, Bing, additional

Published
2021
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40. Additional file 3 of Identification of crucial genes of pyrimidine metabolism as biomarkers for gastric cancer prognosis

Author

Wu, Zhengxin, Tan, Jinshui, Zhuang, Yifan, Zhong, Mengya, Xiong, Yubo, Ma, Jingsong, Yang, Yan, Gao, Zhi, Zhao, Jiabao, Ye, Zhijian, Zhou, Huiwen, Zhu, Yuekun, Lu, Haijie, and Hong, Xuehui

Subjects
fungi, natural sciences
Abstract

Additional file 3: Figure S3. The significantly enriched KEGG pathways by GESA. (A) Five representative KEGG pathways in the high-risk group of GC pyrimidine metabolism in TCGA. (B) Five representative KEGG pathways in the high-risk group of GC pyrimidine metabolism in GEO. (C) Five representative KEGG pathways in the low-risk group of GC pyrimidine metabolism in TCGA. (D) Five representative KEGG pathways in the low-risk group of GC pyrimidine metabolism in GEO.

Published
2021
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41. Additional file 2 of Identification of crucial genes of pyrimidine metabolism as biomarkers for gastric cancer prognosis

Author

Wu, Zhengxin, Tan, Jinshui, Zhuang, Yifan, Zhong, Mengya, Xiong, Yubo, Ma, Jingsong, Yang, Yan, Gao, Zhi, Zhao, Jiabao, Ye, Zhijian, Zhou, Huiwen, Zhu, Yuekun, Lu, Haijie, and Hong, Xuehui

Abstract

Additional file 2: Figure S2. Difference in expression levels of these three DEGS between the high-risk group and the low-risk group. (A) In TCGA database. (B) In GEO database.

Published
2021
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42. Additional file 1 of Carrier-free nanoparticles of camptothecin prodrug for chemo-photothermal therapy: the making, in vitro and in vivo testing

Author

Ao, Mingtao, Yu, Fei, Li, Yixiang, Zhong, Mengya, Tang, Yonghe, Yang, Hua, Wu, Xiaojing, Zhuang, Yifan, Wang, Huiyun, Sun, Xiaolian, Hong, Xuehui, and Chen, Xiao Dong

Abstract

Additional file 1: Figure S1. 1H-NMR spectrum of CPT-SS-OH in DMSO-d6. Figure S2. 13C-NMR spectrum of CPT-SS-OH in DMSO-d6. Figure S3. 1H-NMR spectrum of CPT-SS-LG in CDCl3. Figure S4. 13C-NMR spectrum of CPT-SS-LG in CDCl3. Figure S5. 1H-NMR spectrum of IR820-NH2 in CD3OD. Figure S6. 13C-NMR spectrum of IR820-NH2 in CD3OD. Figure S7. 1H-NMR spectrum of IR820-SS-CPT in DMSO-d6. Figure S8. 13C-NMR spectrum of IR820-SS-CPT in DMSO-d6. Figure S9. ESI���MS spectrum of IR820-SS-CPT. Figure S10. 1H-NMR spectrum of CPT-CC-OH in CDCl3. Figure S11. 1H-NMR spectrum of CPT-CC-LG in CDCl3. Figure S12. 1H-NMR spectrum of IR820-CC-CPT in CD3OD. Figure S13. ESI���MS spectrum of IR820-CC-CPT. Figure S14. UV���vis���NIR absorbance spectra of IR820, IR820-SS-CPT, and CPT in methanol. Figure S15. Stability of the hydrodynamic particle size of the IR820-SS-CPT NPs. Figure S16. Fluorescence spectra of IR820-SS-CPT NPs (10 ��M) incubated with or without 10 mM GSH for 2 h in PBS. Figure S17. Relative fluorescent intensity of IR820-SS-CPT NPs internalized by 4T1 cells treated with PBS, chlorpromazine, nystatin, amiloride at 37 ��C, and PBS at 4 ��C using flow cytometry analysis. Figure S18. Relative viability of LO2 cells treated with various concentrations of CPT and IR820-SS-CPT NPs for 36 h. Error bars indicate SD (n = 3). Figure S19. In vivo pharmacokinetics profiles of IR820-SS-CPT NPs and free CPT in Sprague���Dawley (SD) rats. Error bars indicate SD (n = 3). Figure S20. Representative H&E staining of the major organs and tumors of the mice treated with PBS and IR820-SS-CPT NPs + NIR.

Published
2021
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46. Leflunomide Inhibits rat-to-Mouse Cardiac Xenograft Rejection by Suppressing Adaptive Immune Cell Response and NF-κB Signaling Activation

Author

Ma, Yunhan, primary, Xie, Baiyi, additional, Guo, Junjun, additional, Chen, Yingyu, additional, Zhong, Mengya, additional, Lin, Qingru, additional, Hua, Jianyu, additional, Zhong, Jiaying, additional, Luo, Xuewei, additional, Yan, Guoliang, additional, Dai, Helong, additional, and Qi, Zhongquan, additional

Published
2021
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47. Expression of TIPE family members in human colorectal cancer

Author

Zhong, Mengya, primary, Chen, Zhijian, additional, Yan, Yang, additional, Bahet, Argen, additional, Cai, Xin, additional, Chen, Huiyu, additional, Ran, Honggang, additional, Qu, Kaiyong, additional, Han, Zhaopu, additional, Zhuang, Guohong, additional, Zhang, Shifeng, additional, and Wang, Yinan, additional

Published
2020
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50. UHMK 1 promotes gastric cancer progression through reprogramming nucleotide metabolism

Author

Feng, Xing, primary, Ma, Dong, additional, Zhao, Jiabao, additional, Song, Yongxi, additional, Zhu, Yuekun, additional, Zhou, Qingxin, additional, Ma, Fei, additional, Liu, Xing, additional, Zhong, Mengya, additional, Liu, Yu, additional, Xiong, Yubo, additional, Qiu, Xingfeng, additional, Zhang, Zhen, additional, Zhang, Heng, additional, Zhao, Yongxiang, additional, Zhang, Kaiguang, additional, Hong, Xuehui, additional, and Zhang, Zhiyong, additional

Published
2020
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