9 results on '"Zhou, Quanbo"'
Search Results
2. LncRNA BCAN-AS1stabilizes c-Myc via N6-methyladenosine-mediated binding with SNIP1 to promote pancreatic cancer
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Wu, Guandi, Su, Jiachun, Zeng, Lingxing, Deng, Shuang, Huang, Xudong, Ye, Ying, Li, Rui, Bai, Ruihong, Zhuang, Lisha, Li, Mei, Zhou, Quanbo, Zheng, Yanfen, Deng, Junge, Zhang, Shaoping, Chen, Rufu, Lin, Dongxin, Zhang, Jialiang, and Zheng, Jian
- Abstract
C-Myc overexpression contributes to multiple hallmarks of human cancer but directly targeting c-Myc is challenging. Identification of key factors involved in c-Myc dysregulation is of great significance to develop potential indirect targets for c-Myc. Herein, a collection of long non-coding RNAs (lncRNAs) interacted with c-Myc is detected in pancreatic ductal adenocarcinoma (PDAC) cells. Among them, lncRNA BCAN-AS1is identified as the one with highest c-Myc binding enrichment. BCAN-AS1was abnormally elevated in PDAC tumors and high BCAN-AS1level was significantly associated with poor prognosis. Mechanistically, Smad nuclear-interacting protein 1 (SNIP1) was characterized as a new N6-methyladenosine (m6A) mediator binding to BCAN-AS1via recognizing its m6A modification. m6A-modified BCAN-AS1acts as a scaffold to facilitate the formation of a ternary complex together with c-Myc and SNIP1, thereby blocking S phase kinase-associated protein 2 (SKP2)-mediated c-Myc ubiquitination and degradation. Biologically, BCAN-AS1promotes malignant phenotypes of PDAC in vitro and in vivo. Treatment of metastasis xenograft and patient-derived xenograft mouse models with in vivo-optimized antisense oligonucleotide of BCAN-AS1effectively represses tumor growth and metastasis. These findings shed light on the pro-tumorigenic role of BCAN-AS1and provide an innovant insight into c-Myc-interacted lncRNA in PDAC.
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- 2023
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3. Super-enhancer RNA m6A promotes local chromatin accessibility and oncogene transcription in pancreatic ductal adenocarcinoma
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Li, Rui, Zhao, Hongzhe, Huang, Xudong, Zhang, Jialiang, Bai, Ruihong, Zhuang, Lisha, Wen, Shujuan, Wu, Shaojia, Zhou, Quanbo, Li, Mei, Zeng, Lingxing, Zhang, Shaoping, Deng, Shuang, Su, Jiachun, Zuo, Zhixiang, Chen, Rufu, Lin, Dongxin, and Zheng, Jian
- Abstract
The biological functions of noncoding RNA N6-methyladenosine (m6A) modification remain poorly understood. In the present study, we depict the landscape of super-enhancer RNA (seRNA) m6A modification in pancreatic ductal adenocarcinoma (PDAC) and reveal a regulatory axis of m6A seRNA, H3K4me3 modification, chromatin accessibility and oncogene transcription. We demonstrate the cofilin family protein CFL1, overexpressed in PDAC, as a METTL3 cofactor that helps seRNA m6A methylation formation. The increased seRNA m6As are recognized by the reader YTHDC2, which recruits H3K4 methyltransferase MLL1 to promote H3K4me3 modification cotranscriptionally. Super-enhancers with a high level of H3K4me3 augment chromatin accessibility and facilitate oncogene transcription. Collectively, these results shed light on a CFL1–METTL3–seRNA m6A–YTHDC2/MLL1 axis that plays a role in the epigenetic regulation of local chromatin state and gene expression, which strengthens our knowledge about the functions of super-enhancers and their transcripts.
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- 2023
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4. QDPR deficiency drives immune suppression in pancreatic cancer.
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Liu, Ji, He, Xiaowei, Deng, Shuang, Zhao, Sihan, Zhang, Shaoping, Chen, Ziming, Xue, Chunling, Zeng, Lingxing, Zhao, Hongzhe, Zhou, Yifan, Bai, Ruihong, Xu, Zilan, Liu, Shaoqiu, Zhou, Quanbo, Li, Mei, Zhang, Jialiang, Huang, Xudong, Chen, Rufu, Wang, Liqin, and Lin, Dongxin
- Abstract
The relevance of biopterin metabolism in resistance to immune checkpoint blockade (ICB) therapy remains unknown. We demonstrate that the deficiency of quinoid dihydropteridine reductase (QDPR), a critical enzyme regulating biopterin metabolism, causes metabolite dihydrobiopterin (BH2) accumulation and decreases the ratio of tetrahydrobiopterin (BH4) to BH2 in pancreatic ductal adenocarcinomas (PDACs). The reduced BH4/BH2 ratio leads to an increase in reactive oxygen species (ROS) generation and a decrease in the distribution of H3K27me3 at CXCL1 promoter. Consequently, myeloid-derived suppressor cells are recruited to tumor microenvironment via CXCR2 causing resistance to ICB therapy. We discovered that BH4 supplementation is capable to restore the BH4/BH2 ratio, enhance anti-tumor immunity, and overcome ICB resistance in QDPR-deficient PDACs. Tumors with lower QDPR expression show decreased responsiveness to ICB therapy. These findings offer a novel strategy for selecting patient and combining therapies to improve the effectiveness of ICB therapy in PDAC. [Display omitted] • QDPR deficiency drives immune suppression in pancreatic cancer • QDPR deficiency leads to ICB resistance via biopterin metabolic pathway • QDPR could serve as a predictive biomarker for ICB therapy in PDAC • BH4 supplementation sensitizes QDPR-deficient PDAC models to ICB The critical roles and mechanisms of biopterin metabolism in resistance to immune checkpoint blockade (ICB) therapy remain unknown. Liu et al. demonstrate the interplay between tumor-cell-hijacked biopterin metabolism and tumor immunity in PDAC and propose that QDPR deficiency causes ICB resistance in PDAC. [ABSTRACT FROM AUTHOR]
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- 2024
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5. Cancer-associated fibroblast-induced lncRNA UPK1A-AS1 confers platinum resistance in pancreatic cancer via efficient double-strand break repair
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Zhang, Xiang, Zheng, Shangyou, Hu, Chonghui, Li, Guolin, Lin, Hongcao, Xia, Renpeng, Ye, Yuancheng, He, Rihua, Li, Zhihua, Lin, Qing, Chen, Rufu, and Zhou, Quanbo
- Abstract
The tumor stroma of pancreatic ductal adenocarcinoma (PDAC) is characterized by an abundant and heterogeneous population of cancer-associated fibroblasts (CAFs), which are critically involved in chemoresistance. However, the underlying mechanism of CAFs in chemoresistance is unclear. Here, we show that CAFR, a CAF subset derived from platinum-resistant PDAC patients, assumes an iCAF phenotype and produces more IL8 than CAFSisolated from platinum-sensitive PDAC patients. CAFR-derived IL8 promotes oxaliplatin chemoresistance in PDAC. Based on long noncoding RNA (lncRNA) profiling in tumor cells incubated with CAF-CM, we found that UPK1A-AS1, whose expression is directly induced by IL8/NF-kappa B signaling, functions as a chemoresistance-promoting lncRNA and is critical for active IL8-induced oxaliplatin resistance. Impressively, blocking the activation of UPK1A-AS1 expression increases the oxaliplatin sensitivity of tumor cells in vivo. Mechanistically, UPK1A-AS1 strengthens the interaction between Ku70 and Ku80 to facilitate nonhomologous end joining (NHEJ), thereby enhancing DNA double-strand break (DSB) repair. Clinically, UPK1A-AS1 expression is positively correlated with IL8 expression, a poor chemotherapeutic response and a shorter progression-free survival (PFS) time in advanced PDAC patients. Collectively, our study reveals a lncRNA-mediated mechanism of CAF-derived paracrine IL8-dependent oxaliplatin resistance and highlights UPK1A-AS1 as a potential therapeutic target.
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- 2022
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6. RETRACTED ARTICLE: YAP1-induced MALAT1 promotes epithelial–mesenchymal transition and angiogenesis by sponging miR-126-5p in colorectal cancer
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Sun, Zhenqiang, Ou, Chunlin, Liu, Jinbo, Chen, Chen, Zhou, Quanbo, Yang, Shuaixi, Li, Guiyuan, Wang, Guixian, Song, Junmin, Li, Zhen, Zhang, Zhiyong, Yuan, Weitang, and Li, Xiayu
- Abstract
Yes-associated protein 1 (YAP1) exerts significant effects in various malignancies. However, the oncogenic role of YAP1 remains controversial, and the mechanism by which YAP1 regulates non-coding RNAs is still largely unknown. The present study aimed to assess the effect of YAP1 on the malignant behaviors of colorectal carcinoma (CRC) and explore the underlying regulatory mechanism of the YAP1–MALAT1–miR-126-5p axis. YAP1 was highly expressed in CRC tissues as assessed by GSE20916 and its expression was negatively correlated with overall survival in 83 CRC cases. Meanwhile, YAP1 promoted proliferation, invasion, and migration in colon cancer cells, in vitro and in vivo. MALAT1 was obviously expressed, with differential expression of 11 lncRNAs in HCT116 cells after transfection with siYAP1 or si-Ctl. Based on bioinformatics prediction, immunoprecipitation (IP), and chromatin immunoprecipitation (ChIP), the interaction of YAP1 with TCF4/β-catenin was regulated by MALAT1. Bioinformatics prediction, dual luciferase assay, RNA-IP, and RNA pull-down assay demonstrated that YAP1-induced MALAT1 promoted the expression of metastasis-associated molecules such as VEGFA, SLUG, and TWIST, by sponging miR-126-5p in CRC. These findings indicated that the YAP1–MALAT1–miR-126-5p axis could control angiogenesis and epithelial–mesenchymal transition in CRC, providing potential biomarkers and therapeutic targets for CRC.
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- 2019
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7. Retraction Note: YAP1-induced MALAT1 promotes epithelial–mesenchymal transition and angiogenesis by sponging miR-126-5p in colorectal cancer
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Sun, Zhenqiang, Ou, Chunlin, Liu, Jinbo, Chen, Chen, Zhou, Quanbo, Yang, Shuaixi, Li, Guiyuan, Wang, Guixian, Song, Junmin, Li, Zhen, Zhang, Zhiyong, Yuan, Weitang, and Li, Xiayu
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- 2023
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8. A retrospective cohort study of pancreatic neuroendocrine tumors at single institution over 15 years: New proposal for low- and high-grade groups, validation of a nomogram for prognosis, and novel follow-up strategy for liver metastases.
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Ye, Liangtao, Ye, Huilin, Zhou, Quanbo, Li, Zhihua, Lin, Qing, Tan, Langping, Gao, Wenchao, Fu, Zhiqiang, Zheng, Shangyou, and Chen, Rufu
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COMPARATIVE studies ,CYTOGENETICS ,LIVER tumors ,LONGITUDINAL method ,MATHEMATICAL models ,RESEARCH methodology ,MEDICAL cooperation ,MULTIVARIATE analysis ,NEUROENDOCRINE tumors ,PANCREATIC tumors ,PROGNOSIS ,RESEARCH ,TUMOR classification ,THEORY ,EVALUATION research ,RETROSPECTIVE studies ,STATISTICAL models - Abstract
Purpose: Pancreatic neuroendocrine tumors (PNETs) exhibit various tumor behaviors and symptoms that are difficult for physicians to stage and predict prognosis. We assess prognostic factors combined with staging classifications to optimal the models and try to improve follow-up strategy to monitor liver metastases after surgery.Methods: Patients with PNETs treated at Sun Yat-sen Memorial Hospital between 2000 and 2015 were recruited. Patients were regrouped on the basis of functional status and mitotic rates. Nomograms to predict the prognostic values of classifications (AJCC, ENETS, and WHO) were constructed; the accuracy of the nomograms were quantified by the C-index and calibration plots.Results: We identified 78 PNETs patients with pathological reports. Correlations with OS in univariate analysis included nonfunctional status (P = 0.002), CgA>200 ng/ml (P < 0.001), Ki-67 (3-20%, P = 0.014; >20%, P < 0.001), and mitotic rate (3-20/10HPF, P = 0.011; >20/10HPF, P < 0.001). By multivariate analysis, nonfunctional status and mitotic rate maintained significance (P = 0.039; 3-20/10HPF, P = 0.015; >20/10HPF, P = 0.007). Evaluating the new proposed system, the difference in OS between low- and high-groups was statistically significant (P = 0.001). The C-index of the regrouped nomograms were higher than that of premise ones (AJCC cohort, 0.605 v 0.576, P < 0.01; ENETS cohort, 0.73 v 0.691, P < 0.01; WHO cohort, 0.678 v 0.603, P < 0.01).Conclusion: An prognostic model based on mitotic rates and functional status correlates strongly with survival. PNETs should return visits every 2 months for the first half years, and every 3 months as followed until 2 years after surgery. [ABSTRACT FROM AUTHOR]- Published
- 2016
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9. Pancreatic stellate cells promotes the perineural invasion in pancreatic cancer.
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Zhou, Yu, Zhou, Quanbo, and Chen, Rufu
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PANCREATIC cancer ,CANCER cells ,NERVE growth factor ,NERVE tissue ,EVOKED potentials (Electrophysiology) ,CANCER invasiveness - Abstract
Abstract: Perineural invasion is a prominent characteristic of pancreatic cancer. Pancreatic cancer has an extremely high incidence of perineural invasion which has been associated with poor survival. Early studies mostly focus on the interaction between cancer cells and nerves. Recently, the effect of pancreatic stellate cells in progression of pancreatic cancer has been paid more attention. Both in vitro studies and in vivo ones revealed that pancreatic stellate cells can enhance the proliferation, migration and invasion of pancreatic cancer cells. Pancreatic stellate cells can also regulate the expression and effect of molecules involved in perineural invasion. In addition, pancreatic stellate cells seems to associated with the generation of neuronal plasticity in pancreatic cancer. Herein the hypothesis that pancreatic stellate cells play a potential role in promote the perineural invasion in pancreatic cancer through three mechanisms. One is that pancreatic stellate cells enhance the proliferation, migration and invasion directly through releasing a variety of stimuli and providing a suitable microenvironment. Pancreatic stellate cells also regulate the expression and effects of molecules involved in perineural invasion such as nerve growth factor. Another is that pancreatic stellate cells induce neuronal plasticity, which makes nerves more vulnerable to be invaded. We can conclude that pancreatic stellate cells play a central role in regulating the perineural invasion process by producing different effects on cancer cells and nerve. To inhibit the activity of pancreatic stellate cells or block the interaction between pancreatic stellate cells and cancer cells or nerve tissue might reduce the perineural invasion in pancreatic cancer. [Copyright &y& Elsevier]
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- 2012
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