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21 results on '"Cheng, Rongjie"'

4. Oncogenic KRAS signaling drives evasion of innate immune surveillance in lung adenocarcinoma by activating CD47

Author

Hu, Huanhuan, Cheng, Rongjie, Wang, Yanbo, Wang, Xiaojun, Wu, Jianzhuang, Kong, Yan, Zhan, Shoubin, Zhou, Zhen, Zhu, Hongyu, Yu, Ranran, Liang, Gaoli, Wang, Qingyan, Zhu, Xiaoju, Zhang, Chen- Yu, Yin, Rong, Yan, Chao, and Chen, Xi

Subjects
Gene mutations -- Research, Oncology, Experimental, Immune response -- Genetic aspects, Lung cancer -- Genetic aspects -- Development and progression, Cellular signal transduction -- Research, Oncogenes -- Health aspects, Cancer -- Research, Health care industry
Abstract

KRAS is one of the most frequently activated oncogenes in human cancers. Although the role of KRAS mutation in tumorigenesis and tumor maintenance has been extensively studied, the relationship between KRAS and the tumor immune microenvironment is not fully understood. Here, we identified a role of KRAS in driving tumor evasion from innate immune surveillance. In samples of lung adenocarcinoma from patients and Kras- driven genetic mouse models of lung cancer, mutant KRAS activated the expression of cluster of differentiation 47 (CD47), an antiphagocytic signal in cancer cells, leading to decreased phagocytosis of cancer cells by macrophages. Mechanistically, mutant KRAS activated PI3K/STAT3 signaling, which restrained miR-34a expression and relieved the posttranscriptional repression of miR-34a on CD47. In 3 independent cohorts of patients with lung cancer, the KRAS mutation status positively correlated with CD47 expression. Therapeutically, disruption of the KRAS/CD47 signaling axis with KRAS siRNA, the [KRAS.sup.G12C] inhibitor AMG 510, or a miR-34a mimic suppressed CD47 expression, enhanced the phagocytic capacity of macrophages, and restored innate immune surveillance. Our results reveal a direct mechanistic link between active KRAS and innate immune evasion and identify CD47 as a major effector underlying the KRAS-mediated immunosuppressive tumor microenvironment., Introduction Mutations of the KRAS gene are the most common drivers of tumor development across a spectrum of human cancers, such as cancers of the lung, colon, and pancreas (1-3). [...]

Published
2023
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10. A novel protein RASON encoded by a lncRNA controls oncogenic RAS signaling in KRAS mutant cancers

Author

Cheng, Rongjie, primary, Li, Fanying, additional, Zhang, Maolei, additional, Xia, Xin, additional, Wu, Jianzhuang, additional, Gao, Xinya, additional, Zhou, Huangkai, additional, Zhang, Zhi, additional, Huang, Nunu, additional, Yang, Xuesong, additional, Zhang, Yaliang, additional, Shen, Shunli, additional, Kang, Tiebang, additional, Liu, Zexian, additional, Xiao, Feizhe, additional, Yao, Hongwei, additional, Xu, Jianbo, additional, Yan, Chao, additional, and Zhang, Nu, additional

Published
2022
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17. Long non-coding RNA ZEB1-AS1 promotes cell invasion and epithelial to mesenchymal transition through inducing ZEB1 expression in cervical cancer

Author

Cheng,Rongjie, Li,Nan, Yang,Shuyan, Liu,Lei, Han,Shiyu, Cheng,Rongjie, Li,Nan, Yang,Shuyan, Liu,Lei, and Han,Shiyu

Abstract

Rongjie Cheng,1,* Nan Li,2,* Shuyan Yang,1 Lei Liu,1 Shiyu Han1 1Department of Obstetrics and Gynaecology, The Fourth Affiliated Hospital of Harbin Medical University, Harbin City, Heilongjiang Province, People’s Republic of China; 2Department of Pathology, The Fourth Affiliated Hospital of Harbin Medical University, Harbin City, Heilongjiang Province, People’s Republic of China *These authors contributed equally to this work Background: Long non-coding RNAs (lncRNAs) play important roles in cancer initiation and development. The purpose of the present study was to determine the functions and mechanisms of lncRNA ZEB1-AS1 in human cervical cancer (CC).Methods: A total of 106 pairs of CC tissues and adjacent normal epithelial tissues were collected from CC patients who underwent resection. Three human CC cell lines (HeLa, C33A and SiHa) and a normal cervical cell line Crl-2614 and were transfected with human ZEB1-AS1 cDNA, or empty vector as the control. Then, cells were transfected with ZEB1-AS1-specific small interfering RNA (si-ZEB1-AS1), ZEB1-specific siRNA (si-ZEB1) or negative siRNA control (si-NC). The transfection efficiency was confirmed by RT-qPCR analysis. qPCR was applied to determine the qualification of RNA. Cell proliferation was investigated by MTT assay. The apoptosis rate of cells was detected by flow cytometer. Cell invasion was detected by transwell assay. Western blot was applied to determine the expression of proteins. CC xenografts in 12 male BALB/c athymic nude mice were established. And the tumor volumes were measured by vernier caliper.Results: We found that ZEB1-AS1 expression was remarkably increased in human CC tissue samples and cell lines, and its expression levels were closely associated with poor prognosis of CC patients. Moreover, we found that knockdown of ZEB1-AS1 inhibited the proliferation, migration, invasion and epithelial–mesenchymal transition (EMT) of CC cells in vitro and suppressed CC xenograf

Published
2018

18. The Jun/miR-22/HuR regulatory axis contributes to tumourigenesis in colorectal cancer

Author

Liu, Yanqing, primary, Chen, Xiaorui, additional, Cheng, Rongjie, additional, Yang, Fei, additional, Yu, Mengchao, additional, Wang, Chen, additional, Cui, Shufang, additional, Hong, Yeting, additional, Liang, Hongwei, additional, Liu, Minghui, additional, Zhao, Chihao, additional, Ding, Meng, additional, Sun, Wu, additional, Liu, Zhijian, additional, Sun, Feng, additional, Zhang, Chenyu, additional, Zhou, Zhen, additional, Jiang, Xiaohong, additional, and Chen, Xi, additional

Published
2018
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20. miR-19a promotes colorectal cancer proliferation and migration by targeting TIA1

Author

Liu, Yanqing, primary, Liu, Rui, additional, Yang, Fei, additional, Cheng, Rongjie, additional, Chen, Xiaorui, additional, Cui, Shufang, additional, Gu, Yuanyuan, additional, Sun, Wu, additional, You, Chaoying, additional, Liu, Zhijian, additional, Sun, Feng, additional, Wang, Yanbo, additional, Fu, Zheng, additional, Ye, Chao, additional, Zhang, Chenyu, additional, Li, Jing, additional, and Chen, Xi, additional

Published
2017
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