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Start Over Author "Runbi Ji" Journal cell death and disease
2 results on '"Runbi Ji"'

1. IGF2BP2-meidated m6A modification of CSF2 reprograms MSC to promote gastric cancer progression

Author

Runbi Ji, Chenxi Wu, Jun Yao, Jiajin Xu, Jiang Lin, Hongbing Gu, Min Fu, Xiaoxin Zhang, Yongkang Li, and Xu Zhang

Subjects
Cytology, QH573-671
Abstract

Abstract The interaction between tumor cells and stromal cells within the tumor microenvironment plays a critical role in cancer progression. Mesenchymal stem cells (MSCs) are important tumor stromal cells that exhibit pro-oncogenic activities when reprogrammed by the tumor. However, the precise mechanisms underlying MSC reprogramming in gastric cancer remain not well understood. QRT-PCR, western blot, and immunohistochemistry were used to examine gene and protein expression levels. In vitro and in vivo experiments were conducted to assess the biological functions of gastric cancer cells. RNA-sequencing, RNA immunoprecipitation (RIP), and meRIP assays were performed to investigate underlying molecular mechanisms. We found a significant increase in the expression and N6-methyladenosine (m6A) modification levels of colony-stimulating factor 2 (CSF2) in gastric cancer MSCs. CSF2 gene overexpression induced the reprogramming of normal MSCs into cancer-promoting MSCs, thereby enhancing the proliferation, migration, and drug resistance of gastric cancer cells through the secretion of various pro-inflammatory factors. Additionally, we demonstrated that the m6A reader IGF2BP2 bound to and stabilized CSF2 mRNA in gastric cancer MSCs. Notably, overexpression of IGF2BP2 mimicked the effect of CSF2 on MSCs, promoting gastric cancer progression. Finally, we unveiled that CSF2 induced the ubiquitination of Notch1 to reprogram MSCs. Our study highlights a critical role of IGF2BP2-mediated m6A modification of CSF2 in reprogramming MSCs, which presents a promising therapeutic target for gastric cancer.

Published
2023
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2. LINC00978 promotes the progression of hepatocellular carcinoma by regulating EZH2-mediated silencing of p21 and E-cadherin expression

Author

Zheying Mao, Hui Qian, Fei Mao, Meng Shao, Jiayin Zhang, Feng Wang, Jianmei Gu, Hui Cai, Xu Zhang, Xiaoge Ding, Wenrong Xu, Runbi Ji, Xueyan Zang, Yu Zhang, Xueying Xu, and Guohong Ge

Subjects
Cyclin-Dependent Kinase Inhibitor p21, Cancer Research, Cell cycle checkpoint, Carcinoma, Hepatocellular, Transcription, Genetic, Carcinogenesis, Immunology, Down-Regulation, Mice, Nude, Apoptosis, Biology, Article, Epigenesis, Genetic, Cellular and Molecular Neuroscience, Antigens, CD, Cell Movement, Cell Line, Tumor, medicine, Gene silencing, Animals, Humans, Enhancer of Zeste Homolog 2 Protein, Neoplasm Invasiveness, Gene Silencing, Neoplasm Metastasis, lcsh:QH573-671, neoplasms, Cell Proliferation, Regulation of gene expression, Gene knockdown, Mice, Inbred BALB C, Cadherin, Cell growth, lcsh:Cytology, EZH2, Liver Neoplasms, Diagnostic markers, Cell Biology, medicine.disease, Cadherins, digestive system diseases, Up-Regulation, Gene Expression Regulation, Neoplastic, Hepatocellular carcinoma, Cancer research, Long non-coding RNAs, Disease Progression, RNA, Long Noncoding, Protein Binding
Abstract

Long non-coding RNAs (lncRNAs) have been suggested as important regulators of cancer development and progression in hepatocellular carcinoma (HCC). Nevertheless, the clinical value and biological roles of LINC00978 in HCC remain unclear. In this study, we detected the expression of LINC00978 in tumor tissues and serum of HCC patients, examined the roles of LINC00978 in HCC progression and elucidated the underlying molecular mechanisms. We found that LINC00978 expression was upregulated in tumor tissues and serum of HCC patients. Higher serum levels of LINC00978 could distinguish HCC patients from hepatitis and liver cirrhosis patients and healthy controls. LINC00978 knockdown inhibited HCC cell proliferation, migration and invasion while promoted cell cycle arrest and apoptosis. Overexpression of LINC00978 led to the opposite effects. LINC00978 knockdown also inhibited HCC growth and metastasis in mouse tumor models. Mechanistically, LINC00978 bound to EZH2 and mediated its accumulation at the promoter region of p21 and E-cadherin genes, leading to the trimethylation of H27K3 and the inhibition of p21 and E-cadherin expression. Moreover, the simultaneous depletion of p21 and E-cadherin expression reversed the inhibitory effects of LINC00978 knockdown on HCC cell proliferation, migration, and invasion. Taken together, these findings suggest that LINC00978 promotes HCC progression by inhibiting p21 and E-cadherin expression via EZH2-mediated epigenetic silencing. LINC00978 may represent a novel biomarker for HCC diagnosis, prognosis, and therapy.

Published
2019

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