Ning‐Fang Ma

Guangzhou Medical University

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Trends

Author Order

Document Type

Co-Authors

Xin‐Yuan Guan

Chinese University of Hong Kong

Dan Xie

Sun Yat-sen University

Ming Liu

Peking University Cancer Hospital

Wei Cheng

First Affiliated Hospital of Wenzhou Medical University

Fan-En Kong

Guangzhou Medical University

Rixin Chen

Guangdong Academy of Medical Sciences

Li Huang

Guangzhou Medical University

Xiaohan Jin

Shandong First Medical University

Yuanfeng Gong

Guangzhou Medical University

Mengsu Yang

City University of Hong Kong, Shenzhen Research Institute

Cooperative Institutions

Guangzhou Medical University

119

Sun Yat-sen University

Sun Yat-sen University Cancer Center

University of Hong Kong

Chinese Academy of Sciences

Chinese University of Hong Kong

Southern Medical University

State Key Laboratory of Oncology in South China

State Key Laboratory of Respiratory Disease

Shanghai Jiao Tong University

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Field

Supplementary Data from COOH-Terminal Truncated HBV X Protein Plays Key Role in Hepatocarcinogenesis

Ning‐Fang Ma Sze Hang Lau Liang Hu Dan Xie Jun Wu

Supplementary Data from COOH-Terminal Truncated HBV X Protein Plays Key Role in Hepatocarcinogenesis

10.1158/1078-0432.22439307

Cite

Citations (0)

Supplementary Data from CSTF2-Induced Shortening of the RAC1 3′UTR Promotes the Pathogenesis of Urothelial Carcinoma of the Bladder

Xin Chen Jiaxing Zhang Junhang Luo Song Wu Gangjun Yuan

Supplementary Figure S1. Identification of 3'UTR shortening of RALA and RAC1 from UCB, colorectal carcinoma, hepatocellular carcinoma and non-small cell lung cancer samples. Supplementary Figure S2. RAC1 with short 3'UTR promotes tumorigenesis and produces more protein due to evasion of miRNA-mediated repression. Supplementary Figure S3. Screening of APA factors that contribute to the PAS selection of RAC1 in UCB. Supplementary Figure S4. CSTF2 regulates colony formation and invasiveness abilities of shorter RAC1 isoform in UCB. Supplementary Table S1. PDUI value calculated from DaPars analysis of 15 pairs of UCB and adjacent normal bladder tissues. Supplementary Table S2. KEGG pathway analyses of APA genes identified from RNA-Seq. Supplementary Table S3. RAC1 genomic mutations identified from TCGA UCB database. Supplementary Table S4. Correlation between the expression of CSTF2 and clinicopathologic characteristics of UCB patients

10.1158/0008-5472.22419636.v1

Cite

Citations (0)

Clusterin plays an important role in hepatocellular carcinoma metastasis

Oncogene (2005)

S. H. Lau Jonathan S. T. Sham Dan Xie C-H Tzang Dean G. Tang

Clusterin

HCCS

10.1038/sj.onc.1209141

Cite

Citations (153)

Identification of CHD1L as an Important Regulator for Spermatogonial Stem Cell Survival and Self-Renewal

Stem Cells International (2016)

Shanshan Liu Yinshan Bai Feng Li Wen-Wei Dong Yang Li

Chromodomain helicase/ATPase DNA binding protein 1‐like gene ( Chd1l ) participates in chromatin‐dependent processes, including transcriptional activation and DNA repair. In this study, we have found for the first time that Chd1l is mainly expressed in the testicular tissues of prepubertal and adult mice and colocalized with PLZF, OCT4, and GFR α 1 in the neonatal mouse testis and THY1 + undifferentiated spermatogonia or spermatogonial stem cells (SSCs). Knockdown of endogenous Chd1l in cultured mouse undifferentiated SSCs inhibited the expression levels of Oct4 , Plzf , Gfrα1 , and Pcna genes, suppressed SSC colony formation, and reduced BrdU incorporation, while increasing SSC apoptosis. Moreover, the Chd1l gene expression is activated by GDNF in the cultured mouse SSCs, and the GDNF signaling pathway was modulated by endogenous levels of Chd1l; as demonstrated by the gene expression levels of GDNF, inducible transcripts Etv5 , Bcl6b , Pou3f , and Lhx1 , but not that of GDNF‐independent gene, Taf4b , were significantly downregulated by Chd1l knockdown in mouse SSCs. Taken together, this study provides the first evidence to support the notion that Chd1l is an intrinsic and novel regulator for SSC survival and self‐renewal, and it exerts such regulation at least partially through a GDNF signaling pathway.

Identification

Master regulator

10.1155/2016/4069543

Cite

Citations (10)

Practice of blended learning in physiology teaching based on Rain Classroom

Zhonghua yixue jiaoyu tansuo zazhi (2019)

Yong-Sheng Tu Xiaoyang Xu Ximing Zhang Ning‐Fang Ma Jianhua Li

To effectively urge students to preview lessons before class, carry out efficient precise interactive teaching in class and make an accurate analysis on the teaching effect after class, Rain Classroom was utilized to construct a high-efficient interactive precision before-class-in-class-after-class teaching mode for physiology teaching. A questionnaire survey was conducted for the students, and the results show that the students are very fond of the teaching mode supported by Rain Classroom. The mode effectively promotes the students' daily study and the interaction between teachers and students, makes teachers accurately grasp the students' situation and perform scientific and precise teaching, enhances the teaching efficiency and improves the teaching effect. Key words: Rain Classroom; Precision teaching; Interactive teaching; Blended teaching; Physiology

10.3760/cma.j.issn.2095-1485.2019.07.005

Cite

Citations (0)

CHD1L promotes lineage reversion of hepatocellular carcinoma through opening chromatin for key developmental transcription factors

Hepatology (2016)

Ming Liu Leilei Chen Ning‐Fang Ma Raymond Kwok Kei Chow Yan Li

High‐grade tumors with poor differentiation usually show phenotypic resemblance to their developmental ancestral cells. Cancer cells that gain lineage precursor cell properties usually hijack developmental signaling pathways to promote tumor malignant progression. However, the molecular mechanisms underlying this process remain unclear. In this study, the chromatin remodeler chromodomain‐helicase‐DNA‐binding‐protein 1‐like (CHD1L) was found closely associated with liver development and hepatocellular carcinoma (HCC) tumor differentiation. Expression of CHD1L decreased during hepatocyte maturation and increased progressively from well‐differentiated HCCs to poorly differentiated HCCs. Chromatin immunoprecipitation followed by high‐throughput deep sequencing found that CHD1L could bind to the genomic sequences of genes related to development. Bioinformatics‐aided network analysis indicated that CHD1L‐binding targets might form networks associated with developmental transcription factor activation and histone modification. Overexpression of CHD1L conferred ancestral precursor‐like properties of HCC cells both in vitro and in vivo . Inhibition of CHD1L reversed tumor differentiation and sensitized HCC cells to sorafenib treatment. Mechanism studies revealed that overexpression of CHD1L could maintain an active “open chromatin” configuration at promoter regions of estrogen‐related receptor‐beta and transcription factor 4, both of which are important regulators of HCC self‐renewal and differentiation. In addition, we found a significant correlation of CHD1L with developmental transcriptional factors and lineage differentiation markers in clinical HCC patients. Conclusion: Genomic amplification of chromatin remodeler CHD1L might drive dedifferentiation of HCC toward an ancestral lineage through opening chromatin for key developmental transcriptional factors; further inhibition of CHD1L might “downgrade” poorly differentiated HCCs and provide novel therapeutic strategies. (H epatology 2016;63:1544‐1559)

HCCS

Chromatin immunoprecipitation

10.1002/hep.28437

Cite

Citations (34)

Targeting tumor lineage plasticity in hepatocellular carcinoma using an anti-CLDN6 antibody-drug conjugate

Science Translational Medicine (2021)

Fan-En Kong Guangmeng Li Yunqiang Tang Shaoyan Xi Jane Ho Chun Loong

CLDN6 is not only a marker of hepatocellular carcinoma but also a therapeutic target by promoting sorafenib resistance and lineage plasticity.

Lineage (genetic)

Antibody-drug conjugate

10.1126/scitranslmed.abb6282

Cite

Citations (54)

Ground-source Heat Pump System Design for one Villa in Jiangsu

Refrigeration Air Conditioning & Electric Power Machinery (2011)

Ning‐Fang Ma

According to the request of high level,comfort,function and energy saving for the villa in Jiangsu,the article provided a turnkey solution.Including function analysis,load calculation,design select and project installation,etc.

Source

Cite

Citations (0)

Data from CSTF2-Induced Shortening of the RAC1 3′UTR Promotes the Pathogenesis of Urothelial Carcinoma of the Bladder

Xin Chen Jiaxing Zhang Junhang Luo Song Wu Gangjun Yuan

<div>AbstractShortening of the 3′ untranslated regions (3′UTR) of mRNA is an important mechanism for oncogene activation. However, 3′UTR alteration events, their pathologic functions, and underlying mechanisms in human urothelial carcinoma of the bladder (UCB) are not clear. Here, we combine RNA sequencing, bioinformatics, and clinical studies in two independent cohorts of patients with UCB to identify a novel RAC1 shorter 3′UTR isoform that is frequently expressed in UCB and is critical in the tumorigenesis and acquisition of a poor prognostic phenotype in patients. Short 3′UTR isoform of RAC1 substantially upregulated RAC1 expression by escaping from miRNA-targeted repression and played an essential oncogenic role in UCB pathogenesis. An important cleavage/polyadenylation factor, cleavage stimulation factor 2 (CSTF2), induced 3′UTR shortening of RAC1 in UCB by mediating slow transcriptional elongation at RAC1. Cotranscriptional recruitment of CSTF2 on the GUAAU motif at proximal polyadenylation site of RAC1 attenuated the recruitment of two transcription factors AFF1 and AFF4, causing the defects in elongation. CSTF2 regulated the tumorigenic functions of the shorter RAC1 isoform in UCB cells, enhancing cell proliferation, migration, and invasion. The combination of high expression of CSTF2 and high usage of RAC1 short-3′UTR isoform may be used as a powerful biomarker to predict poor prognosis in UCB. Our findings also suggest a CSTF2-regulated RAC1-3′UTR shortening program as an exploitable therapeutic strategy for patients with UCB.Significance: These findings demonstrate that the short isoform of RAC1 is critical in UCB tumorigenesis and may have implications for developing new therapeutic strategies to treat this disease. Cancer Res; 78(20); 5848–62. ©2018 AACR.</div>

10.1158/0008-5472.c.6510432.v1

Cite

Citations (0)

Correction to: CHD1L prevents lipopolysaccharide-induced hepatocellular carcinomar cell death by activating hnRNP A2/B1-nmMYLK axis

Cell Death and Disease (2022)

Guangliang Wang Xiaofeng Zhang Wei Cheng Y.D. Mo Juan Chen

10.1038/s41419-022-04648-5

Cite

Citations (1)