Related Experiment Video
Updated: Jan 15, 2026

Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo
Published on: July 20, 2019
NSUN2 promotes the growth, metastasis, and glutamine metabolism of non-small cell lung cancer
Yifan Zheng1, Chunhui Ma1, Shengguang Ding1
1Department of Thoracic Surgery, Affiliated Nantong Clinical College of Nantong University, The First People's Hospital of Nantong, 226001, Nantong, China.
Objectives:
As a 5-methylcytosine (m5C) methyltransferase, increased NOP2/Sun RNA methyltransferase 2 (NSUN2) has been revealed to promote the progression of non-small cell lung cancer (NSCLC) through m5C modification. Herein, this study aimed to investigate the potential molecular mechanisms underlying the high NSUN2 expression in NSCLC, and the potential downstream m5C mRNAs of NSUN2 in promoting NSCLC progression.
Methods And Measurements:
Functional analyses were conducted using in vitro 3- (4, 5-dimethylthiazolyl-2)-2, 5-diphenyltetrazolium bromide (MTT), 5-ethynyl-2'-deoxyuridine, Transwell, wound healing, and sphere and tube formation assays, and an in vivo murine model. m5C modification was determined by m5C-methylated RNA immunoprecipitation assay. RNA immunoprecipitation assay determined the binding between NSUN2 and SLC7A5 mRNA. The upstream molecular mechanism of the upregulation of NSUN2 expression was explored using chromatin immunoprecipitation, co-immunoprecipitation, and luciferase reporter assays.
Main Results:
NSUN2 was highly expressed in NSCLC and predicted poor outcomes in NSCLC patients. Functionally, NSUN2 silencing suppressed cancer cell proliferation, migration, stemness properties, angiogenic ability, and glutamine metabolism. Mechanistically, NSUN2 induced m5C methylation modification of SLC7A5, and stabilized SLC7A5 mRNA via a YBX1-dependent mechanism. Accordingly, SLC7A5 overexpression reversed the anticancer effects of NSUN2 on above oncogenic phenotypes. Further upstream molecular mechanism analysis showed that P300 could bind to and cooperate with transcription factor SP1 to increase NSUN2 expression by histone H3 lysine 27 acetylation (H3K27ac). Further in vivo analyses suggested that NSUN2 silencing suppressed NSCLC growth and metastasis in vivo by regulating SLC7A5 expression.
Conclusions:
Increased NSUN2 derived by P300/SP1 complex-mediated histone acetylation promoted the growth, metastasis, and glutamine metabolism of NSCLC by stabilizing SLC7A5 mRNA via m5C modification.
Related Concept Videos
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
Mitogens and the Cell Cycle
Adaptive Mechanisms in Cancer Cells
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
lncRNA - Long Non-coding RNAs
Abnormal Proliferation
The Nucleolus