N6-methyladenosine METTL3 promotes cervical cancer tumorigenesis and Warburg effect through YTHDF1/HK2 modification

Wang, Qianqing; Guo, Xiangcui; Li, Li; Gao, Zhihui; Su, Xiaoke; Ji, Mei; Liu, Juan

doi:10.1038/s41419-020-03071-y

Cited by 194 publications

(201 citation statements)

References 29 publications

Supporting

Mentioning

194

Contrasting

Order By: Relevance

“…21 Thus, an increasing number of studies on cancer metabolism are examining the regulation of HK2 expression as a promising anticancer strategy. 10,21,22 HK2 contributes to increasing the glycolytic capacity and proliferation of GBM cells. 23 Human ATP citrate lyase (ACLY) catalyzes the ATP-dependent synthesis of oxaloacetate and acetyl-coenzyme A (acetyl-CoA) from citrate and coenzyme A (CoA), which is a key enzyme in lipid synthesis.…”

Section: Key Enzymes In Glioma Glycolipid Metabolismmentioning

confidence: 99%

Glioma glycolipid metabolism: MSI2–SNORD12B–FIP1L1–ZBTB4 feedback loop as a potential treatment target

Dong

Liu

Yang

et al. 2021

Clinical & Translational Med

View full text Add to dashboard Cite

1. MSI2 expression was significantly upregulated in GBM, binding to SNORD12B and improving SNORD12B expression by increasing its stability.2. SNORD12B regulated alternative polyadenylation process of transcriptional repressor ZBTB4 by competitively combining with FIP1L1. 3. ZBTB4 transcriptionally suppressed the expression of HK2, ACLY, and MSI2, forming a positive feedback regulatory loop to regulate the glycolipid metabolism and proliferation of GBM cell.

show abstract

Section: Key Enzymes In Glioma Glycolipid Metabolismmentioning

confidence: 99%

Glioma glycolipid metabolism: MSI2–SNORD12B–FIP1L1–ZBTB4 feedback loop as a potential treatment target

Dong

Liu

Yang

et al. 2021

Clinical & Translational Med

View full text Add to dashboard Cite

show abstract

“…It has been reported that HPVs generated circRNAs encompassing the E7 oncogene (circE7), which was subjected to m 6 A modification, and promoted the proliferation of tumor cells ( 39 ). METTL3 promoted the stability of H2K through m 6 A modification, thereby promoting Warburg effect and the proliferation of cervical cancer cells ( 40 ). Here, we found that YTHDF1 is up-regulated in cervical cancer tissues and predicts the poor clinical outcomes.…”

Section: Discussionmentioning

confidence: 99%

YTHDF1 Aggravates the Progression of Cervical Cancer Through m6A-Mediated Up-Regulation of RANBP2

et al. 2021

View full text Add to dashboard Cite

N6-methyladenosine (m6A) is the most common post-transcriptional modification of RNA in eukaryotes, which has been demonstrated to play important roles in various cancers. YTHDF1 acts as a crucial m6A “reader” and regulates the fate of m6A modified mRNA. However, its role in cervical cancer remains unknown. In this study, we showed that YTHDF1 was highly expressed in cervical cancer, and was closely associated with the poor prognosis of cervical cancer patients. YTHDF1 knockdown suppressed the growth, migration and invasion, and induced apoptosis of cervical cancer cells. Moreover, YTHDF1 knockdown inhibited tumorigenesis of cervical cancer cells in vivo. Through combined on-line data analysis of RIP-seq, meRIP-seq and Ribo-seq upon YTHDF1 knockdown, RANBP2 was identified as the key target of YTHDF1 in cervical cancer cells. YTHDF1 regulated RANBP2 translation in an m6A-dependent manner without effect on its mRNA expression. RANBP2 potentiated the growth, migration and invasion of cervical cancer cells. Our study demonstrated the oncogenic role of YTHDF1 in cervical cancer by regulating RANBP2 expression and YTHDF1 represents a potential target for cervical cancer therapy.

show abstract

“…RNA expression levels were measured using quantitative real-time polymerase chain reaction (qRT-PCR) as previously described 26 . Glyceraldehyde-3-phosphate dehydrogenase ( GAPDH ) was used as an endogenous control and Hut78 cells for calibration 29 – 31 . The primers (Supplementary Table 2 ) were provided by Biosune Biotechnology Company (Shanghai, China).…”

Section: Methodsmentioning

confidence: 99%

A novel lncRNA TCLlnc1 promotes peripheral T cell lymphoma progression through acting as a modular scaffold of HNRNPD and YBX1 complexes

Zhao

Fang

et al. 2021

Cell Death Dis

View full text Add to dashboard Cite

Long noncoding RNAs (lncRNAs) play an essential role in tumor progression. Few researches focused on the clinical and biological relevance of lncRNAs in peripheral T cell lymphoma (PTCL). In this research, a novel lncRNA (ENST00000503502) was identified overexpressed in the main subtypes of PTCL, and designated as T cell lymphoma-associated lncRNA1 (TCLlnc1). Serum TCLlnc1 was associated with extranodal involvement, high-risk International Prognostic Index, and poor prognosis of the patients. Both in vitro and in vivo, overexpression of TCLlnc1 promoted T-lymphoma cell proliferation and migration, both of which were counteracted by the knockdown of TCLlnc1 using small interfering RNAs. As the mechanism of action, TCLlnc1 directly interacted with transcription activator heterogeneous nuclear ribonucleoprotein D (HNRNPD) and Y-box binding protein-1 (YBX1) by acting as a modular scaffold. TCLlnc1/HNRNPD/YBX1 complex upregulated transcription of TGFB2 and TGFBR1 genes, activated the tumor growth factor-β signaling pathway, resulting in lymphoma progression, and might be a potential target in PTCL.

show abstract

N6-methyladenosine METTL3 promotes cervical cancer tumorigenesis and Warburg effect through YTHDF1/HK2 modification

Cited by 194 publications

References 29 publications

Glioma glycolipid metabolism: MSI2–SNORD12B–FIP1L1–ZBTB4 feedback loop as a potential treatment target

Glioma glycolipid metabolism: MSI2–SNORD12B–FIP1L1–ZBTB4 feedback loop as a potential treatment target

YTHDF1 Aggravates the Progression of Cervical Cancer Through m6A-Mediated Up-Regulation of RANBP2

A novel lncRNA TCLlnc1 promotes peripheral T cell lymphoma progression through acting as a modular scaffold of HNRNPD and YBX1 complexes

Contact Info

Product

Resources

About