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iNatureN6-methyladenosine (m6A) RNA methylation and circular RNA (circRNA) have been shown to play important roles in a variety of malignancies including gastric cancer (GC)
.
However, little is known about how m6A modification of circRNAs promotes GC progression
.
On February 14, 2022, Shanghai Jiaotong University Zhang Jing and Zhu Jinshui published a joint communication online in Molecular Cancer (IF=27) entitled "METTL14-mediated m6A modification of circORC5 suppresses gastric cancer progression by regulating miR-30c-2-3p /AKT1S1 axis”, which found that METTL14 was downregulated in GC tissue samples and that its low expression was a prognostic factor for poor survival in GC patients
.
Ectopic expression of METTL14 significantly inhibited GC cell growth and invasion in vitro and in vivo, whereas knockdown of METTL14 had the opposite effect
.
Mechanistically, m6A-circRNA epitranscriptome microarray and Me-RIP identified circORC5 as a downstream target of METTL14
.
Silencing of METTL14 decreased the m6A level of circORC5, but increased the expression of circORC5
.
In addition, circORC5 can sponge miR-30c-2-3p and reverse METTL14-induced upregulation of miR-30c-2-3p and downregulation of AKT1S1 and EIF4B
.
Furthermore, circORC5 was negatively correlated with miR-30c-2-3p, indicating a low survival rate in GC
.
Taken together, our findings suggest that METTL14-mediated m6A modification of circORC5 inhibits gastric cancer progression by regulating the miR-30c-2-3p/AKT1S1 axis
.
Although the incidence and mortality of gastric cancer (GC) are declining globally, GC remains the third leading cause of cancer-related death in China
.
Recent decades have witnessed tremendous advances in the treatment of GC, including endoscopic resection, targeted therapy, and immunotherapy
.
However, the prognosis of patients with advanced stage is still poor due to tumor invasion and metastasis
.
Therefore, understanding the molecular mechanism of tumorigenesis is of great significance for the early diagnosis and treatment of gastric cancer
.
As one of the most common chemical modifications in eukaryotic mRNA, N6-methyladenosine (m6A) plays a key role in cancer progression
.
m6A methylation can be catalyzed by methyltransferases such as METTL3/14/16 ("writers"), removed by demethylases FTO and ALKBH5 ("eraser"), and interact with m6A-binding proteins.
roles such as YTHDF1/2/3 and IGF2BP1/2/3 (“readers”)
.
METTL14 has been shown to act as a tumor suppressor in colorectal (CRC), bladder and breast cancer, but not in thyroid, pancreatic and leukemia as a carcinogen
.
However, METTL14-mediated m6A modification in GC remains largely unknown
.
Schematic diagram of the article (picture from Molecular Cancer) Circular RNAs (circRNAs), as another subset of non-coding RNAs, are characterized by closed-loop structures and resistance to RNase
R.
Accumulating evidence suggests that circRNAs can act as miRNA sponges to regulate cancer progression
.
CircRNAs also function in GC by sponging miRNAs
.
For example, circRHOBTB3, circPSMC3, circCCDC9 and hsa_circ_0004872 inhibited GC growth and metastasis by sponge miR-654-3p/-296-5p/-6792-3p/-224, while circNRIP1 and circLMTK2 inhibited GC growth and metastasis by sponge miR-149-5p/ -150-5p promotes GC progress
.
circLARP4 and circYAP1 inhibited GC growth, but circDLST promoted its progression
.
However, how METTL14-mediated m6A modification of circRNAs contributes to GC remains unclear
.
M6A-mediated noncoding RNA (ncRNA) modification has been implicated in cancer
.
METTL14 inhibits carcinogenesis by regulating m6A-dependent miR-375 processing or lncRNA X inactivity-specific transcript (XIST)
.
m6A-modified circ-SORE promotes sorafenib resistance in hepatocellular carcinoma (HCC) by regulating β-catenin signaling
.
Here, we found that METTL14 inhibits GC growth and invasion by regulating the circORC5/miR-30c-2-3p axis, and may provide a potential therapeutic target for GC
.
Reference message: https://molecular-cancer.
biomedcentral.
com/articles/10.
1186/s12943-022-01521-z
.
However, little is known about how m6A modification of circRNAs promotes GC progression
.
On February 14, 2022, Shanghai Jiaotong University Zhang Jing and Zhu Jinshui published a joint communication online in Molecular Cancer (IF=27) entitled "METTL14-mediated m6A modification of circORC5 suppresses gastric cancer progression by regulating miR-30c-2-3p /AKT1S1 axis”, which found that METTL14 was downregulated in GC tissue samples and that its low expression was a prognostic factor for poor survival in GC patients
.
Ectopic expression of METTL14 significantly inhibited GC cell growth and invasion in vitro and in vivo, whereas knockdown of METTL14 had the opposite effect
.
Mechanistically, m6A-circRNA epitranscriptome microarray and Me-RIP identified circORC5 as a downstream target of METTL14
.
Silencing of METTL14 decreased the m6A level of circORC5, but increased the expression of circORC5
.
In addition, circORC5 can sponge miR-30c-2-3p and reverse METTL14-induced upregulation of miR-30c-2-3p and downregulation of AKT1S1 and EIF4B
.
Furthermore, circORC5 was negatively correlated with miR-30c-2-3p, indicating a low survival rate in GC
.
Taken together, our findings suggest that METTL14-mediated m6A modification of circORC5 inhibits gastric cancer progression by regulating the miR-30c-2-3p/AKT1S1 axis
.
Although the incidence and mortality of gastric cancer (GC) are declining globally, GC remains the third leading cause of cancer-related death in China
.
Recent decades have witnessed tremendous advances in the treatment of GC, including endoscopic resection, targeted therapy, and immunotherapy
.
However, the prognosis of patients with advanced stage is still poor due to tumor invasion and metastasis
.
Therefore, understanding the molecular mechanism of tumorigenesis is of great significance for the early diagnosis and treatment of gastric cancer
.
As one of the most common chemical modifications in eukaryotic mRNA, N6-methyladenosine (m6A) plays a key role in cancer progression
.
m6A methylation can be catalyzed by methyltransferases such as METTL3/14/16 ("writers"), removed by demethylases FTO and ALKBH5 ("eraser"), and interact with m6A-binding proteins.
roles such as YTHDF1/2/3 and IGF2BP1/2/3 (“readers”)
.
METTL14 has been shown to act as a tumor suppressor in colorectal (CRC), bladder and breast cancer, but not in thyroid, pancreatic and leukemia as a carcinogen
.
However, METTL14-mediated m6A modification in GC remains largely unknown
.
Schematic diagram of the article (picture from Molecular Cancer) Circular RNAs (circRNAs), as another subset of non-coding RNAs, are characterized by closed-loop structures and resistance to RNase
R.
Accumulating evidence suggests that circRNAs can act as miRNA sponges to regulate cancer progression
.
CircRNAs also function in GC by sponging miRNAs
.
For example, circRHOBTB3, circPSMC3, circCCDC9 and hsa_circ_0004872 inhibited GC growth and metastasis by sponge miR-654-3p/-296-5p/-6792-3p/-224, while circNRIP1 and circLMTK2 inhibited GC growth and metastasis by sponge miR-149-5p/ -150-5p promotes GC progress
.
circLARP4 and circYAP1 inhibited GC growth, but circDLST promoted its progression
.
However, how METTL14-mediated m6A modification of circRNAs contributes to GC remains unclear
.
M6A-mediated noncoding RNA (ncRNA) modification has been implicated in cancer
.
METTL14 inhibits carcinogenesis by regulating m6A-dependent miR-375 processing or lncRNA X inactivity-specific transcript (XIST)
.
m6A-modified circ-SORE promotes sorafenib resistance in hepatocellular carcinoma (HCC) by regulating β-catenin signaling
.
Here, we found that METTL14 inhibits GC growth and invasion by regulating the circORC5/miR-30c-2-3p axis, and may provide a potential therapeutic target for GC
.
Reference message: https://molecular-cancer.
biomedcentral.
com/articles/10.
1186/s12943-022-01521-z
