The m6A methyltransferase METTL3 promotes bladder cancer progression via AFF4/NF-κB/MYC signaling network

N 6 -methyladenosine (m6A) is the most abundant modification in eukaryotic messenger RNAs (mRNAs), and plays important roles in many bioprocesses. However, its functions in bladder cancer (BCa) remain elusive. Here, we discovered that methyltransferase-like 3 (METTL3), a major RNA N 6 -adenosine met...

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Veröffentlicht in:	Oncogene Jg. 38; H. 19; S. 3667 - 3680
Hauptverfasser:	Cheng, Maosheng, Sheng, Lu, Gao, Qian, Xiong, Qiuchan, Zhang, Haojie, Wu, Mingqing, Liang, Yu, Zhu, Fengyu, Zhang, Yingyin, Zhang, Xiuhong, Yuan, Quan, Li, Yang
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	London Nature Publishing Group UK 09.05.2019 Nature Publishing Group
Schlagworte:	13/31 13/89 13/95 38/39 45/91 631/208/176 631/67/589/1336 64/60 96/63 Adenosine Apoptosis Bladder cancer Cell Biology Cell growth Cell proliferation Cell survival DNA-directed RNA polymerase Gene expression Human Genetics Internal Medicine Medicine Medicine & Public Health Myc protein N6-methyladenosine NF-κB protein Oncology Polymerase chain reaction Ribonucleic acid RNA Tumorigenicity
ISSN:	0950-9232, 1476-5594, 1476-5594
Online-Zugang:	Volltext
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Abstract	N 6 -methyladenosine (m6A) is the most abundant modification in eukaryotic messenger RNAs (mRNAs), and plays important roles in many bioprocesses. However, its functions in bladder cancer (BCa) remain elusive. Here, we discovered that methyltransferase-like 3 (METTL3), a major RNA N 6 -adenosine methyltransferase, was significantly up-regulated in human BCa. Knockdown of METTL3 drastically reduced BCa cell proliferation, invasion, and survival in vitro and tumorigenicity in vivo. On the other hand, overexpression of METTL3 significantly promoted BCa cell growth and invasion. Through transcriptome sequencing, m 6 A sequencing and m 6 A methylated RNA immuno-precipitation quantitative reverse-transcription polymerase chain reaction, we revealed the profile of METTL3-mediated m 6 A modification in BCa cells for the first time. AF4/FMR2 family member 4 ( AFF4 ), two key regulators of NF-κB pathway ( IKBKB and RELA ) and MYC were further identified as direct targets of METTL3-mediated m 6 A modification. In addition, we showed that besides NF-κB, AFF4 binds to the promoter of MYC and promotes its expression, implying a novel multilevel regulatory network downstream of METTL3. Our results uncovered an AFF4/NF-κB/MYC signaling network operated by METTL3-mediated m6A modification and provided insight into the mechanisms of BCa progression.
AbstractList	N6-methyladenosine (m6A) is the most abundant modification in eukaryotic messenger RNAs (mRNAs), and plays important roles in many bioprocesses. However, its functions in bladder cancer (BCa) remain elusive. Here, we discovered that methyltransferase-like 3 (METTL3), a major RNA N6-adenosine methyltransferase, was significantly up-regulated in human BCa. Knockdown of METTL3 drastically reduced BCa cell proliferation, invasion, and survival in vitro and tumorigenicity in vivo. On the other hand, overexpression of METTL3 significantly promoted BCa cell growth and invasion. Through transcriptome sequencing, m6A sequencing and m6A methylated RNA immuno-precipitation quantitative reverse-transcription polymerase chain reaction, we revealed the profile of METTL3-mediated m6A modification in BCa cells for the first time. AF4/FMR2 family member 4 (AFF4), two key regulators of NF-κB pathway (IKBKB and RELA) and MYC were further identified as direct targets of METTL3-mediated m6A modification. In addition, we showed that besides NF-κB, AFF4 binds to the promoter of MYC and promotes its expression, implying a novel multilevel regulatory network downstream of METTL3. Our results uncovered an AFF4/NF-κB/MYC signaling network operated by METTL3-mediated m6A modification and provided insight into the mechanisms of BCa progression. N 6 -methyladenosine (m6A) is the most abundant modification in eukaryotic messenger RNAs (mRNAs), and plays important roles in many bioprocesses. However, its functions in bladder cancer (BCa) remain elusive. Here, we discovered that methyltransferase-like 3 (METTL3), a major RNA N 6 -adenosine methyltransferase, was significantly up-regulated in human BCa. Knockdown of METTL3 drastically reduced BCa cell proliferation, invasion, and survival in vitro and tumorigenicity in vivo. On the other hand, overexpression of METTL3 significantly promoted BCa cell growth and invasion. Through transcriptome sequencing, m 6 A sequencing and m 6 A methylated RNA immuno-precipitation quantitative reverse-transcription polymerase chain reaction, we revealed the profile of METTL3-mediated m 6 A modification in BCa cells for the first time. AF4/FMR2 family member 4 ( AFF4 ), two key regulators of NF-κB pathway ( IKBKB and RELA ) and MYC were further identified as direct targets of METTL3-mediated m 6 A modification. In addition, we showed that besides NF-κB, AFF4 binds to the promoter of MYC and promotes its expression, implying a novel multilevel regulatory network downstream of METTL3. Our results uncovered an AFF4/NF-κB/MYC signaling network operated by METTL3-mediated m6A modification and provided insight into the mechanisms of BCa progression. N6-methyladenosine (m6A) is the most abundant modification in eukaryotic messenger RNAs (mRNAs), and plays important roles in many bioprocesses. However, its functions in bladder cancer (BCa) remain elusive. Here, we discovered that methyltransferase-like 3 (METTL3), a major RNA N6-adenosine methyltransferase, was significantly up-regulated in human BCa. Knockdown of METTL3 drastically reduced BCa cell proliferation, invasion, and survival in vitro and tumorigenicity in vivo. On the other hand, overexpression of METTL3 significantly promoted BCa cell growth and invasion. Through transcriptome sequencing, m6A sequencing and m6A methylated RNA immuno-precipitation quantitative reverse-transcription polymerase chain reaction, we revealed the profile of METTL3-mediated m6A modification in BCa cells for the first time. AF4/FMR2 family member 4 (AFF4), two key regulators of NF-κB pathway (IKBKB and RELA) and MYC were further identified as direct targets of METTL3-mediated m6A modification. In addition, we showed that besides NF-κB, AFF4 binds to the promoter of MYC and promotes its expression, implying a novel multilevel regulatory network downstream of METTL3. Our results uncovered an AFF4/NF-κB/MYC signaling network operated by METTL3-mediated m6A modification and provided insight into the mechanisms of BCa progression.N6-methyladenosine (m6A) is the most abundant modification in eukaryotic messenger RNAs (mRNAs), and plays important roles in many bioprocesses. However, its functions in bladder cancer (BCa) remain elusive. Here, we discovered that methyltransferase-like 3 (METTL3), a major RNA N6-adenosine methyltransferase, was significantly up-regulated in human BCa. Knockdown of METTL3 drastically reduced BCa cell proliferation, invasion, and survival in vitro and tumorigenicity in vivo. On the other hand, overexpression of METTL3 significantly promoted BCa cell growth and invasion. Through transcriptome sequencing, m6A sequencing and m6A methylated RNA immuno-precipitation quantitative reverse-transcription polymerase chain reaction, we revealed the profile of METTL3-mediated m6A modification in BCa cells for the first time. AF4/FMR2 family member 4 (AFF4), two key regulators of NF-κB pathway (IKBKB and RELA) and MYC were further identified as direct targets of METTL3-mediated m6A modification. In addition, we showed that besides NF-κB, AFF4 binds to the promoter of MYC and promotes its expression, implying a novel multilevel regulatory network downstream of METTL3. Our results uncovered an AFF4/NF-κB/MYC signaling network operated by METTL3-mediated m6A modification and provided insight into the mechanisms of BCa progression.
Author	Liang, Yu Gao, Qian Sheng, Lu Yuan, Quan Xiong, Qiuchan Zhang, Xiuhong Zhang, Yingyin Wu, Mingqing Zhu, Fengyu Li, Yang Zhang, Haojie Cheng, Maosheng
Author_xml	– sequence: 1 givenname: Maosheng surname: Cheng fullname: Cheng, Maosheng organization: Department of Genetics, School of Life Science, Anhui Medical University – sequence: 2 givenname: Lu surname: Sheng fullname: Sheng, Lu organization: Department of Urology, Huadong Hospital, Fudan University – sequence: 3 givenname: Qian surname: Gao fullname: Gao, Qian organization: Department of Genetics, School of Life Science, Anhui Medical University – sequence: 4 givenname: Qiuchan surname: Xiong fullname: Xiong, Qiuchan organization: State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University – sequence: 5 givenname: Haojie surname: Zhang fullname: Zhang, Haojie organization: Department of Urology, Huadong Hospital, Fudan University – sequence: 6 givenname: Mingqing surname: Wu fullname: Wu, Mingqing organization: Department of Genetics, School of Life Science, Anhui Medical University – sequence: 7 givenname: Yu surname: Liang fullname: Liang, Yu organization: Department of Genetics, School of Life Science, Anhui Medical University – sequence: 8 givenname: Fengyu surname: Zhu fullname: Zhu, Fengyu organization: Department of Genetics, School of Life Science, Anhui Medical University – sequence: 9 givenname: Yingyin surname: Zhang fullname: Zhang, Yingyin organization: Department of Genetics, School of Life Science, Anhui Medical University – sequence: 10 givenname: Xiuhong surname: Zhang fullname: Zhang, Xiuhong organization: Department of Genetics, School of Life Science, Anhui Medical University – sequence: 11 givenname: Quan surname: Yuan fullname: Yuan, Quan organization: State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University – sequence: 12 givenname: Yang orcidid: 0000-0002-9725-8774 surname: Li fullname: Li, Yang email: liyang@ahmu.edu.cn organization: Department of Genetics, School of Life Science, Anhui Medical University
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Snippet	N 6 -methyladenosine (m6A) is the most abundant modification in eukaryotic messenger RNAs (mRNAs), and plays important roles in many bioprocesses. However, its... N6-methyladenosine (m6A) is the most abundant modification in eukaryotic messenger RNAs (mRNAs), and plays important roles in many bioprocesses. However, its...
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SubjectTerms	13/31 13/89 13/95 38/39 45/91 631/208/176 631/67/589/1336 64/60 96/63 Adenosine Apoptosis Bladder cancer Cell Biology Cell growth Cell proliferation Cell survival DNA-directed RNA polymerase Gene expression Human Genetics Internal Medicine Medicine Medicine & Public Health Myc protein N6-methyladenosine NF-κB protein Oncology Polymerase chain reaction Ribonucleic acid RNA Tumorigenicity
Title	The m6A methyltransferase METTL3 promotes bladder cancer progression via AFF4/NF-κB/MYC signaling network
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