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Dysregulated N6‐methyladenosine methylation writer METTL3 contributes to the proliferation and migration of gastric cancer
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| Zeitschriftentitel: | Journal of Cellular Physiology |
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| Personen und Körperschaften: | , , , , , , , , , , |
| In: | Journal of Cellular Physiology, 235, 2020, 1, S. 548-562 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Wiley
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| Schlagwörter: |
| author_facet |
Liu, Tong Yang, Sheng Sui, Jing Xu, Si‐Yi Cheng, Yan‐ping Shen, Bo Zhang, Yan Zhang, Xiao‐mei Yin, Li‐hong Pu, Yue‐pu Liang, Ge‐yu Liu, Tong Yang, Sheng Sui, Jing Xu, Si‐Yi Cheng, Yan‐ping Shen, Bo Zhang, Yan Zhang, Xiao‐mei Yin, Li‐hong Pu, Yue‐pu Liang, Ge‐yu |
|---|---|
| author |
Liu, Tong Yang, Sheng Sui, Jing Xu, Si‐Yi Cheng, Yan‐ping Shen, Bo Zhang, Yan Zhang, Xiao‐mei Yin, Li‐hong Pu, Yue‐pu Liang, Ge‐yu |
| spellingShingle |
Liu, Tong Yang, Sheng Sui, Jing Xu, Si‐Yi Cheng, Yan‐ping Shen, Bo Zhang, Yan Zhang, Xiao‐mei Yin, Li‐hong Pu, Yue‐pu Liang, Ge‐yu Journal of Cellular Physiology Dysregulated N6‐methyladenosine methylation writer METTL3 contributes to the proliferation and migration of gastric cancer Cell Biology Clinical Biochemistry Physiology |
| author_sort |
liu, tong |
| spelling |
Liu, Tong Yang, Sheng Sui, Jing Xu, Si‐Yi Cheng, Yan‐ping Shen, Bo Zhang, Yan Zhang, Xiao‐mei Yin, Li‐hong Pu, Yue‐pu Liang, Ge‐yu 0021-9541 1097-4652 Wiley Cell Biology Clinical Biochemistry Physiology http://dx.doi.org/10.1002/jcp.28994 <jats:title>Abstract</jats:title><jats:p>Accumulating evidence implies that N6‐methyladenosine (m6A) methylation participated in the tumorigenesis of gastric cancer (GC). Here we synthetically analyzing the prognostic value and expression profile of seven m6A methylation‐relevant genes through silico analysis of sequencing data downloaded from The Cancer Genome Atlas, Kaplan–Meier plotter, and Gene Expression Omnibus database. We explored the methyltransferase‐like 3 (METTL3) expression in GC cell line and tumor tissues by reverse transcription quantitative polymerase chain reaction and western blot analysis. The m6A methylation status of total RNA was measured by m6A RNA methylation quantification kit. Small interfering RNA was used to establish METTL3 knockdown cell lines. We also measure the proliferation and migration capability GC cell. Furthermore, we detect the epithelial cell mesenchymal transition marker and m6A methylation level after METTL3 knock down. Our result revealed that METTL3 was significantly increased in GC tissues compared with control in big crowd data sets. Survival analysis showed that METTL3 serve as a poor prognostic factor for GC patients. The expression level of METTL3 gradually increased with the progress of tumor stage and grade. GFI1 is an important transcription factor associated with METTL3. We verified the up‐trend of METTL3 in messenger RNA and protein expression and observed a significant increase in the m6A methylation status of total RNA in the GC cells and tissues. METTL3 knockdown inhibited total RNA m6A methylation level, as well as cell proliferation and migration capacity. Moreover, METTL3 knockdown decreased α‐smooth muscle actin. Taken together, our finding revealed that m6A methylation writer METTL3 serve as an oncogene in tumorigenesis of GC.</jats:p> Dysregulated N6‐methyladenosine methylation writer METTL3 contributes to the proliferation and migration of gastric cancer Journal of Cellular Physiology |
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| title |
Dysregulated N6‐methyladenosine methylation writer METTL3 contributes to the proliferation and migration of gastric cancer |
| title_unstemmed |
Dysregulated N6‐methyladenosine methylation writer METTL3 contributes to the proliferation and migration of gastric cancer |
| title_full |
Dysregulated N6‐methyladenosine methylation writer METTL3 contributes to the proliferation and migration of gastric cancer |
| title_fullStr |
Dysregulated N6‐methyladenosine methylation writer METTL3 contributes to the proliferation and migration of gastric cancer |
| title_full_unstemmed |
Dysregulated N6‐methyladenosine methylation writer METTL3 contributes to the proliferation and migration of gastric cancer |
| title_short |
Dysregulated N6‐methyladenosine methylation writer METTL3 contributes to the proliferation and migration of gastric cancer |
| title_sort |
dysregulated n6‐methyladenosine methylation writer mettl3 contributes to the proliferation and migration of gastric cancer |
| topic |
Cell Biology Clinical Biochemistry Physiology |
| url |
http://dx.doi.org/10.1002/jcp.28994 |
| publishDate |
2020 |
| physical |
548-562 |
| description |
<jats:title>Abstract</jats:title><jats:p>Accumulating evidence implies that N6‐methyladenosine (m6A) methylation participated in the tumorigenesis of gastric cancer (GC). Here we synthetically analyzing the prognostic value and expression profile of seven m6A methylation‐relevant genes through silico analysis of sequencing data downloaded from The Cancer Genome Atlas, Kaplan–Meier plotter, and Gene Expression Omnibus database. We explored the methyltransferase‐like 3 (METTL3) expression in GC cell line and tumor tissues by reverse transcription quantitative polymerase chain reaction and western blot analysis. The m6A methylation status of total RNA was measured by m6A RNA methylation quantification kit. Small interfering RNA was used to establish METTL3 knockdown cell lines. We also measure the proliferation and migration capability GC cell. Furthermore, we detect the epithelial cell mesenchymal transition marker and m6A methylation level after METTL3 knock down. Our result revealed that METTL3 was significantly increased in GC tissues compared with control in big crowd data sets. Survival analysis showed that METTL3 serve as a poor prognostic factor for GC patients. The expression level of METTL3 gradually increased with the progress of tumor stage and grade. GFI1 is an important transcription factor associated with METTL3. We verified the up‐trend of METTL3 in messenger RNA and protein expression and observed a significant increase in the m6A methylation status of total RNA in the GC cells and tissues. METTL3 knockdown inhibited total RNA m6A methylation level, as well as cell proliferation and migration capacity. Moreover, METTL3 knockdown decreased α‐smooth muscle actin. Taken together, our finding revealed that m6A methylation writer METTL3 serve as an oncogene in tumorigenesis of GC.</jats:p> |
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| author | Liu, Tong, Yang, Sheng, Sui, Jing, Xu, Si‐Yi, Cheng, Yan‐ping, Shen, Bo, Zhang, Yan, Zhang, Xiao‐mei, Yin, Li‐hong, Pu, Yue‐pu, Liang, Ge‐yu |
| author_facet | Liu, Tong, Yang, Sheng, Sui, Jing, Xu, Si‐Yi, Cheng, Yan‐ping, Shen, Bo, Zhang, Yan, Zhang, Xiao‐mei, Yin, Li‐hong, Pu, Yue‐pu, Liang, Ge‐yu, Liu, Tong, Yang, Sheng, Sui, Jing, Xu, Si‐Yi, Cheng, Yan‐ping, Shen, Bo, Zhang, Yan, Zhang, Xiao‐mei, Yin, Li‐hong, Pu, Yue‐pu, Liang, Ge‐yu |
| author_sort | liu, tong |
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| container_start_page | 548 |
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| description | <jats:title>Abstract</jats:title><jats:p>Accumulating evidence implies that N6‐methyladenosine (m6A) methylation participated in the tumorigenesis of gastric cancer (GC). Here we synthetically analyzing the prognostic value and expression profile of seven m6A methylation‐relevant genes through silico analysis of sequencing data downloaded from The Cancer Genome Atlas, Kaplan–Meier plotter, and Gene Expression Omnibus database. We explored the methyltransferase‐like 3 (METTL3) expression in GC cell line and tumor tissues by reverse transcription quantitative polymerase chain reaction and western blot analysis. The m6A methylation status of total RNA was measured by m6A RNA methylation quantification kit. Small interfering RNA was used to establish METTL3 knockdown cell lines. We also measure the proliferation and migration capability GC cell. Furthermore, we detect the epithelial cell mesenchymal transition marker and m6A methylation level after METTL3 knock down. Our result revealed that METTL3 was significantly increased in GC tissues compared with control in big crowd data sets. Survival analysis showed that METTL3 serve as a poor prognostic factor for GC patients. The expression level of METTL3 gradually increased with the progress of tumor stage and grade. GFI1 is an important transcription factor associated with METTL3. We verified the up‐trend of METTL3 in messenger RNA and protein expression and observed a significant increase in the m6A methylation status of total RNA in the GC cells and tissues. METTL3 knockdown inhibited total RNA m6A methylation level, as well as cell proliferation and migration capacity. Moreover, METTL3 knockdown decreased α‐smooth muscle actin. Taken together, our finding revealed that m6A methylation writer METTL3 serve as an oncogene in tumorigenesis of GC.</jats:p> |
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| institution | DE-15, DE-Pl11, DE-Rs1, DE-105, DE-14, DE-Ch1, DE-L229, DE-D275, DE-Bn3, DE-Brt1, DE-D161, DE-Gla1, DE-Zi4 |
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| spelling | Liu, Tong Yang, Sheng Sui, Jing Xu, Si‐Yi Cheng, Yan‐ping Shen, Bo Zhang, Yan Zhang, Xiao‐mei Yin, Li‐hong Pu, Yue‐pu Liang, Ge‐yu 0021-9541 1097-4652 Wiley Cell Biology Clinical Biochemistry Physiology http://dx.doi.org/10.1002/jcp.28994 <jats:title>Abstract</jats:title><jats:p>Accumulating evidence implies that N6‐methyladenosine (m6A) methylation participated in the tumorigenesis of gastric cancer (GC). Here we synthetically analyzing the prognostic value and expression profile of seven m6A methylation‐relevant genes through silico analysis of sequencing data downloaded from The Cancer Genome Atlas, Kaplan–Meier plotter, and Gene Expression Omnibus database. We explored the methyltransferase‐like 3 (METTL3) expression in GC cell line and tumor tissues by reverse transcription quantitative polymerase chain reaction and western blot analysis. The m6A methylation status of total RNA was measured by m6A RNA methylation quantification kit. Small interfering RNA was used to establish METTL3 knockdown cell lines. We also measure the proliferation and migration capability GC cell. Furthermore, we detect the epithelial cell mesenchymal transition marker and m6A methylation level after METTL3 knock down. Our result revealed that METTL3 was significantly increased in GC tissues compared with control in big crowd data sets. Survival analysis showed that METTL3 serve as a poor prognostic factor for GC patients. The expression level of METTL3 gradually increased with the progress of tumor stage and grade. GFI1 is an important transcription factor associated with METTL3. We verified the up‐trend of METTL3 in messenger RNA and protein expression and observed a significant increase in the m6A methylation status of total RNA in the GC cells and tissues. METTL3 knockdown inhibited total RNA m6A methylation level, as well as cell proliferation and migration capacity. Moreover, METTL3 knockdown decreased α‐smooth muscle actin. Taken together, our finding revealed that m6A methylation writer METTL3 serve as an oncogene in tumorigenesis of GC.</jats:p> Dysregulated N6‐methyladenosine methylation writer METTL3 contributes to the proliferation and migration of gastric cancer Journal of Cellular Physiology |
| spellingShingle | Liu, Tong, Yang, Sheng, Sui, Jing, Xu, Si‐Yi, Cheng, Yan‐ping, Shen, Bo, Zhang, Yan, Zhang, Xiao‐mei, Yin, Li‐hong, Pu, Yue‐pu, Liang, Ge‐yu, Journal of Cellular Physiology, Dysregulated N6‐methyladenosine methylation writer METTL3 contributes to the proliferation and migration of gastric cancer, Cell Biology, Clinical Biochemistry, Physiology |
| title | Dysregulated N6‐methyladenosine methylation writer METTL3 contributes to the proliferation and migration of gastric cancer |
| title_full | Dysregulated N6‐methyladenosine methylation writer METTL3 contributes to the proliferation and migration of gastric cancer |
| title_fullStr | Dysregulated N6‐methyladenosine methylation writer METTL3 contributes to the proliferation and migration of gastric cancer |
| title_full_unstemmed | Dysregulated N6‐methyladenosine methylation writer METTL3 contributes to the proliferation and migration of gastric cancer |
| title_short | Dysregulated N6‐methyladenosine methylation writer METTL3 contributes to the proliferation and migration of gastric cancer |
| title_sort | dysregulated n6‐methyladenosine methylation writer mettl3 contributes to the proliferation and migration of gastric cancer |
| title_unstemmed | Dysregulated N6‐methyladenosine methylation writer METTL3 contributes to the proliferation and migration of gastric cancer |
| topic | Cell Biology, Clinical Biochemistry, Physiology |
| url | http://dx.doi.org/10.1002/jcp.28994 |