&lt;p&gt;m&lt;sup&gt;6&lt;/sup&gt;A methyltransferase METTL3 suppresses colorectal cancer proliferation and migration through p38/ERK pathways&lt;/p&gt;

Deng, Ruijie; Cheng, Yi‐Kan; Ye, Shubiao; Zhang, Jianwei; Huang, Ruxun; Li, Peisi; Liu, Huashan; Deng, Qi‐Ling; Wu, Xianrui; Lan, Ping; Deng, Yanhong

doi:10.2147/ott.s201052

Cited by 139 publications

(128 citation statements)

References 19 publications

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“…Frontiers in Oncology | www.frontiersin.org colorectal cancer (26). Negative expression of METTL3 was significantly correlated with larger tumor size and metastasis.…”

Section: Mettl3 In Colorectal Cancermentioning

confidence: 92%

“…In contrast, Deng et al showed that high expression of METTL3 was significantly associated with longer survival time and METTL3 played a tumor-suppressive role in colorectal cancer (26).…”

Section: Introductionmentioning

confidence: 91%

“…Negative expression of METTL3 was significantly correlated with larger tumor size and metastasis. Multivariate analysis indicated that METTL3 expression status is an independent prognostic factor for DFS (26). In addition, knockdown of METTL3 promoted tumor proliferation and metastasis.…”

Section: Mettl3 In Colorectal Cancermentioning

confidence: 96%

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Multiple Functions and Mechanisms Underlying the Role of METTL3 in Human Cancers

et al. 2019

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Methyltransferase-like 3 (METTL3), a predominantly catalytic enzyme in the N 6 -methyladenosine (m 6 A) methyltransferase system, is dysregulated and plays a dual role (oncogene or tumor suppressor) in different human cancers. The expression and pro-or anticancer role of METTL3 in different cancers remain controversial. METTL3 is implicated in many aspects of tumor progression, including tumorigenesis, proliferation, invasion, migration, cell cycle, differentiation, and viability. Most underlying mechanisms involve multiple signaling pathways that rely on m 6 A-dependent modification. However, METTL3 can also modulate the cancer process by directly promoting the translation of oncogenes via interaction with the translation initiation machinery through recruitment of eukaryotic translation initiation factor 3 subunit h (eIF3h). In this review, we summarized the current evidence on METTL3 in diverse human malignancies and its potential as a prognostic/ therapeutic target.

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“…Frontiers in Oncology | www.frontiersin.org colorectal cancer (26). Negative expression of METTL3 was significantly correlated with larger tumor size and metastasis.…”

Section: Mettl3 In Colorectal Cancermentioning

confidence: 92%

“…In contrast, Deng et al showed that high expression of METTL3 was significantly associated with longer survival time and METTL3 played a tumor-suppressive role in colorectal cancer (26).…”

Section: Introductionmentioning

confidence: 91%

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Multiple Functions and Mechanisms Underlying the Role of METTL3 in Human Cancers

et al. 2019

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“…In CRC, a recent research has verified that METTL3 could promote cell self‐renewal, stem cell frequency and migration through an m6A‐IGF2BP2‐dependent mechanism . However, another study showed that METTL3 could suppress colorectal cancer proliferation and migration through p38/ERK pathways . Therefore, the role of METTL3 in CRC might be controversial and need to be further explored.…”

Section: Introductionmentioning

confidence: 99%

“…37 However, another study showed that METTL3 could suppress colorectal cancer proliferation and migration through p38/ERK pathways. 38 Therefore, the role of METTL3 in CRC might be controversial and need to be further explored. In our present study, we confirmed that METTL3 could promote CRC cells proliferation and revealed a new mechanism by directly regulating cyclin proteins in an m6A-dependent manner.…”

Section: Introductionmentioning

confidence: 99%

Methyltransferase like 3 promotes colorectal cancer proliferation by stabilizing CCNE1 mRNA in an m6A‐dependent manner

Zhu

et al. 2020

J Cellular Molecular Medi

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m6A modification is the most prevalent RNA modification in eukaryotes. As the critical N6‐methyladenosine (m6A) methyltransferase, the roles of methyltransferase like 3 (METTL3) in colorectal cancer (CRC) are controversial. Here, we confirmed that METTL3, a critical m6A methyltransferase, could facilitate CRC progression in vitro and in vivo. Further, we found METTL3 promoted CRC cell proliferation by methylating the m6A site in 3′‐untranslated region (UTR) of CCNE1 mRNA to stabilize it. Moreover, we found butyrate, a classical intestinal microbial metabolite, could down‐regulate the expression of METTL3 and related cyclin E1 to inhibit CRC development. METTL3 promotes CRC proliferation by stabilizing CCNE1 mRNA in an m6A‐dependent manner, representing a promising therapeutic strategy for the treatment of CRC.

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METTL3/YTHDF2 m6A axis accelerates colorectal carcinogenesis through epigenetically suppressing YPEL5

Zhou

Tang

Xu³

et al. 2021

Molecular Oncology

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N6-methyladenosine (m6A) has emerged as the most prevalent post-transcriptional modification on mRNA that contributes prominently to tumorigenesis. However, the specific function of m6A methyltransferase methyltransferase-like 3 (METTL3) in colorectal cancer (CRC) remains elusive. Herein, we explored the biological function of METTL3 in CRC progression. Clinically, METTL3 was frequently upregulated in CRC tissues, cell lines, and plasma samples and its high expression predicted poor prognosis of CRC patients. Functionally, knockdown of METTL3 significantly repressed CRC cell proliferation and migration in vitro, while its overexpression accelerated CRC tumor formation and metastasis both in vitro and in vivo. Mechanistically, METTL3 epigenetically repressed YPEL5 in an m6A-YTHDF2-dependent manner by targeting the m6A site in the coding sequence region of the YPEL5 transcript. Moreover, overexpression of YPEL5 significantly reduced CCNB1 and PCNA expression. Collectively, we identified the pivotal role of METTL3-catalyzed m6A modification in CRC tumorigenesis, wherein it facilitates CRC tumor growth and metastasis through suppressing YPEL5 expression in an m6A-YTHDF2-dependent manner, suggesting a promising strategy for the diagnosis and therapy of CRC.

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<p>m<sup>6</sup>A methyltransferase METTL3 suppresses colorectal cancer proliferation and migration through p38/ERK pathways</p>

Cited by 139 publications

References 19 publications

Multiple Functions and Mechanisms Underlying the Role of METTL3 in Human Cancers

Multiple Functions and Mechanisms Underlying the Role of METTL3 in Human Cancers

Methyltransferase like 3 promotes colorectal cancer proliferation by stabilizing CCNE1 mRNA in an m6A‐dependent manner

METTL3/YTHDF2 m6A axis accelerates colorectal carcinogenesis through epigenetically suppressing YPEL5

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