The METTL3-m6A-YTHDC1-AMIGO2 axis contributes to cell proliferation and migration in esophageal squamous cell carcinoma

Qiu, Yue; Tian, Zhen; Miao, Ting-Yu; Shen, Lin; Chen, Jing; Li, Pei-Fen; Zhu, Zi-Xuan; Zhu, Zi-Fan; Wu, Wen-Juan; Xu, Xiao; Shen, Wei-Gan

doi:10.1016/j.gene.2024.148281

Cited by 2 publications

(1 citation statement)

References 36 publications

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“…Li et al ( 21 ) confirmed that METTL3 could prompt proliferation and metastasis of ESCC cells by mediating the collagen type XII α1 chain/MAPK signaling pathway. A previous study by the authors explored other underlying mechanisms of METTL3 regulating the biological behaviors of ESCC cells ( 22 ). First, the mRNA, protein and mRNA m 6 A modification levels of AMIGO2 were reduced by METTL3 knockdown.…”

Section: Amigo2 and Cancermentioning

confidence: 99%

Role of AMIGO2 in cancer progression: Novel insights (Review)

Tian,

Zhou,

Jiang

et al. 2024

Oncol Lett

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Adhesion molecule with IgG-like domain 2 (AMIGO2) is a novel scaffold protein initially identified in cerebellar granule neurons, and inhibits apoptosis of neurons. It is also widely expressed in various malignant tumors, including gastric cancer, colorectal carcinoma, ovarian cancer, prostate cancer and melanoma. During the past decades, it has been revealed that AMIGO2 can act as an oncogene, participating in tumor occurrence and development, for example by inhibiting apoptosis, accelerating cell proliferation, migration and adhesion, and promoting tumor metastasis and drug resistance. The present review discusses the recent advancements regarding AMIGO2 in the field of cancer, emphasizing its related molecular mechanisms to identify novel therapeutic strategies targeting AMIGO2 for cancer treatment in the future.

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Section: Amigo2 and Cancermentioning

confidence: 99%

Role of AMIGO2 in cancer progression: Novel insights (Review)

Tian,

Zhou,

Jiang

et al. 2024

Oncol Lett

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AP001885.4 promotes the proliferation of esophageal squamous cell carcinoma cells by histone lactylation- and NF-κB (p65)-dependent transcription activation and METTL3-mediated mRNA stability of c-myc

Fu,

Jiang,

Wang

et al. 2024

Animal Cells and Systems

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Esophageal squamous cell carcinoma (ESCC) is an aggressive malignant neoplasm, and up to now, the role of long non-coding RNA (lncRNA) AP001885.4 in cancer, including ESCC, is absolutely unclear. The GEPIA database was applied to identify differentially expressed and prognosis-associated genes in esophageal cancer (ESCA). CCK-8, colony formation, Western blot, and qRT-PCR methods were harnessed to investigate the role and mechanism of AP001885.4 in esophageal carcinogenesis. By analyzing TCGA data in the GEPIA database, two lncRNAs were selected. AP001885.4 was overexpressed and positively associated with the unfavorable outcome of ESCC patients, and LINC001786 was under-expressed and negatively linked with the poor prognosis. Knockdown of AP001885.4 suppressed the proliferation and colony formation of ESCC cells. Importantly, the silence of AP001885.4 downregulated c-myc. Mechanically, the knockdown of AP001885.4 reduced METTL3 expression and m6A modification in c-myc mRNA, and METTL3 positively regulated c-myc. Furthermore, the knockdown of AP001885.4 diminished histone lactylation and NF-κB (p65) expression, and the protein lactylation inhibitors (2-DG, 2-deoxy-D-glucose and oxamate) and the NF-κB inhibitor (JSH-23) also lessened c-myc expression. Consequently, our findings suggested that AP001885.4 promoted the proliferation of esophageal squamous cell carcinoma cells by histone lactylation- and NF-κB (p65)-dependent transcription activation and METTL3-mediated mRNA stability of c-myc.

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The METTL3-m6A-YTHDC1-AMIGO2 axis contributes to cell proliferation and migration in esophageal squamous cell carcinoma

Cited by 2 publications

References 36 publications

Role of AMIGO2 in cancer progression: Novel insights (Review)

Role of AMIGO2 in cancer progression: Novel insights (Review)

AP001885.4 promotes the proliferation of esophageal squamous cell carcinoma cells by histone lactylation- and NF-κB (p65)-dependent transcription activation and METTL3-mediated mRNA stability of c-myc

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