N6‐methyladenosine modification participates in neoplastic immunoregulation and tumorigenesis

Zhao, W.; Li, Jianjun; Ma, Qiang; Cai, Jijie; Li, Aixin; Wu, Weijun; Lv, Yun-Cheng; Cai, Manbo

doi:10.1002/jcp.30730

Cited by 9 publications

(5 citation statements)

References 74 publications

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“…N6-methyladenosine (m6A) is the most common modification in the mammalian RNA transcriptome and is broadly present in mRNAs and certain noncoding RNAs [ 41 ]. Recent studies have suggested that alterations in m6A modification patterns are deeply involved in tumorigenesis [ 42 ]. Methyltransferase-like 14 ( METTL14 ) is a key RNA methyltransferase involved in m6A modification.…”

Section: Discussionmentioning

confidence: 99%

Oncogenic Targets Regulated by Tumor-Suppressive miR-30c-1-3p and miR-30c-2-3p: TRIP13 Facilitates Cancer Cell Aggressiveness in Breast Cancer

Mitsueda,

Toda,

Shinden

et al. 2023

Cancers

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Accumulating evidence suggests that the miR-30 family act as critical players (tumor-suppressor or oncogenic) in a wide range of human cancers. Analysis of microRNA (miRNA) expression signatures and The Cancer Genome Atlas (TCGA) database revealed that that two passenger strand miRNAs, miR-30c-1-3p and miR-30c-2-3p, were downregulated in cancer tissues, and their low expression was closely associated with worse prognosis in patients with BrCa. Functional assays showed that miR-30c-1-3p and miR-30c-2-3p overexpression significantly inhibited cancer cell aggressiveness, suggesting these two miRNAs acted as tumor-suppressors in BrCa cells. Notably, involvement of passenger strands of miRNAs is a new concept of cancer research. Further analyses showed that seven genes (TRIP13, CCNB1, RAD51, PSPH, CENPN, KPNA2, and MXRA5) were putative targets of miR-30c-1-3p and miR-30c-2-3p in BrCa cells. Expression of seven genes were upregulated in BrCa tissues and predicted a worse prognosis of the patients. Among these genes, we focused on TRIP13 and investigated the functional significance of this gene in BrCa cells. Luciferase reporter assays showed that TRIP13 was directly regulated by these two miRNAs. TRIP13 knockdown using siRNA attenuated BrCa cell aggressiveness. Inactivation of TRIP13 using a specific inhibitor prevented the malignant transformation of BrCa cells. Exploring the molecular networks controlled by miRNAs, including passenger strands, will facilitate the identification of diagnostic markers and therapeutic target molecules in BrCa.

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Section: Discussionmentioning

confidence: 99%

Oncogenic Targets Regulated by Tumor-Suppressive miR-30c-1-3p and miR-30c-2-3p: TRIP13 Facilitates Cancer Cell Aggressiveness in Breast Cancer

Mitsueda,

Toda,

Shinden

et al. 2023

Cancers

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“…In atherosclerosis (AS), the activity of vascular endothelial cells could reflect cells’ metabolism and proliferation [ 17 – 19 ]. AS is a life-threatening vascular disease, and m 6 A modification level is dysregulated in its pathophysiologic processes of AS [ 20 , 21 ]. Here, we found that m 6 A writer KIAA1429 upregulated in ox-LDL-induced HUVECs.…”

Section: Discussionmentioning

confidence: 99%

m6A ‘writer’ KIAA1429 regulates the proliferation and migration of endothelial cells in atherosclerosis

2022

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Increasing evidences have illustrated the important role of N 6 -methyladenosine (m 6 A) in atherosclerosis (AS). However, the role of m 6 A modification in AS pathophysiological process is still unknown. Here, the present work tried to investigate the expression and function of m 6 A methyltransferase KIAA1429 in AS pathology and explored its undergoing m 6 A-dependent molecular mechanism. Results indicated that KIAA1429 remarkedly up-regulated in oxidative low-density lipoprotein (ox-LDL)-treated human umbilical vein endothelial cells (HUVECs). KIAA1429 over-expression inhibited the proliferation/migration in ox-LDL-treated HUVECs, while, KIAA1429 knockdown up-regulated the proliferation and migration. Mechanistically, via m 6 A modification sites binding, ROCK2 mRNA was post-transcriptionally upregulated by KIAA1429 in response to Actinomycin D. Collectively, our study demonstrated the regulation of KIAA1429 on ox-LDL-induced HUVECs via m 6 A/ROCK2 pathway. These findings provide new insights for m 6 A-mediated epigenetics in AS. Supplementary Information The online version contains supplementary material available at 10.1007/s12033-022-00614-w.

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“…m6A modifications were found to alters HCC progression by affecting immune cell recruitment and pro-tumor inflammation [10]. In addition, m6A modifications altered the proliferation and metastasis of gastric cancer by participating in the infiltration of immune cells and activation of immune pathways [11].…”

Section: Introductionmentioning

confidence: 99%

Comprehensive analysis of IGF2BP3 with expression features, prognosis, immune modulation and stemness in hepatocellular carcinoma and pan-cancer

Qin,

Jin,

et al. 2024

J. Cancer

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Insulin like growth factor 2 mRNA binding protein 3 (IGF2BP3) is a critical m6A reader. It encodes proteins that contain several KH domains, which are important in RNA binding, RNA synthesis and metabolism. Lots of researches have studied the malignant potential of m6A readers in tumors. However, the biological functional analysis of IGF2BP3 in hepatocellular carcinoma (HCC) and pan-cancer is not comprehensive. In this study, we used a bioinformatics approach to comprehensively analyze the significance of IGF2BP3 in HCC through analyzing its expression, mutation, prognosis, protein-protein interaction (PPI) network, functional enrichment, and the correlation with ferroptosis, stemness as well as immune modulation in HCC. IGF2BP3 presented a negative correlation with the ferroptosis molecule NFE2L2, and a positive correlation with the ferroptosis molecule SLC1A5 as well as the immune checkpoint HAVCR2. In addition, we also analyzed IGF2BP3 expression, prognosis and immune modulation in pan-cancer, revealing the prognostic value of IGF2BP3 in a variety of tumors. Finally, we verified the biological functions of IGF2BP3 in HCC through various experiments. The data showed that IGF2BP3 may enhance the proliferation, colony formation and invasion capacities of HCC cells, and IGF2BP3 is mainly positively correlated with the expression level of stemness marker SOX2. In conclusion, IGF2BP3 had a potential to be a new perspective biomarker in forecasting the immune response, ferroptosis, stemness and prognosis of HCC or even pan-cancer.

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N6‐methyladenosine modification participates in neoplastic immunoregulation and tumorigenesis

Cited by 9 publications

References 74 publications

Oncogenic Targets Regulated by Tumor-Suppressive miR-30c-1-3p and miR-30c-2-3p: TRIP13 Facilitates Cancer Cell Aggressiveness in Breast Cancer

Oncogenic Targets Regulated by Tumor-Suppressive miR-30c-1-3p and miR-30c-2-3p: TRIP13 Facilitates Cancer Cell Aggressiveness in Breast Cancer

m6A ‘writer’ KIAA1429 regulates the proliferation and migration of endothelial cells in atherosclerosis

Comprehensive analysis of IGF2BP3 with expression features, prognosis, immune modulation and stemness in hepatocellular carcinoma and pan-cancer

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