YTHDF2 inhibit the tumorigenicity of endometrial cancer via downregulating the expression of IRS1 methylated with m<sup>6</sup>A

Li, Hong; Pu, Xiaowen; Gan, Haili; Weng, Lichun; Zheng, Qi-Teng

doi:10.7150/jca.54527

Cited by 15 publications

(12 citation statements)

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“…But YTHDF2 was identified to inhibit the proliferation and invasion of EC cell lines. Mechanistically, the m6A reader YTHDF2 bind the methylation sites of target transcripts Insulin Receptor Substrate 1 (IRS1) and promoted IRS1 mRNA degradation, consequently inhibiting the expression of IRS1 and inhibiting IRS1/AKT signaling pathway, finally inhibit the tumorigenicity of EC [89]. IRS1 plays a key role in cancer cell proliferation and mediates the resistance to anticancer drugs [90].…”

Section: Endometrial Cancermentioning

confidence: 99%

Role of m6A modification in female infertility and reproductive system diseases

Chen

Fang

et al. 2022

Int. J. Biol. Sci.

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Gamete abnormalities and reproductive system tumors have become a dominant cause of infertility, troubling people globally. In recent years, increasing evidence emerged and found that N6-methyladenosine (m6A) played a leading role in reproduction. The biological effects of m6A modification are dynamically and reversibly regulated by methyltransferases (writers), WTAP, METTL3, METTL14 and KIAA1429, demethylases (erasers), FTO and ALKBH5, and m6A binding proteins (readers), including YTH domain. In this review, we highlight the change of m6A modification in abnormal oogenesis, female reproductive system diseases including reproductive system tumors, adenomyosis, endometriosis, premature ovarian failure and polycystic ovary syndrome. Moreover, we review some of the mechanisms and the specific modified genes that have been identified. Especially, with the underlying mechanisms being uncovered, m6A and its protein machineries are expected to be the markers and targets for the diagnosis and treatment of female reproductive dysfunction.

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Section: Endometrial Cancermentioning

confidence: 99%

Role of m6A modification in female infertility and reproductive system diseases

Chen

Fang

et al. 2022

Int. J. Biol. Sci.

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“…It indicates that the upregulation of these protein may inhibit antitumor immune responses in HCC. In fact, previous studies have demonstrated their oncogenic and antitumor immunosuppressive roles ( Bouameur et al, 2014 ; Jinesh et al, 2017 ; Wang et al, 2020 ; Hong et al, 2021 ).…”

Section: Resultsmentioning

confidence: 99%

Identifying tumor immunity-associated molecular features in liver hepatocellular carcinoma by multi-omics analysis

Shen

Yin

Qian

et al. 2022

Front. Mol. Biosci.

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Background: Although current immunotherapies have achieved some successes for hepatocellular carcinoma (HCC) patients, their benefits are limited for most HCC patients. Therefore, the identification of biomarkers for promoting immunotherapeutic responses in HCC is urgently needed.Methods: Using the TCGA HCC cohort, we investigated correlations of various molecular features with antitumor immune signatures (CD8+ T cell infiltration and cytolytic activity) and an immunosuppressive signature (PD-L1 expression) in HCC. These molecular features included mRNAs, microRNAs (miRNAs), long non-coding RNAs (lncRNAs), proteins, and pathways.Results: We found that the mutations of several oncogenes and tumor suppressor genes significantly correlated with reduced antitumor immune signatures, including TTN, CTNNB1, RB1, ZFHX4, and TP53. It indicates that these genes’ mutations may inhibit antitumor immune responses in HCC. Four proteins (Syk, Lck, STAT5, and Caspase-7) had significant positive expression correlations with CD8+ T cell enrichment, cytolytic activity, and PD-L1 expression in HCC. It suggests that these proteins’ expression could be useful biomarkers for the response to immune checkpoint inhibitors Similiarly, we identified other types of biomarkers potentially useful for predicting the response to ICIs, including miRNAs (hsa-miR-511-5p, 150-3p, 342-3p, 181a-3p, 625-5p, 4772-3p, 155-3p, 142-5p, 142-3p, 155-5p, 625-3p, 1976, 7702), many lncRNAs, and pathways (apoptosis, cytokine-cytokine receptor interaction, Jak-STAT signaling, MAPK signaling, PI3K-AKT signaling, HIF-1 signaling, ECM receptor interaction, focal adhesion, and estrogen signaling). Further, tumor mutation burden showed no significant correlation with antitumor immunity, while tumor aneuploidy levels showed a significant negative correlation with antitumor immunity.Conclusion: The molecular features significantly associated with HCC immunity could be predictive biomarkers for immunotherapeutic responses in HCC patients. They could also be potential intervention targets for boosting antitumor immunity and immunotherapeutic responses in HCC.

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“…YTHDF2 was significantly upregulated in EC. According to Hong et al ( 119 ), YTHDF2 knockdown markedly accelerated endometrial cell proliferation, migration and invasion. Conversely, overexpression of YTHDF2 exerted a significant inhibitory role, indicating that YTHDF2 may inhibit the activity of EC cells.…”

Section: M6a and Ecmentioning

confidence: 94%

RNA m6A methylation regulators in endometrial cancer (Review)

Shen

Guo

et al. 2022

Int J Oncol

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As one of the three major malignant tumor types of the female reproductive system, endometrial cancer (EC) is the most prevalent gynecologic cancer in developed countries. In recent years, the incidence of EC has increased worldwide, threatening the health and well-being of women. Recent research has indicated that the expression of multiple N6-methyladenosine (m6A) regulators is up-or downregulated in EC and that abnormalities in m6A methylation and the expression of associated regulators are critical to the pathogenesis and progression of EC. m6A is the most abundant internal modification of mRNA. Several studies have demonstrated a close association between the development and progression of malignant tumors and the epigenetic phenomenon of m6A methylation. In the present study, the current status of research on m6A methylation in EC was reviewed. The mechanisms of methyltransferase, demethylase and m6A binding protein in regulating the development and progression of EC by modifying mRNA were introduced. The related research results will provide novel methods and approaches for the prevention and treatment of EC.

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YTHDF2 inhibit the tumorigenicity of endometrial cancer via downregulating the expression of IRS1 methylated with m⁶A

Cited by 15 publications

References 0 publications

Role of m6A modification in female infertility and reproductive system diseases

Role of m6A modification in female infertility and reproductive system diseases

Identifying tumor immunity-associated molecular features in liver hepatocellular carcinoma by multi-omics analysis

RNA m6A methylation regulators in endometrial cancer (Review)

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YTHDF2 inhibit the tumorigenicity of endometrial cancer via downregulating the expression of IRS1 methylated with m6A

Cited by 15 publications

References 0 publications

Role of m6A modification in female infertility and reproductive system diseases

Role of m6A modification in female infertility and reproductive system diseases

Identifying tumor immunity-associated molecular features in liver hepatocellular carcinoma by multi-omics analysis

RNA m6A methylation regulators in endometrial cancer (Review)

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YTHDF2 inhibit the tumorigenicity of endometrial cancer via downregulating the expression of IRS1 methylated with m⁶A