RNA Modifications Meet Tumors

Yang, Zhaohui; Zhang, Siyu; Xia, Tian; Yang, Fan; Shi, Ying; Zhang, Kaiwen; Xiong, Jiayan; Gu, Miao; You, Bo

doi:10.2147/cmar.s391067

Cited by 7 publications

(5 citation statements)

References 193 publications

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“…m 6 A modification plays a key role in the growth and metastasis of NPC tumors by regulating the immune microenvironment of tumor cells [ 29 ]. Therefore, m 6 A modification is considered an important RNA modification that runs through the whole process from transcription to translation regulation [ 31 ]. m 6 A modification can regulate the expression of downstream targets by maintaining the stability of coding and noncoding RNAs in NPC cells [ 30 , 32 ].…”

Section: Discussionmentioning

confidence: 99%

The m6A demethylases FTO and ALKBH5 aggravate the malignant progression of nasopharyngeal carcinoma by coregulating ARHGAP35

Yang,

Zhang,

Xiong

et al. 2024

Cell Death Discov.

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N6-methyladenosine (m6A) is an RNA modification that can be removed by demethylases [fat mass and obesity-associated protein (FTO) and AlkB homolog 5 (ALKBH5)], which regulate gene expression and cell function. We show that m6A levels and m6A demethylase levels are altered in nasopharyngeal carcinoma (NPC) tissues vs. normal tissues. High FTO and ALKBH5 predict a poor prognosis in NPC patients. Silencing FTO and ALKBH5 inhibited the malignant behavior of patient-derived NPC cells in a short time. However, as time progressed, the inhibitory effect of FTO or ALKBH5 was weakened, and the cosilencing of FTO and ALKBH5 maintained a better inhibitory effect. Combined transcriptome and m6A-seq analysis revealed a downstream target gene that was jointly regulated by FTO and ALKBH5 in NPC, and ARHGAP35 was chosen to do further study. The synergistic silencing of FTO and ALKBH5 increased the methylation level on the mRNA CDS of a new transcription factor (ARHGAP35) and positively regulate the protein coding capacity and mRNA stability of ARHGAP35, thus leading to increased expression of ARHGAP35 and inhibition of the malignant phenotype of tumor cells. Our study revealed that the growth and metastasis of NPC can be stably inhibited through synergistic silencing of the demethylases FTO and ALKBH5, which play a positive role in the treatment of NPC by regulating the downstream transcript ARHGAP35 and increasing its m6A level.

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Section: Discussionmentioning

confidence: 99%

The m6A demethylases FTO and ALKBH5 aggravate the malignant progression of nasopharyngeal carcinoma by coregulating ARHGAP35

Yang,

Zhang,

Xiong

et al. 2024

Cell Death Discov.

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“…Clinical information, including age, sex, and TNM stage was collected. In total, 29 m7G-related regulatory genes were identified by screening the Gene Set Enrichment Analysis database (GSEA; https://www.gsea-msigdb.org/gsea/index.jsp) and by performing literature searches (18)(19)(20)(21)(22)(23). In the BLCA cohort from TCGA, the expression data of these 29 m7G-related genes were extracted for subsequent analysis.…”

Section: R Na-sequencing T Ra Nscriptomic Data Collectionmentioning

confidence: 99%

Expression pattern, tumor immune landscape, and prognostic value of N7‑methylguanosine regulators in bladder urothelial carcinoma

et al. 2023

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N7-Methylguanosine (m7G) modification is important in post-transcriptional regulation. dysregulation of m7G RNA modification has been reported to be markedly associated with cancer. However, its importance in bladder urothelial carcinoma (BLCA) remains poorly characterized. The present study systematically analyzed mRNA gene expression data and clinical information from The Cancer Genome Atlas and further constructed robust risk signatures for the four regulators of m7G RNA modification (nudix hydrolase 11, gem nuclear organelle-associated protein 5, eukaryotic translation initiation factor 3 subunit D and cytoplasmic FMR1 interacting protein 1). The differential expression and cell function of m7G-related genes in bladder cancer cells were verified by reverse transcription-quantitative PCR, Cell Counting Kit-8 and colony formation assays. The four-gene-based model could accurately predict the prognosis of BLCA. Nomogram-based clinical decisions had a higher net benefit compared with that of individual predictors. Through immune infiltration analysis, it was found that immune cell infiltration affected the prognosis of patients with BLCA. Finally, the present study identified potential therapeutics that differ between high and low-risk groups based on four genes. In summary, the current findings revealed an essential role for m7G RNA modification regulators in BLCA, and developed risk signatures as promising prognostic markers in patients with BLCA.

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“…For example, it contributes to tumorigenesis by perturbing the stability of relevant RNA molecules and further fuels cancer progression by modulating the translation of target mRNA, among other mechanisms. It also has implications for the diagnosis, prognosis, and treatment of cancer patients [ 14 ]. Recent research has increasingly demonstrated the involvement of “writer,” “reader,” and “eraser” regulators of m1A in regulating cancer occurrence and progression [ 3 , 5 , 10 ].…”

Section: Introductionmentioning

confidence: 99%

Research progress of N1-methyladenosine RNA modification in cancer

Liu,

Zhang,

Gao

et al. 2024

Cell Commun Signal

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N1-methyladenosine (m1A) is a post-transcriptionally modified RNA molecule that plays a pivotal role in the regulation of various biological functions and activities. Especially in cancer cell invasion, proliferation and cell cycle regulation. Over recent years, there has been a burgeoning interest in investigating the m1A modification of RNA. Most studies have focused on the regulation of m1A in cancer enrichment areas and different regions. This review provides a comprehensive overview of the methodologies employed for the detection of m1A modification. Furthermore, this review delves into the key players in m1A modification, known as the “writers,” “erasers,” and “readers.” m1A modification is modified by the m1A methyltransferases, or writers, such as TRMT6, TRMT61A, TRMT61B, TRMT10C, NML, and, removed by the demethylases, or erasers, including FTO and ALKBH1, ALKBH3. It is recognized by m1A-binding proteins YTHDF1, TYHDF2, TYHDF3, and TYHDC1, also known as “readers”. Additionally, we explore the intricate relationship between m1A modification and its regulators and their implications for the development and progression of specific types of cancer, we discuss how m1A modification can potentially facilitate the discovery of novel approaches for cancer diagnosis, treatment, and prognosis. Our summary of m1A methylated adenosine modification detection methods and regulatory mechanisms in various cancers provides useful insights for cancer diagnosis, treatment, and prognosis.

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RNA Modifications Meet Tumors

Cited by 7 publications

References 193 publications

The m6A demethylases FTO and ALKBH5 aggravate the malignant progression of nasopharyngeal carcinoma by coregulating ARHGAP35

The m6A demethylases FTO and ALKBH5 aggravate the malignant progression of nasopharyngeal carcinoma by coregulating ARHGAP35

Expression pattern, tumor immune landscape, and prognostic value of N7‑methylguanosine regulators in bladder urothelial carcinoma

Research progress of N1-methyladenosine RNA modification in cancer

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