Post-transcriptional regulation of tumor suppressor gene lncRNA CARMN via m6A modification and miRNA regulation in cervical cancer

Yu, Bingjia; Li, Xiuting; Yan, Wenjing; Ding, Bo; Zhang, X.-R.; Shen, Siyuan; Xie, Shuqian; Hu, Jing; Liu, Haohan; Xue, Chen; Nie, Yan; Liu, Fengying; Zhang, Yan; Wang, Shizhi

doi:10.1007/s00432-023-04893-x

Cited by 10 publications

(2 citation statements)

References 41 publications

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“…YTHDF2 was shown to recognize m6A modification in LINC02038 and trigger its degradation [ 38 ]. Consistently, Ye et al reported that YTHDF2 sensed m 6 A modifications in the tumor-suppressive lncRNA CARMN and enabled m 6 A-caused breakdown of this lncRNA in cervical cancer [ 41 ]. Another study reported that METTL3-mediated m6A modification could stabilize LINC00839, an oncogenic lncRNA, in a YTHDF2-dependent manner.…”

Section: Discussionmentioning

confidence: 84%

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METTL3-mediated deficiency of lncRNA HAR1A drives non-small cell lung cancer growth and metastasis by promoting ANXA2 stabilization

Ling,

Qi,

Cao

et al. 2024

Cell Death Discov.

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We previously reported lncRNA HAR1A as a tumor suppressor in non-small cell lung cancer (NSCLC). However, the delicate working mechanisms of this lncRNA remain obscure. Herein, we demonstrated that the ectopic expression of HAR1A inhibited the proliferation, epithelial-mesenchymal transition (EMT), migration, and invasion of NSCLC cells and enhanced paclitaxel (PTX) sensitivity in vitro and in vivo. We identified the oncogenic protein annexin 2 (ANXA2) as a potential interacting patterner of HAR1A. HAR1A overexpression enhanced ANXA2 ubiquitination and accelerated its degradation via the ubiquitin–proteasome pathway. We further uncovered that HAR1A promoted the interaction between E3 ubiquitin ligase TRIM65 and ANXA2. Moreover, the ANXA2 plasmid transfection could reverse HAR1A overexpression-induced decreases in proliferation, migration, and invasion of NSCLC cells and the activity of the NF-κB signaling pathway. Finally, we found that HAR1A loss in NSCLC might be attributed to the upregulated METTL3. The m6A modification levels of HAR1A were increased in cancer cells, while YTHDF2 was responsible for recognizing m6A modification in the HAR1A, leading to the disintegration of this lncRNA. In conclusion, we found that METTL3-mediated m6A modification decreased HAR1A in NSCLC. HAR1A deficiency, in turn, stimulated tumor growth and metastasis by activating the ANXA2/p65 axis.

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Section: Discussionmentioning

confidence: 84%

“…Apart from mRNAs, lncRNAs can also be regulated by m 6 A modification. Many studies demonstrated that YTHDF2 mediated the stability of m 6 A-modified RNAs in a cotext-dependent manner [ 38 – 41 ]. LINC02038, subjected to METTL3-mediated m6A modification, was a tumor suppressor and decreased in CRC.…”

Section: Discussionmentioning

confidence: 99%

METTL3-mediated deficiency of lncRNA HAR1A drives non-small cell lung cancer growth and metastasis by promoting ANXA2 stabilization

Ling,

Qi,

Cao

et al. 2024

Cell Death Discov.

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The roles of LncRNA CARMN in cancers: biomarker potential, therapeutic targeting, and immune response

Liu,

2024

Discov Onc

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Long non-coding RNAs (LncRNAs) are crucial regulators of gene expression and cellular processes, with significant implications for cancer research. This review focuses on the role of LncRNA CARMN (Cardiac Arrest and Regulated Myocyte Nuclear Protein) in various cancers. CARMN, originally identified for its function in cardiac tissues, has shown dysregulated expression in several tumor types, including cervical, breast, colorectal, and esophageal cancers. Its altered expression often correlates with tumor progression, metastasis, and patient prognosis, suggesting its potential as both a biomarker and therapeutic target. In cervical cancer, CARMN's role as a tumor suppressor is highlighted by its ability to inhibit cell proliferation, migration, and invasion through interaction with the miR-92a-3p/BTG2 axis and modulation of the Wnt/β-catenin signaling pathway. In breast cancer, CARMN acts as an enhancer RNA, affecting epithelial-mesenchymal transition and metastasis by regulating MMP2 via DHX9. The downregulation of CARMN in triple-negative breast cancer is associated with enhanced sensitivity to chemotherapy. In colorectal cancer, CARMN’s expression is regulated by m6A methylation and mutant p53, influencing tumor growth through miR-5683 and FGF2. Lastly, in esophageal cancer, genetic variations in CARMN affect cancer susceptibility, with certain SNPs and haplotypes associated with either increased or decreased risk. Additionally, the relationship between CARMN and immune cell dynamics highlights its potential role in cancer immune surveillance and therapy. Finally, we found that CARMN may regulate immune cell exhaustion in the tumor microenvironment by influencing the recruitment and activation of NK cells and T cells, as well as modulating macrophage polarization. This review emphasizes the diverse roles of CARMN across different cancers and its potential as a diagnostic and therapeutic tool. Future research should address the mechanistic details of CARMN’s involvement in cancer, validate its clinical utility, and explore its therapeutic potential in combination with existing treatments.

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From diagnosis to therapy: The transformative role of lncRNAs in eye cancer management

Hazazi,

AlShehah,

Khan

et al. 2024

Pathology - Research and Practice

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Post-transcriptional regulation of tumor suppressor gene lncRNA CARMN via m6A modification and miRNA regulation in cervical cancer

Cited by 10 publications

References 41 publications

METTL3-mediated deficiency of lncRNA HAR1A drives non-small cell lung cancer growth and metastasis by promoting ANXA2 stabilization

METTL3-mediated deficiency of lncRNA HAR1A drives non-small cell lung cancer growth and metastasis by promoting ANXA2 stabilization

The roles of LncRNA CARMN in cancers: biomarker potential, therapeutic targeting, and immune response

From diagnosis to therapy: The transformative role of lncRNAs in eye cancer management

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