LINC02159 promotes non-small cell lung cancer progression via ALYREF/YAP1 signaling

Yang, Qing; Wang, Maoye; Xu, Jianming; Yu, Dae‐Yeul; Li, Yixin; Chen, Yanke; Zhang, Xiaoxin; Zhang, Jiahui; Gu, Jianmei; Zhang, Xu

doi:10.1186/s12943-023-01814-x

Cited by 25 publications

(6 citation statements)

References 36 publications

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“…ALYREF, an important m5C reader, has been proven to maintain mRNA stability [ 20 – 22 ]. To verify whether ALYREF is a functional m5C reader in lung cancer cells, we performed RIP assay with ALYREF antibody in H1650 and H1299 cells, and the RT-qPCR results showed that ALYREF could bind to EZH2 mRNA, suggesting that ALYREF might be the m5C reader (Fig.…”

Section: Resultsmentioning

confidence: 99%

NOP2 facilitates EZH2-mediated epithelial–mesenchymal transition by enhancing EZH2 mRNA stability via m5C methylation in lung cancer progression

Yang,

Fan,

Liu

et al. 2024

Cell Death Dis

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NOP2, a member of the NOL1/NOP2/SUN domain (NSUN) family, is responsible for catalyzing the posttranscriptional modification of RNA through 5-methylcytosine (m5C). Dysregulation of m5C modification has been linked to the pathogenesis of various malignant tumors. Herein, we investigated the expression of NOP2 in lung adenocarcinoma (LUAD) tissues and cells, and found that it was significantly upregulated. Moreover, lentivirus-mediated overexpression of NOP2 in vitro resulted in enhanced migration and invasion capabilities of lung cancer cells, while in vivo experiments demonstrated its ability to promote the growth and metastasis of xenograft tumors. In contrast, knockdown of NOP2 effectively inhibited the growth and metastasis of lung cancer cells. RNA-sequencing was conducted to ascertain the downstream targets of NOP2, and the findings revealed a significant upregulation in EZH2 mRNA expression upon overexpression of NOP2. Subsequent validation experiments demonstrated that NOP2 exerted an m5C-dependent influence on the stability of EZH2 mRNA. Additionally, our investigations revealed a co-regulatory relationship between NOP2 and the m5C reader protein ALYREF in modulating the stability of EZH2 mRNA. Notably, the NOP2/EZH2 axis facilitated the malignant phenotype of lung cancer cells by inducing epithelial–mesenchymal transition (EMT) both in vitro and in vivo. Mechanistically, ChIP analysis proved that EZH2 counteracted the impact of NOP2 on the occupancy capacity of EZH2 and H3K27me3 in the promoter regions of E-cadherin, a gene crucial for regulating EMT. In a word, our research highlights the significant role of NOP2 in LUAD and offers novel mechanistic insights into the NOP2/ALYREF/EZH2 axis, which holds promise as a potential target for lung cancer therapy.

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Section: Resultsmentioning

confidence: 99%

NOP2 facilitates EZH2-mediated epithelial–mesenchymal transition by enhancing EZH2 mRNA stability via m5C methylation in lung cancer progression

Yang,

Fan,

Liu

et al. 2024

Cell Death Dis

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“…LncRNAs not only regulate gene expression and participate in signal transduction pathways but also regulate epigenetic, transcriptional, and post-transcriptional modifications [ 45 ]. LncRNA expression is closely related to a variety of biological functions, including cell survival, cancer progression and metastasis [ 46 , 47 ]. Recent studies have shown that abnormal expression levels of lncRNAs are closely related to the pathology and prognosis of glioma [ 48 ].…”

Section: Discussionmentioning

confidence: 99%

LINC00606 promotes glioblastoma progression through sponge miR-486-3p and interaction with ATP11B

Dong,

Qi,

et al. 2024

J Exp Clin Cancer Res

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Background LncRNAs regulate tumorigenesis and development in a variety of cancers. We substantiate for the first time that LINC00606 is considerably expressed in glioblastoma (GBM) patient specimens and is linked with adverse prognosis. This suggests that LINC00606 may have the potential to regulate glioma genesis and progression, and that the biological functions and molecular mechanisms of LINC00606 in GBM remain largely unknown. Methods The expression of LINC00606 and ATP11B in glioma and normal brain tissues was evaluated by qPCR, and the biological functions of the LINC00606/miR-486-3p/TCF12/ATP11B axis in GBM were verified through a series of in vitro and in vivo experiments. The molecular mechanism of LINC00606 was elucidated by immunoblotting, FISH, RNA pulldown, CHIP-qPCR, and a dual-luciferase reporter assay. Results We demonstrated that LINC00606 promotes glioma cell proliferation, clonal expansion and migration, while reducing apoptosis levels. Mechanistically, on the one hand, LINC00606 can sponge miR-486-3p; the target gene TCF12 of miR-486-3p affects the transcriptional initiation of LINC00606, PTEN and KLLN. On the other hand, it can also regulate the PI3K/AKT signaling pathway to mediate glioma cell proliferation, migration and apoptosis by binding to ATP11B protein. Conclusions Overall, the LINC00606/miR-486-3p/TCF12/ATP11B axis is involved in the regulation of GBM progression and plays a role in tumor regulation at transcriptional and post-transcriptional levels primarily through LINC00606 sponging miR-486-3p and targeted binding to ATP11B. Therefore, our research on the regulatory network LINC00606 could be a novel therapeutic strategy for the treatment of GBM. Graphical Abstract LINC00606 is highly expressed in GBM patients with carcinogenic function and correlated with poor prognosis. LINC00606 regulates glioblastoma progression by sponging miR-486-3p and interacting with ATP11B.

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“…In vitro and in vivo studies have identifiedthe RNA methyltransferase NSUN2 as primarily enzyme catalyzing m5C production in mRNAs, with m5C specifically recognized by the mRNA export adaptor ALYREF [ 46 ]. Recent research has linked ALYREF to the development of various tumors, including bladder cancer [ 47 , 48 ], breast cancer [ 49 ], neuroblastoma [ 50 ], hepatocellular carcinoma [ 51 , 52 ], glioblastoma [ 53 ], and non-small cell lung cancer [ 54 ]. These findings underscore the gene’s critical role in human cancer.…”

Section: Discussionmentioning

confidence: 99%

Pan-cancer analysis of RNA 5-methylcytosine reader (ALYREF)

YE,

TUO,

CHEN

et al. 2024

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The increasing interest in RNA modifications has significantly advanced epigenomic and epitranscriptomic technologies. This study focuses on the immuno-oncological impact of ALYREF in human cancer through a pancancer analysis, enhancing understanding of this gene's role in cancer. We observed differential ALYREF expression between tumor and normal samples, correlating strongly with prognosis in various cancers, particularly kidney renal papillary cell carcinoma (KIRP) and liver hepatocellular carcinoma (LIHC). ALYREF showed a negative correlation with most tumor-infiltrating cells in lung squamous cell carcinoma (LUSC) and lymphoid neoplasm diffuse large Bcell lymphoma (DLBC), while positive correlations were noted in LIHC, kidney chromophobe (KICH), mesothelioma (MESO), KIRP, pheochromocytoma and paraganglioma (PARD), and glioma (GBMLGG). Additionally, ALYREF expression was closely associated with tumor heterogeneity, stemness indices, and a high mutation rate in TP53 across these cancers. In conclusion, ALYREF may serve as an oncogenic biomarker in numerous cancers, meriting further research attention.

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LINC02159 promotes non-small cell lung cancer progression via ALYREF/YAP1 signaling

Cited by 25 publications

References 36 publications

NOP2 facilitates EZH2-mediated epithelial–mesenchymal transition by enhancing EZH2 mRNA stability via m5C methylation in lung cancer progression

NOP2 facilitates EZH2-mediated epithelial–mesenchymal transition by enhancing EZH2 mRNA stability via m5C methylation in lung cancer progression

LINC00606 promotes glioblastoma progression through sponge miR-486-3p and interaction with ATP11B

Pan-cancer analysis of RNA 5-methylcytosine reader (ALYREF)

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