YTHDF2 promotes the liver cancer stem cell phenotype and cancer metastasis by regulating OCT4 expression via m6A RNA methylation

Zhang, Chuanzhao; Huang, Shanzhou; Zhuang, Hongkai; Ruan, Su; Zhou, Zixuan; Huang, Kaijun; Ji, Fei; Ma, Zuyi; Hou, Baohua; He, Xiaoshun

doi:10.1038/s41388-020-1303-7

Cited by 268 publications

(235 citation statements)

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“…30 Additionally, YTHDF2 has been found to promote liver cancer stem cell phenotypes and cancer metastasis by modulating the m 6 A methylation of OCT4 mRNA. 31 Aberrant overexpression of YTHDC1 in colon adenocarcinoma has also been previously reported. 32 Our findings and these results suggest that m 6 A readers may be a potential therapeutic target.…”

Section: Discussionmentioning

confidence: 68%

Downregulation of m⁶A reader YTHDC2 promotes tumor progression and predicts poor prognosis in non‐small cell lung cancer

et al. 2020

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Background m 6 A modification affects the pathological progress of many diseases by affecting RNA stability and translocation. YTHDC2, a m 6 A reader, is associated with multiple cancers; however, little is known of its role in non‐small cell lung cancer (NSCLC). Methods The GEPIA, Oncomine and GEO databases were analyzed to assess expression of YTHDC2 in NSCLC patients. Quantitative polymerase chain reaction, western blot and immunohistochemistry were used to detect YTHDC2 expression in different NSCLC cell lines (H1299, H460, H292 and A549) and patients. The effects of YTHDC2 on NSCLC cell lines (A549 and H1299) proliferation and migration were employed using CCK8 and transwell assays. The potential target RNAs of YTHDC2 were obtained from the POSTAR database. Functional enrichment analysis of YTHDC2 targeted RNAs was performed using the Metascape database. Results GEPIA, Oncomine and GEO databases showed low expression of YTHDC2 in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC) patients. YTHDC2 expression was significantly decreased in different NSCLC cell lines and our clinical samples. Moreover, low expression of YTHDC2 was significantly associated with poor differentiation, lymph node metastasis, tumor size and stage. In addition, YTHDC2 could suppress the proliferation and migration ability of A549 and H1299 cell lines. Kaplan‐Meier Plotter database analysis revealed that patients with low level of YTHDC2 had a significantly poor prognosis. Finally, functional enrichment analysis of YTHDC2 targeted RNAs indicated several enriched pathways related to cancer. Conclusions These findings elucidate that YTHDC2 suppresses tumorigenesis in NSCLC, indicating that YTHDC2 may be a promising therapeutic target for NSCLC. Key points Significant findings of the study This study demonstrated that the downregulation of YTHDC2 promotes tumor progression and predicts poor prognosis in non‐small cell lung cancer (NSCLC). What this study adds YTHDC2 might be a promising therapeutic target for non‐small cell lung cancer (NSCLC).

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Section: Discussionmentioning

confidence: 68%

Downregulation of m⁶A reader YTHDC2 promotes tumor progression and predicts poor prognosis in non‐small cell lung cancer

et al. 2020

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“…Besides, YTHDF2 can suppress tumor growth through modulating the m 6 A methylation of EGFR mRNA by the m 6 A/mRNA degradation pathway. However, YTHDF2 promotes the cancer stem cell liver phenotype and cancer metastasis by binding m 6 A-modified OCT4 mRNA (Zhang et al, 2020). YTHDF2 can also interact with miRNA, miR-145 targets YTHDF2 and results in its degradation (Yang Z. et al, 2017).…”

Section: Ythdf2mentioning

confidence: 99%

The Potential Roles of RNA N6-Methyladenosine in Urological Tumors

Yang

et al. 2020

Front. Cell Dev. Biol.

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N6-methyladenosine (m 6 A) is regarded as the most abundant, prevalent and conserved internal mRNA modification in mammalian cells. M 6 A can be catalyzed by m 6 A methyltransferases METTL3, METTL14 and WTAP (writers), reverted by demethylases ALKBH5 and FTO (erasers), and recognized by m 6 A-binding proteins such as YTHDF1/2/3, IGF2BP1/2/3 and HNRNPA2B1 (readers). Emerging evidence suggests that m 6 A modification is significant for regulating many biological and cellular processes and participates in the pathological development of various diseases, including tumors. This article reviews recent studies on the biological function of m 6 A modification and the methylation modification of m 6 A in urological tumors.

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“…13 Some previous studies showed that the critical role of CSCs in initiation and development of lung cancer, liver cancer, breast cancer, head and neck squamous cell carcinomas, pancreatic cancer and glioblastoma. [14][15][16][17][18][19] Lung CSCs are considered as the cancer initiating and maintaining cells of lung cancer. 15 Lin et al reported that lung CSCs are responsible for lung cancer initiation and local or metastatic recurrence, the mitochondrial deoxyguanosine kinase is required for CSCs stemness in lung adenocarcinoma.…”

Section: Cancer Stem Cells Play a Key Role In Tumorigenesis And Develmentioning

confidence: 99%

<p>Tobacco Smoke Plays an Important Role in Initiation and Development of Lung Cancer by Promoting the Characteristics of Cancer Stem Cells</p>

Lü¹,

Liang

Shen

et al. 2020

CMAR

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Lung cancer is one of the most common causes of cancer-related deaths worldwide. Tobacco smoke is the single greatest risk factor of lung cancer. Although enormous progress in understanding the molecular mechanisms by which tobacco smoke leading to lung cancer has been made, the molecular pathogenesis remains largely unclear. Cancer stem cells have been implicated in cancer initiation, development, and drug resistance. In this review, we reviewed the relationship between tobacco smoke and lung cancer, the key role of cancer stem cells in lung cancer and other tumors. More importantly, we elucidate the mechanism of tobacco smoke promoting lung cancer from the perspective of the characteristics of cancer stem cells induced by tobacco smoke.

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YTHDF2 promotes the liver cancer stem cell phenotype and cancer metastasis by regulating OCT4 expression via m6A RNA methylation

Cited by 268 publications

References 23 publications

Downregulation of m⁶A reader YTHDC2 promotes tumor progression and predicts poor prognosis in non‐small cell lung cancer

Downregulation of m⁶A reader YTHDC2 promotes tumor progression and predicts poor prognosis in non‐small cell lung cancer

The Potential Roles of RNA N6-Methyladenosine in Urological Tumors

<p>Tobacco Smoke Plays an Important Role in Initiation and Development of Lung Cancer by Promoting the Characteristics of Cancer Stem Cells</p>

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YTHDF2 promotes the liver cancer stem cell phenotype and cancer metastasis by regulating OCT4 expression via m6A RNA methylation

Cited by 268 publications

References 23 publications

Downregulation of m6A reader YTHDC2 promotes tumor progression and predicts poor prognosis in non‐small cell lung cancer

Downregulation of m6A reader YTHDC2 promotes tumor progression and predicts poor prognosis in non‐small cell lung cancer

The Potential Roles of RNA N6-Methyladenosine in Urological Tumors

<p>Tobacco Smoke Plays an Important Role in Initiation and Development of Lung Cancer by Promoting the Characteristics of Cancer Stem Cells</p>

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Downregulation of m⁶A reader YTHDC2 promotes tumor progression and predicts poor prognosis in non‐small cell lung cancer

Downregulation of m⁶A reader YTHDC2 promotes tumor progression and predicts poor prognosis in non‐small cell lung cancer