Hypoxia induces the breast cancer stem cell phenotype by HIF-dependent and ALKBH5-mediated m6A-demethylation of NANOG mRNA
By Chuanzhao Zhang, Debangshu Samanta, Haiquan Lu, John W. Bullen, Huimin Zhang, Ivan Chen, Xiaoshun He, G. Semenza. Proceedings of the National Academy of Sciences of the United States of America, 2016
967 citations recorded by the source corpus.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/9a44c3ce2b97d81ab099e3274f7d7feca675923b
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Citations in the corpus
- RNA N6-methyladenosine modification in cancers: current status and perspectives (2018, background): “Thus, FTO likely also plays a critical oncogenic role in self-renewal of GSCs and is required for the development of GBM.”
- m6A RNA methylation: from mechanisms to therapeutic potential (2021, positive): “Moreover, ALKBH5 appears to promote tumorigenesis in breast cancer and glioblastoma (Zhang et al , 2016, 2017b) in addition to affecting innate immune responses to viral infections (Zheng et al , 2017; Liu et al , 2019).”
- Critical Roles of N6-Methyladenosine (m6A) in Cancer and Virus Infection (2020, background): “In breast cancer, overexpression of ALKBH5 promotes mRNA stability and expression of the pluripotency factor NANOG, which is required for primary tumor formation, and metastasis by catalyzing m6A demethylation [100].”
- Functions of N6-methyladenosine and its role in cancer (2019, background): “Breast cancer ALKBH5 NANOG stabilization inhibits tumor formation and breast cancer stem cell population [120]”
- The role of m6A RNA methylation in cancer metabolism (2022, background): “In breast cancer, hypoxia induces demethylation of m6A, mainly HIF-1α and HIF-2α, which is highly expressed under hypoxia, can activate the gene transcription of ALKBH5, reduce NANOG m6A methylation and stabilize its stability, increase its protein expression, and promote the phenotype of breast can”
- Where, when and how: context-dependent functions of RNA methylation writers, readers, and erasers (2019, background): “(Zhang et al., 2016), regulating glioblastoma proliferation and tumorigenesis through the ALKBH5-FOXM1 pathway (Zhang et al.”
- m6A RNA Methylation Regulates the Self-Renewal and Tumorigenesis of Glioblastoma Stem Cells (2017, background): “On the other hand, elevated levels of the S-adenosyl methionine (SAM) donor of the methyl group in the m6A methylation process have been shown to suppress cell growth in cancer (Pascale et al., 2002; Pakneshan et al., 2004; Guruswamy et al., 2008; Lu et al., 2009; Zhao et al., 2010).”