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N6-methyladenosine RNA modification is associated with enzalutamide resistance in prostate cancer (MeRIP-Seq)

ABSTRACT: Our study examines the role of m6A RNA modification in regulating gene expression of transcripts promoting enzalutamide resistance in prostate cancer.

ORGANISM(S): Homo sapiens

PROVIDER: GSE249748 | GEO | 2024/05/01

REPOSITORIES: GEO

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N6-methyladenosine RNA modification is associated with enzalutamide resistance in prostate cancer (RNA-seq)

Project description:Our study examines the role of m6A RNA modification in regulating gene expression of transcripts promoting enzalutamide resistance in prostate cancer.

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N6-methyladenosine RNA modification is associated with enzalutamide resistance in prostate cancer (MeRIP-Seq)

Project description:N6-methyladenosine RNA modification is associated with enzalutamide resistance in prostate cancer (MeRIP-Seq)

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Structure and Thermodynamics of N6-methyladenosine in RNA: a Spring-Loaded Base Modification

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N6-methyladenosine RNA modification is associated with enzalutamide resistance in prostate cancer

Project description:This SuperSeries is composed of the SubSeries listed below.

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Project description:N6-methyladenosine (m6A) modification of messenger RNAs (mRNAs) is a pivotal mechanism controlling mRNA fate in cells. RNA m6A modification is regulated by the functional balance between methyltransferases and demethylases. Here we demonstrated that FTO-IT1 enhancer RNA (eRNA), a long non-coding RNA (lncRNA) transcribed from the last intron of FTO gene is significantly upregulated in CRPC and aggressive tumors compared to primary tumors. FTO-IT1 knockout by CRISPR/Cas9 almost completely blocks growth and G1-S cell cycle transition of both androgen-sensitive and castration-resistant prostate cancer cells. Meanwhile, the mRNA m6A was dramatically increased in FTO-IT knockout PCa cells and we identified FTO-IT1 as a binding partner of FTO. From m6A-seq, we unexpectedly found hypermethylated m6A associated with upregulated levels of the mRNAs for p53 signaling pathway genes in 22Rv1 prostate cancer cells. Mechanistic study showed that FTO-IT1 recruits FTO to the P53 target mRNA to promote their m6A demethylation, which leads to their degradation.

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