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YTHDF3 Induces the Translation of m6A-enriched Metastasis-associated Gene Transcripts to Promote Breast Cancer Brain Metastasis [RIP-Seq]

ABSTRACT: Brain metastasis is a major cause of cancer mortality, but its molecular mechanisms are severely understudied. We found that YTHDF3 overexpression clinically correlates with brain metastases in breast cancer patients and is required for brain metastasis. Silencing YTHDF3 suppressed the brain metastasis of breast cancer cells in vitro and in vivo. Integrated transcriptome and m6A-seq analysis revealed alter expression of selected YTHDF3 target genes, including ST6GALNAC5, GJA1, and EGFR by promoting m6A-dependent translation of these target transcripts. Our work uncovers an essential role of YTHDF3 in controlling the interaction between cancer cells and brain microenvironment, thereby gaining brain metastatic competence.

ORGANISM(S): Homo sapiens

PROVIDER: GSE130171 | GEO | 2020/09/30

REPOSITORIES: GEO

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YTHDF3 Induces the Translation of m6A-enriched Metastasis-associated Gene Transcripts to Promote Breast Cancer Brain Metastasis [m6A-seq]

Project description:Brain metastasis is a major cause of cancer mortality, but its molecular mechanisms are severely understudied. We found that YTHDF3 overexpression clinically correlates with brain metastases in breast cancer patients and is required for brain metastasis. Silencing YTHDF3 suppressed the brain metastasis of breast cancer cells in vitro and in vivo. Integrated transcriptome and m6A-seq analysis revealed alter expression of selected YTHDF3 target genes, including ST6GALNAC5, GJA1, and EGFR by promoting m6A-dependent translation of these target transcripts. Our work uncovers an essential role of YTHDF3 in controlling the interaction between cancer cells and brain microenvironment, thereby gaining brain metastatic competence.

2020-09-30 | GSE130172 | GEO

Gene expression in breast cancer cell with shYTHDF3 [mouse]

Project description:Knocking down YTHDF3 in breast cancer cells resulted in an altered gene expression profile N6-methyl-adenosine (m6A) is the most prevalent internal chemical modification in eukaryotic messenger RNAs and emerging as a critical mRNA chemical mark that mediates post-transcriptional gene expression regulation. YTHDF3 facilitates translation and decay of m6A-modified mRNAs. However, the role for YTHDF3 protein in breast cancer brain metastasis remain to be elucidated. We found that YTHDF3 is overexpressed in brain metastasis of breast cancer cells. Our study will characterize the expression profiling in YTHDF3 silencing breast cancer cells compared to shControl breast cancers cells. The objectives are to identify expression profiles that are specific to shYTHDF3 breast cancer cell to identify new the signaling pathway of YTHDF3 for brain metastasis of breast cancer cells.

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YTHDF3 Induces the Translation of m6A-enriched Metastasis-associated Gene Transcripts to Promote Breast Cancer Brain Metastasis

Project description:YTHDF3 Induces the Translation of m6A-enriched Metastasis-associated Gene Transcripts to Promote Breast Cancer Brain Metastasis

| PRJNA534211 | ENA

YTHDF3 Induces the Translation of m6A-enriched Metastasis-associated Gene Transcripts to Promote Breast Cancer Brain Metastasis [m6A-seq]

Project description:YTHDF3 Induces the Translation of m6A-enriched Metastasis-associated Gene Transcripts to Promote Breast Cancer Brain Metastasis [m6A-seq]

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YTHDF3 improves translation initiation of mRNAs with N6-methyladenosine methylation at 5’ untranslated region by facilitating eIF2AK2 recruitment in oxaliplatin-resistant colorectal cancer - RIP-seq dataset

Project description:Oxaliplatin as a first-line drug frequently causes the chemo-resistance on colorectal cancer (CRC). N6-methyladenosine (m6A) methylation has been largely acknowledged in multiple biological functions. However, the molecular mechanisms underlying the m6A methylation in modulating anticancer drug resistance in CRC are still obscure. In present study, RIP-seq was conducted to investigate the occupancy of N6-methyladenosine RNA binding protein 3 (YTHDF3) served as “readers” that can recognize m6A modification site in HCT116 cells with oxaliplatin resistance (HCT116R). Then, YTHDF3 was knockdown by siRNA in HCT116 cells with oxaliplatin resistance, and RIP-seq was further conducted to investigate m6A methylation of HCT116, HCT116R and HCT116R cells with YTHDF3 knockdown.

2022-02-04 | E-MTAB-11321 | biostudies-arrayexpress

YTHDF3 Induces the Translation of m6A-enriched Metastasis-associated Gene Transcripts to Promote Breast Cancer Brain Metastasis [RIP-Seq]

Project description:YTHDF3 Induces the Translation of m6A-enriched Metastasis-associated Gene Transcripts to Promote Breast Cancer Brain Metastasis [RIP-Seq]

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Genes that mediate breast cancer metastasis to the brain

2009-05-06 | GSE12237 | GEO

Transcription profiling of human breast cancer metastasis to the brain to identify genes involved

Project description:Brain metastasis is one of the most feared complications of cancer and the most common intracranial malignancy in adults. Its underlying mechanisms remain unknown. From breast cancer patients with metastatic disease we isolated cell populations that aggressively colonize the brain. Transcriptomic analysis of these cells yielded overlapping gene sets whose expression is selectively associated with brain metastasis. The expression of seventeen of these genes in primary breast tumors is associated with brain relapse in breast cancer patients. Some of these genes are also associated with metastasis to lung but not to liver, bone or lymph nodes, providing a molecular basis for the long-observed clinical link between brain and lung metastasis. Among the functionally validated brain metastasis genes, the cyclooxygenase COX-2, the EGFR ligand HB-EGF, and the brain-specific Î±2-6 sialyltransferase ST6GALNAC5 mediate cancer cell passage through the blood-brain barrier. Other brain metastasis genes encode inflammatory factors and brain-specific proteolytic regulators, suggesting a multifaceted program for breast cancer colonization of the brain. Experiment Overall Design: Two different breast cancer cell lines, MDA-MB-231 and freshly isolated pleural effusion CN34 were used in this study. The MDA-MB-231 group contains three biological replicates of the parental, unselected population, and 4 brain metastatic isolates. CN34 contains 2 biological replicates of the parental, unselected population, and 4 brain metastatic isolates. In each case, the parental population was compared to the brain metastatic isolates to identify gene expression changes associated with the brain metastatic phenotype.

2009-05-16 | E-GEOD-12237 | biostudies-arrayexpress

Transcription profiling of human primary breast tumors

Project description:Brain metastasis is one of the most feared complications of cancer and the most common intracranial malignancy in adults. Its underlying mechanisms remain unknown. From breast cancer patients with metastatic disease we isolated cell populations that aggressively colonize the brain. Transcriptomic analysis of these cells yielded overlapping gene sets whose expression is selectively associated with brain metastasis. The expression of seventeen of these genes in primary breast tumors is associated with brain relapse in breast cancer patients. Some of these genes are also associated with metastasis to lung but not to liver, bone or lymph nodes, providing a molecular basis for the long-observed link between brain and lung metastasis. Among the functionally validated brain metastasis genes, the cyclooxigenase COX-2, the EGFR ligand HB-EGF, and the brain-specific 2-6 sialyltransferase ST6GALNAC5 mediate cancer cell passage through the blood-brain barrier. Other brain metastasis genes encode inflammatory factors and brain-specific proteolytic regulators, suggesting a multifaceted program for breast cancer colonization of the brain. Experiment Overall Design: 204 primary tumors from breast cancer patients with known site of relapse were studied, focussing on brain relapse versus other relapse. Identified genes were validated in this cohort.

2009-06-23 | E-GEOD-12276 | biostudies-arrayexpress

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