RNA-Seq of Myf6-knockout versus Wild-type satellite cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA551653 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11351149.fastq.gz | Fastqsanger.gz | |||
| SRR11351150.fastq.gz | Fastqsanger.gz | |||
| SRR11351151.fastq.gz | Fastqsanger.gz | |||
| SRR11351152.fastq.gz | Fastqsanger.gz | |||
| SRR11351153.fastq.gz | Fastqsanger.gz |
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Project description:In metazoans, skeletal muscle evolved to contract and produce force. Recent experimental evidence, however, suggests that skeletal muscle has also acquired endocrine functions and produces a vast array of muscle-derived cytokines and growth factors, collectively called myokines. The mechanisms that regulate myokine production and their effect on the resident stem cell population inskeletal muscle remain unknown. Here, we report that in adult skeletal muscle, Myf6/MRF4 is a major regulator of myokine expression. Genetic deletion of Myf6 in skeletal muscle leads to reduction of the muscle stem cell (MuSCs) pool in adult mice in a myokine-dependent manner but, surprisingly, does not disrupt muscle differentiation. Using ChIP-Seq and gene expression analyses of myogenic factors, we show that Myf6/MRF4 is a direct regulator of many myokines and muscle-secreted proteins, including ligands for canonical signaling pathways such as EGFR and VEGFR. Consequently, in Myf6-deficient animals,MuSCs increasingly break quiescence, but can nevertheless undergo differentiation. Lastly, we show that Myf6 and its gene network rapidly respondto aerobic and anaerobic exercise. Together, these findings indicate that control of myokine signaling by Myf6 is critical to maintain muscle stem cell pool and skeletal muscle function via myokine signaling.
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Project description:In metazoans, skeletal muscle evolved to contract and to produce force. Recent experimental evidence suggests, however, that skeletal muscle has also acquired endocrine functions and produces a vast array of myokines, but how myokine production is regulated and how they affect the resident stem cell population of the skeletal muscle is unknown. Here, we show that in adult skeletal muscle, Myf6/MRF4 is a major regulator of myokine expression. Genetic deletion of Myf6 in skeletal muscles leads to exhaustion of the muscle stem cell (MuSCs) pool in adult mice in a myokine-dependent manner but, surprisingly, does not disrupt muscle differentiation. Using ChIP-Seq and gene expression analyses of myogenic factors, we show that Myf6/MRF4 is essential for the transcriptional activation of many myokines and muscle-secreted proteins, including ligands for canonical signaling pathways such as EGFR, VEGFR and STAT3. Consequently, MuSCs from Myf6 knockout animals show impaired activation of those signaling pathways and exhibit impaired quiescence, defective self-renewal, but nevertheless undergo differentiation. Lastly, we show that induction of myokine expression during aerobic and anaerobic exercise closely correlates with Myf6 expression. Together, these findings indicate that control of myokine signaling by Myf6 is critical to maintain muscle stem cell pool in adult skeletal muscle.
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Project description:Background: Proliferation is an important hallmark of cancer development and progression. Tumor growth rate significantly influences the course of the disease, and patients with tumors that have a high proliferation rate have an increased risk (10-20%) of metastasis and death. The genomic region encoding the transcription factor MYF6 is often altered in breast cancer, and alterations in MYF6 methylation have been linked to several different cancer types. However, the functional role of MYF6 in cancer remain unknown. Here, we have dissected the functional role of MYF6 in ER+ breast cancer. Methods: We analyzed cancer cell growth, proliferation, apoptosis, in vivo tumor formation, EMT phenotype and BCSC propagation in MCF7 and T47D ER+ breast cancer models with inducuble MYF6 overexpression or MYF6 knockdown. Additionally, we performed detailed molecular profiling and network analysis, and Western blot validation of identified targets. Results: We show that MYF6 suppresses PI3K/Akt/mTOR and Wnt pathway signaling, two important pathways of cell proliferation, and suppression was accompanied by reduced cell growth in vitro and in vivo, and G0/G1 phase cell cycle arrest. MYF6 also induced an EMT phenotype and forced the cells into a cancer stem cell-like state, leading to resistance to -irradiation. Network analysis of molecular profiling data revealed that MYF6 activates hypoxia signaling and HIF1A was identified as a downstream target and an upstream regulator of MYF6. Conclusion: Our results suggest both a tumor-suppressive and oncogenic role of MYF6 in ER+ breast cancer, and we theorize that, subject to the presence or absence of yet unidentified cellular factors, MYF6 can switch from a growth-inhibiting tumor suppressor to an oncogene state, associated with cancer stem cells and treatment resistance.
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Project description:Background: Proliferation is an important hallmark of cancer development and progression. Tumor growth rate significantly influences the course of the disease, and patients with tumors that have a high proliferation rate have an increased risk (10-20%) of metastasis and death. The genomic region encoding the transcription factor MYF6 is often altered in breast cancer, and alterations in MYF6 methylation have been linked to several different cancer types. However, the functional role of MYF6 in cancer remain unknown. Here, we have dissected the functional role of MYF6 in ER+ breast cancer. Methods: We analyzed cancer cell growth, proliferation, apoptosis, in vivo tumor formation, EMT phenotype and BCSC propagation in MCF7 and T47D ER+ breast cancer models with inducuble MYF6 overexpression or MYF6 knockdown. Additionally, we performed detailed molecular profiling and network analysis, and Western blot validation of identified targets. Results: We show that MYF6 suppresses PI3K/Akt/mTOR and Wnt pathway signaling, two important pathways of cell proliferation, and suppression was accompanied by reduced cell growth in vitro and in vivo, and G0/G1 phase cell cycle arrest. MYF6 also induced an EMT phenotype and forced the cells into a cancer stem cell-like state, leading to resistance to -irradiation. Network analysis of molecular profiling data revealed that MYF6 activates hypoxia signaling and HIF1A was identified as a downstream target and an upstream regulator of MYF6. Conclusion: Our results suggest both a tumor-suppressive and oncogenic role of MYF6 in ER+ breast cancer, and we theorize that, subject to the presence or absence of yet unidentified cellular factors, MYF6 can switch from a growth-inhibiting tumor suppressor to an oncogene state, associated with cancer stem cells and treatment resistance.
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