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Temporal chromatin accessibility changes define transcriptional states essential for osteosarcoma metastasis

ABSTRACT: Temporal chromatin accessibility changes define transcriptional states essential for osteosarcoma metastasis

PROVIDER: PRJNA890572 | ENA |

REPOSITORIES: ENA

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Temporal chromatin accessibility changes define transcriptional states essential for osteosarcoma metastasis [scATAC-Seq]

Project description:Temporal profiling of chromatin accessibility during metastasis revealed dynamic changes in chromatin accessibility during osteosarcoma lung colonization. We sought to determine whether these changes were due to epigenomic reprogramming, or shifts in subclonal frequency. To do this we performed scATAC-seq on MG63.3-GFP cells grown in vitro.

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Temporal chromatin accessibility changes define transcriptional states essential for osteosarcoma metastasis [RNA-Seq]

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Temporal chromatin accessibility changes define transcriptional states essential for osteosarcoma metastasis

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

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Temporal chromatin accessibility changes define transcriptional states essential for osteosarcoma metastasis [143b_ATACseq]

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Temporal chromatin accessibility changes define transcriptional states essential for osteosarcoma metastasis [mg633_ATACseq]

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AMTB, a TRPM8 Antagonist, Suppresses Growth and Metastasis of Osteosarcoma through Repressing the TGFβ Signaling Pathway

Project description:Since its first identification in prostate cancers and prostate tissues, transient receptor potential melastatin-subfamily member 8 (TRPM8) is subsequently found to be overexpressed in a wide range of cancers and is shown to be implicated in tumorigenesis and tumor progression. Here, we used N-(3-aminopropyl)-2-[(3-methylphenyl) methoxy] -N-(2-thienylmethyl) benzamide hydrochloride (AMTB), a specific TRPM8 antagonist, to explore its antitumoral effect on osteosarcoma. We find that AMTB suppress osteosarcoma cell proliferation, metastasis and induce cellular apoptosis. Xenograft model in nude mice experiments also define that AMTB can increase the sensitivity of tumor cells to cisplatin, the cytotoxic chemotherapeutic regimens in treating osteosarcoma. Molecularly, AMTB specific antagonizes TRPM8 which is upregulated in osteosarcoma and its expression level in osteosarcoma tissues is negatively related to patients’ prognosis. Finally, RNA sequencing analysis was performed to explore the mechanism underlying the antitumoral effect of AMTB on osteosarcoma cells and the results prove that AMTB suppresses the Transforming Growth Factor β (TGFβ) signaling pathway. Our study provides evidence that TRPM8 could be a potential therapeutic target and AMTB can suppress growth and metastasis of osteosarcoma cells through repressing the TGFβ signaling pathway and increase the sensitivity of tumor cells to cisplatin.

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