YAP1 and TAZ knockdown in human keratinocytes
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA565787 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10126581_1.fastq.gz | Fastqsanger.gz | |||
| SRR10126581_2.fastq.gz | Fastqsanger.gz | |||
| SRR10126582_1.fastq.gz | Fastqsanger.gz | |||
| SRR10126582_2.fastq.gz | Fastqsanger.gz | |||
| SRR10126583_1.fastq.gz | Fastqsanger.gz |
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Project description:Promoting rumen development is closely related to the health and efficient growth of ruminants. In the present study, we aimed to assess the impact of YAP1/TAZ on RE proliferation. The transcriptomic expression was analyzed to investigate the potential regulatory networks. The results indicated that GA promoted RE cell proliferation, while VP disrupted RE cell proliferation. The Hippo, Wnt, and calcium signaling pathways were altered in cells following the regulation of YAP1/TAZ. Upon YAP1/TAZ activation through GA, the CCN1/2 increased to promote RE cell proliferation. While when the YAP1/TAZ was inhibited by VP, the BIRC3 decreased to suppress RE cell proliferation. Thus, YAP1/TAZ may be potential targets for regulating RE cell proliferation. These findings broaden our understanding of the role of YAP1/TAZ and their regulators in RE and offer a potential target for promoting rumen development.
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Project description:The Hippo signaling pathway is evolutionarily well conserved, and all core components have one or more mammalian orthologs, including MST1/2 (Hippo), SAV1 (Salvador), LATS1/2 (Warts), MOB1 (Mats), YAP1/TAZ (Yorkie), and TEAD1/2/3/4 (Scalloped) (Halder and Johnson, 2011; Pan, 2007; Dong et al., 2007; Saucedo and Edgar, 2007). When Hippo signaling is active, YAP1/TAZ is phosphorylated by LATS1/2 and sequestered by 14-3-3 proteins in cytoplasm. When Hippo signaling is absent, unphosphorylated YAP1/TAZ enters the nucleus and increases transcriptional activation of genes involved in cell proliferation and survival. The indispensability of the Hippo pathway in restricting cell growth and proliferation has prompted speculation that many members of the pathway might be involved in tumorigenesis. To see the effect of YAP1 and TAZ in HCC cell, we generated gene expression profile.
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Project description:Targeted therapies in cancer are limited by cells exhibiting drug tolerance. We aimed to target drug tolerance in order to delay the development of acquired resistance. In melanoma, tolerance to MAPK pathway inhibitors is associated with loss of SOX10 and an enhanced TEAD transcriptional program. We show that loss of SOX10 is sufficient to up-regulate TEAD targets with dependence on the co-activator, TAZ. Active TAZ was sufficient to mediate tolerance to BRAF inhibitors and MEK inhibitors. We developed novel covalent inhibitors, OPN-9643 and OPN-9652, designed to target the central palmitate binding pocket of TEADs. In SOX10-deficient cells, OPN-9643 and OPN-9652 reduced TEAD-dependent reporter activity and expression of TEAD targets, CTGF and CYR61. OPN-9643 and OPN-9652 treatment enhanced the inhibitory effects of MAPK-targeted therapies in 2D and 3D growth assays and reversed tolerance mediated by active TAZ. In vivo, OPN-9652 delayed the onset of acquired resistance to BRAF inhibitors and MEK inhibitors from minimal residual disease. Thus, TAZ-TEAD activity plays an important role in melanoma drug tolerance and the development of acquired resistance.
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