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Homo sapiens

ABSTRACT: TGF-beta orchestrates proliferation and migration of cancer cells via KRTAP2-3

PROVIDER: PRJDB12717 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	DRR333361_1.fastq.gz	Fastqsanger.gz
	DRR333361_2.fastq.gz	Fastqsanger.gz
	DRR333362_1.fastq.gz	Fastqsanger.gz
	DRR333362_2.fastq.gz	Fastqsanger.gz
	DRR392346_1.fastq.gz	Fastqsanger.gz

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TGF-β orchestrates proliferation and migration of cancer cells via KRTAP2-3

Project description:TGF-β orchestrates proliferation and migration of cancer cells via KRTAP2-3

| PRJNA761118 | ENA

TGF-β orchestrates proliferation and migration of cancer cells via KRTAP2-3

Project description:The proliferation and migration of cancer cells are regulated by stimuli from the tumour microenvironment during tumour progression and metastasis. While transforming growth factor-β (TGF-β) increases migration and metastasis of various types of epithelial cancer cells via induction of epithelial-mesenchymal transition (EMT), it also inhibits their proliferation by inducing cell cycle arrest in the G1 phase. However, the correlation between the tumour promoting and suppressing effects of TGF-β remains elusive because of the lack of analysis at the single-cell level. Here, we showed that TGF-β conferred higher motility and mesenchymal phenotypes to oral cancer cells residing in the G1 phase, suggesting a correlation between TGF-β-dependent cell cycle arrest and increased cell migration. We identified keratin-associated protein 2-3 (KRTAP2-3) as a regulator of these dual effects of TGF-β and showed that the expression of KRTAP2-3 was associated with TGF-β-induced cell cycle arrest and increased migration and correlated with poor prognosis in patients with head and neck cancer. Deletion of the KRTAP2-3 gene decreased in vitro migration and in vivo metastasis of oral cancer cells via induction of mesenchymal-epithelial transition. KRTAP2-3 also induced the expression of the zinc finger BED domain-containing protein 2 and ectodermal-neural cortex 1, which suppressed proliferation and increased migration of oral cancer cells, respectively. The present findings revealed the mechanisms by which TGF-β orchestrates proliferation and migration of cancer cells by inducing the expression of KRTAP2-3 and highlighted the importance of targeting motile cancer cells under cell cycle arrest in the G1 phase to suppress metastasis. Identification of marker genes for KRTAP2-3 induced gene

2024-09-02 | GSE183524 | GEO

RNA-seq analysis evaluating cell cycle specific gene expression and the effect of KRTAP2-3 gene inactivation in SAS cells expressing Fucci.

Project description:Proliferation and migration of cancer cells are regulated by the stimuli from tumour microenvironment during its progression and metastasis. While transforming growth factor-β (TGF-β) increases migration and metastasis of various types of epithelial cancer cells via induction of epithelial-mesenchymal transition (EMT), it also decreases their proliferation by inducing G1 cell cycle arrest. However, the correlation of these tumour promoting and suppressing effects of TGF-β remains to be elusive because of the lack of analysis at a single cell level. Here, we showed that TGF-β confers the oral cancer cells residing in G1 phase with higher motility and mesenchymal phenotypes, suggesting a correlation between TGF-β-dependent cell cycle arrest and increased migration. We identified keratin-associated protein 2-3 (KRTAP2-3) as a regulator of these dual effects of TGF-β. Expression of KRTAP2-3 was associated with both TGF-β-induced cell cycle arrest and increased migration, and also was correlated with poor prognosis of head and neck cancer patients. We found that deletion of KRTAP2-3 gene decreased in vitro migration and in vivo metastasis of oral cancer cells via induction of mesenchymal-epithelial transition (MET). KRTAP2-3 also induces the expression of Regulator of G-protein signalling 4 (RGS4) and Zinc finger BED domain-containing protein 2 (ZBED2), which suppresses proliferation and increases migration of oral cancer cells, respectively. Present findings revealed novel mechanisms how TGF-β orchestrates proliferation and migration of cancer cells by inducing the expression of KRTAP2-3, and highlighted the importance of targeting the motile cancer cells under G1 cell cycle arrest to suppress metastasis.

2022-09-27 | GSE179223 | GEO

The phosphorylation of the Smad2/3 linker region by Nemo-like kinase regulates TGF-β signaling

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2021-09-10 | PXD023957 | Pride

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