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Breast tumor from Pik3caH1047R/+ mammary gland transduced with single or pooled lentivirus.

ABSTRACT: Breast tumor from Pik3caH1047R/+ mammary gland transduced with single or pooled lentivirus.

PROVIDER: PRJNA505888 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8204070_1.fastq.gz	Fastqsanger.gz
	SRR8204070_2.fastq.gz	Fastqsanger.gz
	SRR8204080_1.fastq.gz	Fastqsanger.gz
	SRR8204080_2.fastq.gz	Fastqsanger.gz
	SRR8204090_1.fastq.gz	Fastqsanger.gz

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Project description:Identify gene expression changes in the absence of Plk2 Disruptions in polarity and mitotic spindle orientation contribute to the progression and evolution of tumorigenesis. However, little is known about the molecular mechanisms regulating these processes in vivo. Here we demonstrate that Polo-like kinase 2 (Plk2) regulates mitotic spindle orientation in the mammary gland and is a putative tumor suppressor. Plk2 is highly expressed in the mammary gland and is required for proper mammary gland development. Loss of Plk2 leads to increased mammary epithelial cell proliferation and ductal hyperbranching. Additionally a novel role for Plk2 in regulating the orientation of the mitotic spindle and maintaining proper cell polarity in the ductal epithelium was discovered. In support of a tumor suppressor function for Plk2, loss of Plk2 increased the formation of lesions in multiparous glands. Collectively, these results demonstrate a novel role for Plk2 in regulating mammary gland development and as a tumor suppressor in mammary tumorigenesis. Disruptions in polarity and mitotic spindle orientation contribute to the progression and evolution of tumorigenesis. However, little is known about the molecular mechanisms regulating these processes in vivo. Here we demonstrate that Polo-like kinase 2 (Plk2) regulates mitotic spindle orientation in the mammary gland and is a putative tumor suppressor. Plk2 is highly expressed in the mammary gland and is required for proper mammary gland development. Loss of Plk2 leads to increased mammary epithelial cell proliferation and ductal hyperbranching. Additionally a novel role for Plk2 in regulating the orientation of the mitotic spindle and maintaining proper cell polarity in the ductal epithelium was discovered. In support of a tumor suppressor function for Plk2, loss of Plk2 increased the formation of lesions in multiparous glands. Collectively, these results demonstrate a novel role for Plk2 in regulating mammary gland development and as a tumor suppressor in mammary tumorigenesis.

Dataset Information

Breast tumor from Pik3caH1047R/+ mammary gland transduced with single or pooled lentivirus.

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