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Basic Information

Classification Information

Regulatory Mechanism		Biological Function		Clinical Application
TF		Immune		Survival
Enhancer		Apoptosis	apoptosis	Drug
Variant		Cell Growth		Circulating
MiRNA		EMT		Metastasis
Methylation		Coding Ability		Recurrence

Cancer&Entry Information

Cancer Name	cervical cancer
ICD-0-3	C53
Methods	qPCR, Western blot, etc.
Sample	MS751, SiHa, HeLa, HT-3, NCSC1, and NCSC2 cells
Expression Pattern	down-regulated
Function Description	DGCR5 was downregulated in human cervical cancer cell lines (MS751, SiHa, HeLa, and HT 3) compared with the primary normal cervical squamous cells (NCSC1 and NCSC2). Then, DGCR5 was restrained by transfection with lenti-virus-short hairpin RNA (LV shRNA) while induced by LV DGCR5 in HeLa and C33A cells. Silence of DGCR5 obviously induced cervical cancer cell viability and cell proliferation. Reversely, upregulation of DGCR5 inhibited HeLa and C33A cell survival and proliferation. Furthermore, silencing of DGCR5 increased cervical cancer cell colony formation ability and decreased cell apoptosis, whereas its overexpression exhibited an opposite process. Moreover, DGCR5 suppressed migration and invasion capacity of cervical cancer cells. The Wnt signaling is integral in numerous biological processes. Here, we found that Wnt signaling was strongly activated in cervical cancer cells. Downregulation of DGCR5 contributed to cervical cancer progression by activating Wnt signaling. Subsequently, in vivo animal models were used to confirm that DGCR5 suppressed cervical cancer via targeting Wnt signaling.
Pubmed ID	30552671
Year	2018
Title	Downregulation of Long Noncoding RNA DGCR5 Contributes to the Proliferation, Migration, and Invasion of Cervical Cancer by Activating Wnt Signaling Pathway

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