Research Papers:

Upregulation of miR-572 transcriptionally suppresses SOCS1 and p21 and contributes to human ovarian cancer progression

Xin Zhang, Junling Liu, Dan Zang, Shu Wu, Aibin Liu, Jinrong Zhu, Geyan Wu, Jun Li and Lili Jiang _

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Oncotarget. 2015; 6:15180-15193. https://doi.org/10.18632/oncotarget.3737

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Xin Zhang1,2,*, Junling Liu3,*, Dan Zang1, Shu Wu2, Aibin Liu4, Jinrong Zhu4, Geyan Wu4, Jun Li4 and Lili Jiang1

1 Department of Pathophysiology, Guangzhou Medical University, Guangzhou, China

2 Department of Experimental Research, State Key Laboratory of Oncology in Southern China, Sun Yat-sen University Cancer Centre, Guangzhou, China

3 Department of Medical Oncology, State Key Laboratory of Oncology in Southern China, Sun Yat-sen University Cancer Center, Guangzhou, China

4 Department of Biochemistry, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong, China

* These authors have contributed equally to this work

Correspondence to:

Lili Jiang, email:

Keywords: ovarian cancer, miR-572, proliferation, SOCS1, p21

Received: January 27, 2015 Accepted: March 05, 2015 Published: March 30, 2015


Ovarian cancer is a gynecological malignancy with high mortality rates worldwide and novel diagnostic and prognostic markers and therapeutic targets are urgently required. The suppressor of cytokine signaling 1 (SOCS1) and cyclin-dependent kinase inhibitor 1A (p21KIP) are known to regulate tumor cell proliferation. However, the mechanisms that regulate these genes have not yet been completely elucidated. In the present study, analysis of a published microarray-based high-throughput assessment (NCBI/E-MTAB-1067) and real-time PCR demonstrated that miR-572 was upregulated in human ovarian cancer tissues and cell lines. Kaplan-Meir analysis indicated that high level expression of miR-572 was associated with poorer overall survival. Ectopic miR-572 promoted ovarian cancer cell proliferation and cell cycle progression in vitro and tumorigenicity in vivo. SOCS1 and p21 were identified as direct targets of miR-572 and suppression of SOCS1 or p21 reversed the inhibiting-function of miR-572-silenced cell on proliferation and tumorigenicity in ovarian cancer cells. Additionally, the expression of miR-572 correlated inversely with the protein expression levels of SOCS1, p21 and positively with Cyclin D1 in ovarian carcinoma specimens. This study demonstrates that miR-572 post-transcriptionally regulates SOCS1 and p21 and may play an important role in ovarian cancer progression; miR-572 may represent a potential therapeutic target for ovarian cancer therapy.

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