Research Papers:

MicroRNA-940 promotes tumor cell invasion and metastasis by downregulating ZNF24 in gastric cancer

Xinyang Liu, Xiaoxiao Ge, Zhe Zhang, Xiaowei Zhang, Jinjia Chang, Zheng Wu, Wenbo Tang, Lu Gan, Menghong Sun and Jin Li _

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Oncotarget. 2015; 6:25418-25428. https://doi.org/10.18632/oncotarget.4456

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Xinyang Liu1,*, Xiaoxiao Ge1,*, Zhe Zhang2, Xiaowei Zhang2, Jinjia Chang1, Zheng Wu1, Wenbo Tang1, Lu Gan1, Menghong Sun3, Jin Li4

1Shanghai Medical College, Fudan University, Shanghai, 200032, P.R. China

2Department of Medical Oncology, Fudan University Shanghai Cancer Center, Shanghai, 200032, P.R. China

3Department of Pathology, Fudan University Shanghai Cancer Center, Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, P.R. China

4Department of Medical Oncology, Shanghai Tianyou Hospital of Tongji University, Shanghai, 200032, P.R. China

*These authors have contributed equally to this work

Correspondence to:

Jin Li, e-mail: [email protected]

Keywords: gastric cancer, miR-940, ZNF24, metastasis, epithelial-mesenchymal transition

Received: March 23, 2015     Accepted: June 15, 2015     Published: June 27, 2015


Growing evidence indicates that microRNA (miRNA) plays a vital role in progression and metastasis of gastric cancer (GC). However, the underlying mechanism of miRNA-mediated metastasis has not been fully understood. Recently, miRNA-940 (miR-940) was found to be overexpressed in GC, which correlated with malignant progression and poor survival. Mechanistically, we found that miR-940 promoted GC cell migration, invasion, and metastasis in vivo by directly and functionally repressing the expression of Zinc Finger Transcription Factor 24 (ZNF24). Importantly, upregulation of ZNF24 could re-inhibit miR-940-induced migration and invasion. Hence, we demonstrated the oncogenic role of miR-940 in GC, finding that miR-940 promoted GC progression by directly downregulating ZNF24 expression, and targeting miR-940 could serve as a novel strategy for future GC therapy.

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