Oncotarget

Research Papers:

miR-1290 promotes lung adenocarcinoma cell proliferation and invasion by targeting SOCS4

Xuelian Xiao, Daheng Yang, Xue Gong, Dongping Mo, Shiyang Pan and Jian Xu _

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Oncotarget. 2018; 9:11977-11988. https://doi.org/10.18632/oncotarget.24046

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Abstract

Xuelian Xiao1,*, Daheng Yang1,*, Xue Gong1, Dongping Mo1, Shiyang Pan1,2 and Jian Xu1,2

1Department of Laboratory Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China

2National Key Clinical Department of Laboratory Medicine, Nanjing 210029, China

*These authors contributed equally to this work

Correspondence to:

Jian Xu, email: 13813849621@163.com

Keywords: lung adenocarcinoma; miR-1290; SOCS4; proliferation; invasion

Received: September 12, 2017     Accepted: January 03, 2018     Published: January 08, 2018

ABSTRACT

miRNAs play important roles in lung adenocarcioma (LADC) progression. We previously found that miR-1290 expression was upregulated in LADC tissue and serum samples from patients with LADC, and correlated with prognosis. However, the biological role of miR-1290 in LADC and mechanism of such role are poorly understood. Here, we found that miR-1290 overexpression promoted LADC cell proliferation, cell cycle progression and invasion, while suppressing cell apoptosis in vitro. Furthermore, miR-1290 promoted tumor growth, invasion and metastasis in vivo. miR-1290 downregulated suppressor of cytokine signaling 4 (SOCS4) at both the mRNA and protein levels by targeting SOCS4. Reduced SOCS4 level reversed the inhibitory effect of miR-1290 downregulation on cell proliferation and invasion. miR-1290 activated the JAK/STAT3 and PI3K/AKT signaling pathways by targeting SOCS4. An inverse correlation was observed between miR-1290 and SOCS4 expression in LADC tissues. Clinicopathological characteristics analysis showed that SOCS4 expression was negatively associated with higher clinical stage and lymph node metastasis. These observations suggest that miR-1290 promotes LADC cell proliferation and invasion by targeting SOCS4.


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