Oncotarget

Research Papers:

Co-expression analysis revealed PTCH1-3’UTR promoted cell migration and invasion by activating miR-101-3p/SLC39A6 axis in non-small cell lung cancer: implicating the novel function of PTCH1

Xuechao Wan, Zhe Kong, Kaili Chu, Chuanyou Yi, Jian Hu, Rui Qin, Chen Zhao, Fangqiu Fu, Hai Wu, Yao Li and Yan Huang _

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Oncotarget. 2018; 9:4798-4813. https://doi.org/10.18632/oncotarget.23219

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Abstract

Xuechao Wan1,*, Zhe Kong1,*, Kaili Chu1, Chuanyou Yi1, Jian Hu1, Rui Qin1, Chen Zhao1, Fangqiu Fu1, Hai Wu1, Yao Li1 and Yan Huang1

1State Key Laboratory of Genetic Engineering, Shanghai Engineering Research Center of Industrial Microorganisms, School of Life Sciences, Fudan University, Shanghai 200433, PR China

*These authors have contributed equally to this work

Correspondence to:

Yan Huang, email: huangyan@fudan.edu.cn

Keywords: PTCH1-3'UTR; metastasis; miR-101-3p; WGCNA; non-small cell lung cancer

Received: May 04, 2017     Accepted: November 16, 2017     Published: December 13, 2017

ABSTRACT

Metastasis is the most common cause of mortality for non-small cell lung cancer (NSCLC). PTCH1, a receptor of Hedgehog (Hh) pathway, is reported to suppress cell proliferation. Interestingly, our previous study showed PTCH1 silencing promoted cell proliferation but inhibited cell migration and invasion of NSCLC cells. However, the precise mechanisms of PTCH1 regulating NSCLC metastasis remain unclear. PTCH1 has multiple splicing variants, which all share the same 3’UTR sequence, meanwhile, emerging studies have shown competing endogenous RNAs (ceRNAs) play important roles in regulating cancer progression. Therefore, we hypothesized the functions of PTCH1-3’UTR in NSCLC in present study to reveal its role as a ceRNA. Here, we find overexpression of PTCH1-3’UTR promotes cell migration, invasion and adhesion, but does not affect cell proliferation in NSCLC cells. By combining weighted correlation network analysis (WGCNA) analysis and experimental validation, we reported PTCH1-3’UTR acted as a sponge to absorb miR-101-3p and promoted SLC39A6 expression. Moreover, we observed low expression of miR-101-3p and PTCH1 and high SLC39A6 levels were positively correlated with NSCLC progression. Therefore, our results help to understand the function of PTCH1 in NSCLC tumorigenesis and provide novel insights for the prevention of NSCLC metastasis.


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