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Multi-layered proteogenomic analysis unravels cancer metastasis directed by MMP-2 and focal adhesion kinase signaling

 Yumi Kwon  ;  Seong-Jun Park  ;  Binh Thanh Nguyen  ;  Mi Jeong Kim  ;  Sejin Oh  ;  Hwanho Lee  ;  Narae Park  ;  Hyun Seok Kim  ;  Min-Jung Kang  ;  Byung Soh Min  ;  Jin-Won Lee  ;  Eun Gyeong Yang  ;  Cheolju Lee 
 SCIENTIFIC REPORTS, Vol.11(1) : 17130, 2021-08 
Journal Title
Issue Date
Cells, Cultured ; Colorectal Neoplasms / genetics ; Colorectal Neoplasms / metabolism* ; Colorectal Neoplasms / pathology ; Epithelial-Mesenchymal Transition ; Focal Adhesion Kinase 1 / genetics ; Focal Adhesion Kinase 1 / metabolism* ; HCT116 Cells ; Humans ; Matrix Metalloproteinase 2 / genetics ; Matrix Metalloproteinase 2 / metabolism* ; Neoplasm Metastasis ; Proteome / genetics ; Proteome / metabolism ; Signal Transduction ; Tetraspanin 29 / genetics ; Tetraspanin 29 / metabolism
The role of matrix metalloproteinase-2 (MMP-2) in tumor cell migration has been widely studied, however, the characteristics and effects of MMP-2 in clinical sample of metastatic colorectal cancer (CRC) remain poorly understood. Here, in order to unveil the perturbed proteomic signal during MMP-2 induced cancer progression, we analyzed plasma proteome of CRC patients according to disease progression, HCT116 cancer secretome upon MMP-2 knockdown, and publicly available CRC tissue proteome data. Collectively, the integrative analysis of multi-layered proteomes revealed that a protein cluster containing EMT (Epithelial-to-Mesenchymal Transition)-associated proteins such as CD9-integrin as well as MMP-2. The proteins of the cluster were regulated by MMP-2 perturbation and exhibited significantly increased expressions in tissue and plasma as disease progressed from TNM (Tumor, Node, and Metastasis) stage I to II. Furthermore, we also identified a plausible association between MMP-2 up-regulation and activation of focal adhesion kinase signaling in the proteogenomic analysis of CRC patient tissues. Based on these comparative and integrative analyses, we suggest that the high invasiveness in the metastatic CRC resulted from increased secretion of MMP-2 and CD9-integrin complex mediated by FAK signaling activation.
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1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
Yonsei Authors
Kim, Hyun Seok(김현석) ORCID logo https://orcid.org/0000-0003-4498-8690
Min, Byung Soh(민병소) ORCID logo https://orcid.org/0000-0003-0180-8565
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