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Open AccessArticle

PSPC1 Potentiates IGF1R Expression to Augment Cell Adhesion and Motility

1
Graduate Institute of Life Sciences, National Defense Medical Center, Taipei 11490, Taiwan
2
Institute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan
*
Author to whom correspondence should be addressed.
Cells 2020, 9(6), 1490; https://doi.org/10.3390/cells9061490
Received: 30 April 2020 / Revised: 6 June 2020 / Accepted: 16 June 2020 / Published: 18 June 2020
(This article belongs to the Section Cell Motility and Adhesion)
Paraspeckle protein 1 (PSPC1) overexpression in cancers is known to be the pro-metastatic switch of tumor progression associated with poor prognosis of cancer patients. However, the detail molecular mechanisms to facilitate cancer cell migration remain elusive. Here, we conducted integrated analysis of human phospho-kinase antibody array, transcriptome analysis with RNA-seq, and proteomic analysis of protein pulldown to study the molecular detail of PSPC1-potentiated phenotypical transformation, adhesion, and motility in human hepatocellular carcinoma (HCC) cells. We found that PSPC1 overexpression re-assembles and augments stress fiber formations to promote recruitment of focal adhesion contacts at the protruding edge to facilitate cell migration. PSPC1 activated focal adhesion-associated kinases especially FAK/Src signaling to enhance cell adhesion and motility toward extracellular matrix (ECM). Integrated transcriptome and gene set enrichment analysis indicated that PSPC1 modulated receptor tyrosine kinase IGF1R involved in the focal adhesion pathway and induction of diverse integrins expression. Knockdown IGF1R expression and treatment of IGF1R inhibitor suppressed PSPC1-induced cell motility. Interestingly, knockdown PSPC1-interacted paraspeckle components including NONO, FUS, and the lncRNA Neat1 abolished PSPC1-activated IGF1R expression. Together, PSPC1 overexpression induced focal adhesion formation and facilitated cell motility via activation of IGF1R signaling. PSPC1 overexpression in tumors could be a potential biomarker of target therapy with IGF1R inhibitor for improvement of HCC therapy. View Full-Text
Keywords: PSPC1; paraspeckle; IGF1R; NONO; FUS; lncRNA Neat1; FAK/Src; cell motility PSPC1; paraspeckle; IGF1R; NONO; FUS; lncRNA Neat1; FAK/Src; cell motility
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MDPI and ACS Style

Jen, H.-W.; Gu, D.-L.; Lang, Y.-D.; Jou, Y.-S. PSPC1 Potentiates IGF1R Expression to Augment Cell Adhesion and Motility. Cells 2020, 9, 1490. https://doi.org/10.3390/cells9061490

AMA Style

Jen H-W, Gu D-L, Lang Y-D, Jou Y-S. PSPC1 Potentiates IGF1R Expression to Augment Cell Adhesion and Motility. Cells. 2020; 9(6):1490. https://doi.org/10.3390/cells9061490

Chicago/Turabian Style

Jen, Hsin-Wei; Gu, De-Leung; Lang, Yaw-Dong; Jou, Yuh-Shan. 2020. "PSPC1 Potentiates IGF1R Expression to Augment Cell Adhesion and Motility" Cells 9, no. 6: 1490. https://doi.org/10.3390/cells9061490

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