Dysregulation of the MiR-449b target TGFBI alters the TGFβ pathway to induce cisplatin resistance in nasopharyngeal carcinoma

Despite the improvement in locoregional control of nasopharyngeal carcinoma (NPC), distant metastasis (DM), and chemoresistance persist as major causes of mortality. This study identified a novel role for miR-449b, an overexpressed gene in a validated four-miRNA signature for NPC DM, leading to chem...

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Veröffentlicht in:Oncogenesis (New York, NY) NY), 2018-05, Vol.7 (5), p.40-13, Article 40
Hauptverfasser: Bissey, Pierre-Antoine, Law, Jacqueline H., Bruce, Jeff P., Shi, Wei, Renoult, Aline, Chua, Melvin L. K., Yip, Kenneth W., Liu, Fei-Fei
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container_start_page 40
container_title Oncogenesis (New York, NY)
container_volume 7
creator Bissey, Pierre-Antoine
Law, Jacqueline H.
Bruce, Jeff P.
Shi, Wei
Renoult, Aline
Chua, Melvin L. K.
Yip, Kenneth W.
Liu, Fei-Fei
description Despite the improvement in locoregional control of nasopharyngeal carcinoma (NPC), distant metastasis (DM), and chemoresistance persist as major causes of mortality. This study identified a novel role for miR-449b, an overexpressed gene in a validated four-miRNA signature for NPC DM, leading to chemoresistance via the direct targeting of transforming growth factor beta-induced (TGFBI). In vitro shRNA-mediated downregulation of TGFBI induced phosphorylation of PTEN and AKT, increasing cisplatin resistance. Conversely, the overexpression of TGFBI sensitized the NPC cells to cisplatin. In NPC patients treated with concurrent chemoradiotherapy (CRT), the overall survival (OS) was significantly inversely correlated with miR-449b, and directly correlated with both TGFBI mRNA and protein expression, as assessed by RNA sequencing and immunohistochemistry (IHC). Mechanistically, co-immunoprecipitation demonstrated that TGFBI competes with pro-TGFβ1 for integrin receptor binding. Decreased TGFBI led to increased pro-TGFβ1 activation and TGFβ1 canonical/noncanonical pathway-induced cisplatin resistance. Thus, overexpression of miR-449b decreases TGFBI, thereby altering the balance between TGFBI and pro-TGFβ1, revealing a novel mechanism of chemoresistance in NPC.
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K.</au><au>Yip, Kenneth W.</au><au>Liu, Fei-Fei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dysregulation of the MiR-449b target TGFBI alters the TGFβ pathway to induce cisplatin resistance in nasopharyngeal carcinoma</atitle><jtitle>Oncogenesis (New York, NY)</jtitle><stitle>Oncogenesis</stitle><addtitle>Oncogenesis</addtitle><date>2018-05-22</date><risdate>2018</risdate><volume>7</volume><issue>5</issue><spage>40</spage><epage>13</epage><pages>40-13</pages><artnum>40</artnum><issn>2157-9024</issn><eissn>2157-9024</eissn><abstract>Despite the improvement in locoregional control of nasopharyngeal carcinoma (NPC), distant metastasis (DM), and chemoresistance persist as major causes of mortality. This study identified a novel role for miR-449b, an overexpressed gene in a validated four-miRNA signature for NPC DM, leading to chemoresistance via the direct targeting of transforming growth factor beta-induced (TGFBI). 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subjects 13/106
13/109
13/2
13/89
38/90
38/91
631/67
631/80
82/1
82/51
82/80
AKT protein
Apoptosis
Cell Biology
Chemoradiotherapy
Chemoresistance
Chemotherapy
Cisplatin
Gene expression
Human Genetics
Immunohistochemistry
Immunoprecipitation
Internal Medicine
Medicine
Medicine & Public Health
Metastases
miRNA
mRNA
Nasopharyngeal carcinoma
Oncology
Phosphorylation
PTEN protein
Throat cancer
Transforming growth factor-b
Transforming growth factor-b1
title Dysregulation of the MiR-449b target TGFBI alters the TGFβ pathway to induce cisplatin resistance in nasopharyngeal carcinoma
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