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Dinitrosopiperazine-decreased PKP3 through upregulating miR-149 participates in nasopharyngeal carcinoma metastasis.

Mol Carcinog. 2018 Dec;57(12):1763-1779. doi:10.1002/mc.22895. Epub 2018 Sep 19
Yuejin Li 1 , Kunyu Ju 2 , Weiwei Wang 3 , Zheliang Liu 3 , Haitao Xie 4 , Yuan Jiang 3 , Guanmin Jiang 3 , Jinping Lu 1 , Zigang Dong 5 , Faqing Tang 1
Yuejin Li 1 , Kunyu Ju 2 , Weiwei Wang 3 , Zheliang Liu 3 , Haitao Xie 4 , Yuan Jiang 3 , Guanmin Jiang 3 , Jinping Lu 1 , Zigang Dong 5 , Faqing Tang 1
+ et al

[No authors listed]

Author information
  • 1 Zhuhai Hospital of Jinan University, Zhuhai, China.
  • 2 Metallurgical Science and Engineering, Central South University, Changsha, China.
  • 3 Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, China.
  • 4 The First Affiliated Hospital of University of South China, Hengyang, China.
  • 5 Hormel Institute, University of Minnesota, Austin, Minnesota.

摘要

Nasopharyngeal carcinoma (NPC) has a high metastatic clinicopathological feature. As a carcinogen factor, N,N'-dinitrosopiperazine (DNP) is involved in NPC metastasis, but its precise mechanism has not been fully elucidated. Herein, we showed that DNP promotes NPC metastasis through upregulating miR-149. DNP was found to decrease Plakophilin3 (PKP3) expression, further DNP-decreased PKP3 was verified to be through upregulating miR-149. We also found that DNP induced proliferation, adhesion, migration and invasion of NPC cell, which was inhibited by miR-149-inhibitor. DNP may promote NPC metastasis through miR-149-decreased PKP3 expression. Therefore, DNP-increased miR-149 expression may be an important factor of NPC high metastasis, and miR-149 may serve as a molecular target for anti-metastasis therapy of NPC.

KEYWORDS: N,N′-dinitrosopiperazine, Plakophilin3, metastasis, miR-149, nasopharyngeal carcinoma

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