QYQun Yan

Qun Yan

*This is an algorithmically generated author record based on publicly available information.

Current Organizations / Institutes

The organizations/institutes from the scholar's latest article

Research Subjects


Qun Yan has a total of 12 co-authors. Here are the top co-authors by number of shared publications:

  • Guiyuan Li

    The Key Laboratory of Carcinogenesis of the Chinese Ministry of Health, Xiangya Hospital, Central South University, Changsha, Hunan, China

    1 shared publication
  • Hailin Tang

    Central South University

    1 shared publication
  • Jian Ma

    Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital/The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan 410013, P.R. China

    1 shared publication
  • Min Deng

    Cancer Research Institute, Central South University, Hunan Key Laboratory of Nonresolving Inflammation and Cancer, Changsha, China

    1 shared publication
  • Ming Zhou

    Central South University

    1 shared publication
  • Qiurong Ye

    Central South University

    1 shared publication

Latest Publications

  • miR-214 promotes tumorigenesis by targeting lactotransferrin in nasopharyngeal carcinoma

    by Min Deng, Qiurong Ye, Zailong Qin, Ying Zheng, Wei He, Hailin Tang, Yanhong Zhou, Wei Xiong, Ming Zhou, Xiaoling Li, et al.

    LTF (lactotransferrin, or lactoferrin) plays important role in innate immunity, and its anti-tumor function has also been reported in multiple cancers. We previously reported that LTF is significantly down-regulated in nasopharyngeal carcinoma (NPC) and acts as a tumor suppressor by suppressing AKT signaling. However, the exact mechanism of the down-regulation of LTF in NPC has not been revealed. In the current study, we screened and identified LTF is a bona fide target of miR-214 in NPC cells. miR-214 mimics significantly suppressed LTF mRNA and protein expression levels in NPC cells. miR-214 not only can promote NPC cell proliferation and invasion abilities in vitro, but also can accelerate tumor formation and lung metastasis in a mouse xenograft model. The pro-tumor function of miR-214 was depended on LTF suppression since LTF re-expression can reverse it. miR-214 can also activate AKT signaling by suppressing LTF expression. Furthermore, miR-214 expression level was up-regulated in NPC especially in metastasis-prone NPC tumor tissues compared with normal nasopharyngeal epithelial tissues, while the LTF expression level was negatively correlated with miR-214, suggesting that miR-214 targeting is partly responsible for LTF down-regulation in NPC specimens.