Research Papers:

FAM83D, a microtubule-associated protein, promotes tumor growth and progression of human gastric cancer

Minlu Huang, Xinjie Ma, Hongpeng Shi, Lei Hu, Zhiyuan Fan, Li Pang, Fan Zhu, Xiao Yang, Wei Xu, Binya Liu, Zhenggang Zhu and Chen Li _

PDF  |  HTML  |  Supplementary Files  |  How to cite

Oncotarget. 2017; 8:74479-74493. https://doi.org/10.18632/oncotarget.20157

Metrics: PDF 1671 views  |   HTML 3053 views  |   ?  


Minlu Huang1, Xinjie Ma1, Hongpeng Shi1, Lei Hu1, Zhiyuan Fan1, Li Pang1, Fan Zhu1, Xiao Yang1, Wei Xu1, Binya Liu1, Zhenggang Zhu1 and Chen Li1

1Shanghai Key Laboratory of Gastric Neoplasms, Department of Surgery, Shanghai Institute of Digestive Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, People’s Republic of China

Correspondence to:

Chen Li, email: [email protected]

Keywords: FAM83D, gastric cancer, proliferation, HMMR, TPX2

Received: August 17, 2016    Accepted: June 02, 2017    Published: August 10, 2017


FAM83D, a microtubule-associated protein (MAP), is overexpressed in diverse types of human cancer. The expression and critical role of FAM83D in human gastric cancer (GC), however, remains largely unknown. Here, we conducted molecular, cellular and clinical analyses to evaluate the functional link of FAM83D to GC. FAM83D expression was elevated in gastric tumors, and its expression strongly correlated with lymph node metastasis and TNM stage. In addition, over-expression of FAM83D in GC cell lines enhanced cell proliferation, cycle progression, migration, invasion, as well as tumor growth and metastatic dissemination in vivo. Furthermore, FAM83D exhibited a strong cell cycle correlated expression. The knockdown of FAM83D inhibited the regrowth of microtubules in GC cells. FAM83D was co-immunoprecipitated with HMMR, TPX2, and AURKA, a set of drivers of mitosis progression. Taken together, our results demonstrate FAM83D as an important player in the development of human gastric cancer, and as a potential therapeutic target for the treatment of cancer.

Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 20157