Abstract
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.
Highlights
Gastric cancer (GC) is one of the leading causes of cancer-related death worldwide [1,2,3]
We show that Family with sequence similarity 83 member D (FAM83D) is overexpressed in human gastric tumors, and its overexpression strongly correlates with lymph node metastasis and TNM stage
Our functional analyses reveal that FAM83D overexpression promotes tumor cell proliferation, colony formation, migration, and invasion, as well as tumor growth and metastatic dissemination
Summary
Gastric cancer (GC) is one of the leading causes of cancer-related death worldwide [1,2,3]. With sequence similarity 83 member D (FAM83D), known as C20Orf129 or CHICA, has been implicated as a crucial player in the GC malignancy. This gene was initially identified as a novel spindle component by mass-spectrometry [4]. FAM83D is implicated in promoting tumor cell proliferation, migration, and invasion through activation of the mTOR- and MAPK- signaling pathway [6, 10]. These observations implicate FAM83D as a strong driver of tumor development and progression in human cancer
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