FAM216A Promotes Hepatocellular Carcinoma Proliferation and Invasion through the PLK1/ERK Signaling Pathway

Abstract

Background and Aims:

Family with sequence similarity 216 member A (FAM216A) is overexpressed in several cancer tissues, but its prognostic value and pathological effect in hepatocellular carcinoma (HCC) have not been fully elucidated.

Materials and Methods:

FAM216A expression in HCC specimens and cell lines was determined by real-time PCR and western blotting. FAM216A expression was knocked down in HCCLM3 and Huh7 cells, and overexpressed in Hep3B and PLC/PRF/5 cells. The proliferation, migration, and invasion of different HCC cell lines were assessed by colony formation and Transwell assays. The expression of epithelial–mesenchymal transition (EMT)-related proteins and the level of polo-like kinase 1/extracellular regulated protein kinase (PLK1/ERK) were determined.

Results:

Increased FAM216A expression was observed in HCC tissues, a result that is consistent with outcomes obtained from an online database, and patient prognosis was negatively correlated with the FAM216A expression level. Additionally, FAM216A overexpression promoted the proliferation, migration, and invasion of HCC cells and activated EMT via the PLK1/ERK signaling pathway.

Conclusions:

FAM216A is overexpressed in HCC tissues and is associated with poor clinical outcomes. Mechanistically, FAM216A promotes aggressive tumor behavior by activating the PLK1/ERK signaling pathway.

Graphical Abstract

This is a visual representation of the abstract.

Keywords

hepatocellular carcinoma FAM216A PLK1 ERK proliferation

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