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The recepteur d'origine nantais (RON) receptor tyrosine kinase is highlyexpressed in various cancers including human hepatocellular carcinoma (HCC) andinvolved in tumor progression. The aims of the current study were to evaluatewhether RON affects tumor cell behavior and oncogenic signaling cascades in HCCcells. We investigated the biologic role of RON on tumor cell behavior and oncogenicsignaling cascades including Akt, c-Raf and extracellular signal-regulated kinase(ERK) by using the small interfering RNA (siRNA) in HCC cell lines, chang, HepG2and Huh7. Knockdown of RON suppressed tumor cell migration and invasion in alltested HCC cell lines. The proportion of apoptotic cells induced by knockdownof RON was greater than that induced by transfection of the scramble siRNA inall tested HCC cell lines. Knockdown of RON resulted in cell cycle arrest in theG2/M phase of chang and Huh7 cells, and sub G1 phase of HepG2 cells. Knockdownof RON activated cleaved caspase-3 and PARP, and down-regulated the expressionof Bcl-2, Bcl-xL and survivin, leading to induction of apoptosis in all testedcell lines. Knockdown of RON negatively regulates the progression of the cellcycle by decreasing cyclin D1 and D3, and increasing p21 and p27 in all testedcell lines. The phosphorylation of Akt, c-Raf and ERK1/2 signal proteins was significantlyblocked by knockdown of RON in all tested cell lines. These results suggest thatRON is associated with invasive and oncogenic phenotypes such as tumor cell migration,invasion, resistance to apoptosis and cell cycle arrest through the modulationof Akt, c-Raf and ERK signaling cascades in HCC cells.

Small interfering RNA-directed targeting of RON alters invasive and oncogenic phenotypes of human hepatocellular carcinoma cells