To　investigate　the　interaction　between　interleukin-17　(IL-17)　and　interferon-γ　(IFN-γ)　and　how　their　interaction　affects　the　growth　of　mouse　hepatoma　Hepa1-6　cells.Hepa1-6　cells　treated　with　IL-17　and　IFN-γ　either　alone　or　in　combination　were　examined　for　changes　in　cell　proliferation　using　MTT　assay　and　in　cell　cycle　distribution　using　flow　cytometry.　Western　blotting　was　used　to　detect　the　protein　expression　levels　of　proliferating　cell　nuclear　antigen　(PCNA),　cyclin　D1,　P21　and　P16　and　the　phosphorylation　of　p38MAPK,　ERK1/2　and　Stat1　in　the　cells.Compared　with　control　group,　IFN-γ　treatment　obviously　inhibited　the　growth　and　proliferation　of　Hepa1-6　cells,　induced　cell　cycle　arrest　at　G0/G1　phase,　reduced　the　protein　expression　of　PCNA　and　cyclin　D1,　and　increased　the　protein　expression　of　P21.　IL-17　alone　had　no　effect　on　the　growth　of　Hepa1-6　cells.　In　the　combined　treatment,　IL-17　significantly　antagonized　the　effects　of　IFN-γ.　Compared　with　those　treated　with　IFN-γ　alone,　the　cells　with　the　combined　treatment　showed　significantly　decreased　G0/G1　cell　population,　increased　the　protein　expressions　of　PCNA　and　cyclin　D1,　and　decreased　the　protein　expression　of　P21.　IL-17　significantly　inhibited　IFN-γ-induced　phosphorylation　of　p38MAPK　and　ERK1/2　without　affecting　the　phosphorylation　of　Stat1.IL-17　obviously　reverses　the　antitumor　effects　of　IFN-γ　to　promote　the　proliferation　of　mouse　hepatoma　cells　and　accelerate　the　development　of　hepatocellular　carcinoma.