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An Oncogenic Hepatocyte-Induced Orthotopic Mouse Model of Hepatocellular Cancer Arising in the Setting of Hepatic Inflammation and Fibrosis
Published on: September 12, 2019
Targeting FAM64A: a promising strategy to halt liver cancer angiogenesis and enhance immunity
Liping Bai1, Xueyan Yang1, Lixian Bai2
1Department of Gastroenterology, The Affiliated Hospital of Yunnan University Kunming, Yunnan, China.
Abstract:
Liver cancer, a primary malignancy of liver cells, exhibits high morbidity and mortality. Family with sequence similarity 64, member A (FAM64A) acts as an oncogene and modulates tumor progression in multiple cancers. However, the specific role of FAM64A in liver cancer development remains poorly elucidated. Thus, this work uncovered the action of FAM64A on liver cancer pathogenesis and cancer immunity and reveals the underlying mechanism. In this study, the FAM64A expression in liver cancer and its association with the overall survival were investigated using bioinformatics analysis. Tumor tissues and adjacent normal tissues were obtained from 64 liver cancer cases. Cell viability, invasion, and angiogenesis were assessed by CCK-8 method, Transwell invasion assay, and tube formation assay, respectively. The secretion levels of IFN-γ, IL-2, IL-10 and TGF-β were tested utilizing the ELISA assay. A xenograft tumor was created to monitor tumor growth in vivo. Results revealed that FAM64A expression was elevated in liver cancer. Clinically, high FAM64A levels correlated with shorter overall survival. Silencing of FAM64A restricted the malignant phenotypes of liver cancer cells, including proliferation, invasion, angiogenesis and immune escape. Furthermore, FAM64A knockdown restricted the activation of the VEGFA/AKT signaling. Conversely, VEGFA overexpression offset the above influences of FAM64A on liver cancer cells. Moreover, silenced FAM64A suppressed tumor growth, decreased CD31 and PD-L1 levels, increased CD8 and IFN-γ level, and reduced activation of the VEGFA/AKT signaling. Taken together, FAM64A is up-regulated in liver cancer and closely correlated with poor prognosis. Silenced FAM64A restrained proliferation ability, invasion capacity, angiogenesis and immune escape of liver cancer cells through inactivating the VEGFA/AKT signaling. FAM64A may be a valuable candidate target for liver cancer therapy.
Insights
Family with sequence similarity 64, member A (FAM64A) is elevated in liver cancer, correlating with poor prognosis. Silencing FAM64A inhibits cancer cell proliferation, invasion, angiogenesis, and immune escape by inactivating the VEGFA/AKT pathway, suggesting FAM64A as a therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Immunology
Background:
- Liver cancer is a significant health concern with high mortality.
- Family with sequence similarity 64, member A (FAM64A) is implicated as an oncogene in various cancers.
- The precise role of FAM64A in liver cancer pathogenesis and its impact on anti-tumor immunity are not well understood.
Purpose of the Study:
- To investigate the role of FAM64A in liver cancer development.
- To elucidate the underlying mechanisms by which FAM64A influences liver cancer progression and immune evasion.
- To assess FAM64A as a potential therapeutic target for liver cancer.
Main Methods:
- Bioinformatic analysis of FAM64A expression in liver cancer tissues and correlation with patient survival.
- In vitro assays (CCK-8, Transwell, tube formation) to evaluate cell viability, invasion, and angiogenesis.
- ELISA to measure cytokine levels (IFN-γ, IL-2, IL-10, TGF-β).
- In vivo xenograft models to assess tumor growth and immune cell infiltration.
- Western blot analysis to examine signaling pathway activation (VEGFA/AKT).
Main Results:
- FAM64A expression is significantly upregulated in liver cancer tissues compared to normal tissues.
- High FAM64A levels are associated with shorter overall survival in liver cancer patients.
- FAM64A knockdown suppressed liver cancer cell proliferation, invasion, angiogenesis, and immune escape.
- FAM64A silencing inhibited the VEGFA/AKT signaling pathway.
- Overexpression of VEGFA partially reversed the effects of FAM64A knockdown.
- FAM64A knockdown suppressed tumor growth, reduced CD31 and PD-L1 expression, increased CD8 and IFN-γ levels, and deactivated the VEGFA/AKT pathway in vivo.
Conclusions:
- FAM64A is oncogenic in liver cancer, promoting proliferation, invasion, angiogenesis, and immune evasion.
- FAM64A exerts its effects by activating the VEGFA/AKT signaling pathway.
- Targeting FAM64A may represent a promising therapeutic strategy for liver cancer, potentially enhancing anti-tumor immunity.
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