الفهرس 
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Abstract
Aim: Investigating the silencing of NUPR1 in HepG2 cells using the breakthrough genome editing technique CRISPR/Cas9.
Methods: HepG2 cells were seeded and transfected with specific NUPR1 crRNA:tracrRNA mixture and Cas9 plasmids. Cell viability was measured via MTT assay, cytokines secretions, and the expression levels of some genes were analyzed 24 hours after transfection.
Results: The viability of HepG2 is not affected following the NUPR1 silencing. Several modulators (AFP, TGF-β1, IL-2, and IL-6) involved in the HCC development and immune defense mechanisms are significantly down regulated. In addition, the expression levels of TGF-β2 and IGFBP7 are suppressed, while FGF19 unchanged.
Conclusion: Our study verifies that targeting NUPR1 as a possible treatment for HCC may lead to unexpected outcomes as it is involved in various pathways and its role differs according to cancer cell type.