<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>20(5)</volume><submitter>Qu J</submitter><pubmed_abstract>The development of an effective therapeutic intervention for liver cancer is a worldwide challenge that remains to be adequately addressed. Of note, &lt;i>TP53&lt;/i>, which encodes the p53 protein, is an important tumor suppressor gene, 61% of &lt;i>TP53&lt;/i> is functionally inactivated in liver cancer. Recombinant human adenovirus p53 (rAd-p53) is the first commercial product that has been used for gene therapy. In the present study, the combined mechanistic effects of rAd-p53 and curcumin, a naturally occurring compound with previously reported anti-inflammatory, antioxidant and anti-cancer properties, were assessed in liver cancer cells, using HepG2 cells as the model cell line. The administration of either curcumin or rAd-p53 promoted apoptosis, suppressed epithelial-mesenchymal transition (EMT) and blocked G2/M phase progression in HepG2 cells, which were potentiated further when both agents were applied together. Combined rAd-p53 and curcumin treatment resulted in higher p53 (P&lt;0.01) and p21 (P&lt;0.01) expression compared with rAd-p53 or curcumin were added alone, suggesting an additive effect on &lt;i>TP53&lt;/i> expression. Additionally, curcumin and rAd-p53 were demonstrated to regulate the activation of mitogen-activated protein kinases (MAPKs) ERK1/2, p38 MAPK and JNK. These results indicated that the combination of rAd-p53 with curcumin synergistically potentiates apoptosis and inhibit EMT compared with either rAd-p53 or curcumin treatment alone via the regulation of &lt;i>TP53&lt;/i> regulation. Mechanistically, this effect on &lt;i>TP53&lt;/i> expression may involve the ERK1/2, p38 MAPK and JNK signaling pathways. The current study provides new insights that can potentially advance the development of therapeutic strategies for liver cancer treatment.</pubmed_abstract><journal>Experimental and therapeutic medicine</journal><pagination>18</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7471865</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Combined effect of recombinant human adenovirus p53 and curcumin in the treatment of liver cancer.</pubmed_title><pmcid>PMC7471865</pmcid><pubmed_authors>Yang J</pubmed_authors><pubmed_authors>Lu W</pubmed_authors><pubmed_authors>Chen M</pubmed_authors><pubmed_authors>Qu J</pubmed_authors><pubmed_authors>Gao W</pubmed_authors><pubmed_authors>Zhang C</pubmed_authors><pubmed_authors>Guo B</pubmed_authors></additional><is_claimable>false</is_claimable><name>Combined effect of recombinant human adenovirus p53 and curcumin in the treatment of liver cancer.</name><description>The development of an effective therapeutic intervention for liver cancer is a worldwide challenge that remains to be adequately addressed. Of note, &lt;i>TP53&lt;/i>, which encodes the p53 protein, is an important tumor suppressor gene, 61% of &lt;i>TP53&lt;/i> is functionally inactivated in liver cancer. Recombinant human adenovirus p53 (rAd-p53) is the first commercial product that has been used for gene therapy. In the present study, the combined mechanistic effects of rAd-p53 and curcumin, a naturally occurring compound with previously reported anti-inflammatory, antioxidant and anti-cancer properties, were assessed in liver cancer cells, using HepG2 cells as the model cell line. The administration of either curcumin or rAd-p53 promoted apoptosis, suppressed epithelial-mesenchymal transition (EMT) and blocked G2/M phase progression in HepG2 cells, which were potentiated further when both agents were applied together. Combined rAd-p53 and curcumin treatment resulted in higher p53 (P&lt;0.01) and p21 (P&lt;0.01) expression compared with rAd-p53 or curcumin were added alone, suggesting an additive effect on &lt;i>TP53&lt;/i> expression. Additionally, curcumin and rAd-p53 were demonstrated to regulate the activation of mitogen-activated protein kinases (MAPKs) ERK1/2, p38 MAPK and JNK. These results indicated that the combination of rAd-p53 with curcumin synergistically potentiates apoptosis and inhibit EMT compared with either rAd-p53 or curcumin treatment alone via the regulation of &lt;i>TP53&lt;/i> regulation. Mechanistically, this effect on &lt;i>TP53&lt;/i> expression may involve the ERK1/2, p38 MAPK and JNK signaling pathways. The current study provides new insights that can potentially advance the development of therapeutic strategies for liver cancer treatment.</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Nov</publication><modification>2024-12-04T12:18:35.233Z</modification><creation>2020-09-26T07:13:39Z</creation></dates><accession>S-EPMC7471865</accession><cross_references><pubmed>32934683</pubmed><doi>10.3892/etm.2020.9145</doi></cross_references></HashMap>