RGD Reference Report - Licochalcone B Ameliorates Liver Cancer via Targeting of Apoptotic Genes, DNA Repair Systems, and Cell Cycle Control. - Rat Genome Database

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Licochalcone B Ameliorates Liver Cancer via Targeting of Apoptotic Genes, DNA Repair Systems, and Cell Cycle Control.

Authors: Sadek, Kadry  Abouzed, Tarek  Nasr, Sherif  Shoukry, Moustafa 
Citation: Sadek K, etal., Iran J Pharm Res. 2020 Fall;19(4):372-386. doi: 10.22037/ijpr.2020.1101292.
RGD ID: 152998960
Pubmed: PMID:33841550   (View Abstract at PubMed)
PMCID: PMC8019863   (View Article at PubMed Central)
DOI: DOI:10.22037/ijpr.2020.1101292   (Journal Full-text)

Apurinic/apyrimidinic endonuclease 1/redox factor-1 (APE1/Ref-1) is a ubiquitous multifunctional protein required in the DNA base excision repair pathway and a noteworthy reducing-oxidizing factor that regulates the activity of various transcription factors. Cyclin-dependent kinases (CDKs) assume a key role in directing the progression of the cell- cycle. The present study evaluated the synergistic efficacy of using licochalcone B (LCB) and fullerene C60 (FnC60) nanoparticles against diethylnitrosamine (DEN)-induced hepatocarcinoma in rats and relevant signaling pathways, with APE1/Ref-1 and CDK-4, as novel anti-cancer- targeting. LCB alone and in combination with FnC60 significantly decreased DNA fragmentation, oxidative DNA damage (8-hydroxy-2'-deoxyguanosine levels), APE1/Ref-1, CDK-4, retinoblastoma, B- cell lymphoma-2 (Bcl-2), B-cell lymphoma-xL (Bcl-xL), and β-arrestin-2 mRNA expression, and APE1/Ref-1 and CDK-4 protein expression. In contrast, these treatments significantly increased the expression of protein 53 (p53), Bcl-2-associated X protein (Bax), and caspase-3. These data suggest that LCB either alone or in combination with FnC60 elicited significant protective effects against DEN-induced hepatocarcinogenesis, which may have occurred because of the regulation of enzymes involved in DNA repair and cell-cycle control at S phase progression as well as the induction of apoptosis at the gene and protein expression levels. Furthermore, FnC60 potentiated the effect of LCB at the molecular level, possibly through targeting of cancerous cells.

Objects Annotated

Genes (Rattus norvegicus)
Apex1  (apurinic/apyrimidinic endodeoxyribonuclease 1)
Arrb2  (arrestin, beta 2)
Bax  (BCL2 associated X, apoptosis regulator)
Bcl2  (BCL2, apoptosis regulator)
Bcl2l1  (Bcl2-like 1)
Casp3  (caspase 3)
Cdk4  (cyclin-dependent kinase 4)
Rb1  (RB transcriptional corepressor 1)
Tp53  (tumor protein p53)

Genes (Mus musculus)
Apex1  (apurinic/apyrimidinic endonuclease 1)
Arrb2  (arrestin, beta 2)
Bax  (BCL2-associated X protein)
Bcl2  (B cell leukemia/lymphoma 2)
Bcl2l1  (BCL2-like 1)
Casp3  (caspase 3)
Cdk4  (cyclin dependent kinase 4)
Rb1  (RB transcriptional corepressor 1)
Trp53  (transformation related protein 53)

Genes (Homo sapiens)
APEX1  (apurinic/apyrimidinic endodeoxyribonuclease 1)
ARRB2  (arrestin beta 2)
BAX  (BCL2 associated X, apoptosis regulator)
BCL2  (BCL2 apoptosis regulator)
BCL2L1  (BCL2 like 1)
CASP3  (caspase 3)
CDK4  (cyclin dependent kinase 4)
RB1  (RB transcriptional corepressor 1)
TP53  (tumor protein p53)


Additional Information