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Title: AKR7A3 suppresses tumorigenicity and chemoresistance in hepatocellular carcinoma through attenuation of ERK, c-Jun and NF-?B signaling pathways
Authors: Chow, R.K.K
Sin, S.T
Liu, M
Li, Y
Chan, T.H.M 
Song, Y 
Chen, L 
Kwong, D.L
Guan, X.-Y
Keywords: aldo keto reductase family 7A isoform 3
alpha fetoprotein
immunoglobulin enhancer binding protein
mitogen activated protein kinase
protein c jun
unclassified drug
animal experiment
animal model
animal tissue
cancer cell line
cancer inhibition
cancer tissue
colony formation
controlled study
down regulation
drug resistance
heterozygosity loss
human cell
human tissue
in vitro study
in vivo study
liver cell carcinoma
major clinical study
nude mouse
overall survival
promoter region
real time polymerase chain reaction
Western blotting
Issue Date: 2017
Citation: Chow, R.K.K, Sin, S.T, Liu, M, Li, Y, Chan, T.H.M, Song, Y, Chen, L, Kwong, D.L, Guan, X.-Y (2017). AKR7A3 suppresses tumorigenicity and chemoresistance in hepatocellular carcinoma through attenuation of ERK, c-Jun and NF-?B signaling pathways. Oncotarget 8 (48) : 83469-83479. ScholarBank@NUS Repository.
Rights: Attribution 4.0 International
Abstract: Hepatocellular carcinoma (HCC), which accounts for 85-90% of primary liver cancer, is now the second leading cause of cancer-related mortality worldwide. Here we reported that Aldo-Keto Reductase family 7A isoform 3 (AKR7A3) is frequently down-regulated in HCC, associating with poor overall survival rate, elevated serum �-fetoprotein (AFP) and poor differentiation of HCC. The promoter region of AKR7A3 was detected to be hypermethylated. Loss of heterozygosity (LOH) was also detected in AKR7A3. Functional assays on both AKR7A3 overexpressed and knockdown cells, including foci formation, colony formation in soft agar, migration, invasion and tumor formation in nude mice, demonstrated the strong tumor suppressive functions of AKR7A3. In addition, treatment of chemotherapy drug cisplatin showed that AKR7A3 sensitizes tumor cells to apoptosis. Mechanistically, western blot analysis showed that overexpression of AKR7A3 inhibits the activation of ERK, c-Jun and NF-?B. In summary, we found that AKR7A3 functions as a tumor suppressor gene in HCC through attenuating c-Jun, ERK and NF-?B signaling pathways. ? Chow et al.
Source Title: Oncotarget
ISSN: 19492553
DOI: 10.18632/oncotarget.12726
Rights: Attribution 4.0 International
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