Please use this identifier to cite or link to this item: https://doi.org/10.18632/oncotarget.12726
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dc.titleAKR7A3 suppresses tumorigenicity and chemoresistance in hepatocellular carcinoma through attenuation of ERK, c-Jun and NF-?B signaling pathways
dc.contributor.authorChow, R.K.K
dc.contributor.authorSin, S.T
dc.contributor.authorLiu, M
dc.contributor.authorLi, Y
dc.contributor.authorChan, T.H.M
dc.contributor.authorSong, Y
dc.contributor.authorChen, L
dc.contributor.authorKwong, D.L
dc.contributor.authorGuan, X.-Y
dc.date.accessioned2020-10-23T04:55:38Z
dc.date.available2020-10-23T04:55:38Z
dc.date.issued2017
dc.identifier.citationChow, 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. https://doi.org/10.18632/oncotarget.12726
dc.identifier.issn19492553
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/179543
dc.description.abstractHepatocellular 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.
dc.rightsAttribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.sourceUnpaywall 20201031
dc.subjectaldo keto reductase family 7A isoform 3
dc.subjectalpha fetoprotein
dc.subjectcisplatin
dc.subjectimmunoglobulin enhancer binding protein
dc.subjectmitogen activated protein kinase
dc.subjectoxidoreductase
dc.subjectprotein c jun
dc.subjectunclassified drug
dc.subjectadult
dc.subjectallele
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectArticle
dc.subjectcancer cell line
dc.subjectcancer inhibition
dc.subjectcancer tissue
dc.subjectcarcinogenicity
dc.subjectcolony formation
dc.subjectcontrolled study
dc.subjectdown regulation
dc.subjectdrug resistance
dc.subjectfemale
dc.subjectheterozygosity loss
dc.subjecthuman
dc.subjecthuman cell
dc.subjecthuman tissue
dc.subjectin vitro study
dc.subjectin vivo study
dc.subjectliver cell carcinoma
dc.subjectmajor clinical study
dc.subjectmale
dc.subjectmouse
dc.subjectnonhuman
dc.subjectnude mouse
dc.subjectoverall survival
dc.subjectpromoter region
dc.subjectreal time polymerase chain reaction
dc.subjectWestern blotting
dc.typeArticle
dc.contributor.departmentCANCER SCIENCE INSTITUTE OF SINGAPORE
dc.contributor.departmentANATOMY
dc.description.doi10.18632/oncotarget.12726
dc.description.sourcetitleOncotarget
dc.description.volume8
dc.description.issue48
dc.description.page83469-83479
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