Evidence map›Paper›PMID 29137357›Full record

ArticleOncotarget2017

AKR7A3 suppresses tumorigenicity and chemoresistance in hepatocellular carcinoma through attenuation of ERK, c-Jun and NF-κB signaling pathways.

Raymond Kwok Kei Chow, Sarah Tsz-Kwan Sin, Ming Liu, Yan Li, Tim Hon Man Chan, Yangyang Song, Leilei Chen, Dora Lai-Wan Kwong, Xin-Yuan Guan

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.1field-weighted citation impact, top 23% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 40 citations in OpenAlex.

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  11. Investigation of Anti-Liver Cancer Activity of the Herbal Drug FDY003 Using Network Pharmacology.Evidence-based complementary and alternative medicine : eCAM · 2022
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  16. Studying the Role and Molecular Mechanisms ofBioMed research international · 2020
    Article
  17. Article
  18. Article
  19. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 6 institutions in 3 countries.

Raymond Kwok Kei Chow *Department of Clinical Oncology, Li Ka Shing Faculty of Medicine, the University of Hong Kong, Hong Kong.
Sarah Tsz-Kwan Sin *Department of Clinical Oncology, Li Ka Shing Faculty of Medicine, the University of Hong Kong, Hong Kong.
Ming LiuSchool of Basic Sciences, Guangzhou Medical University, Guangzhou, China.
Yan LiDepartment of Biology, South University of Science and Technology of China, Shenzhen, China.
Tim Hon Man ChanCancer Science Institute of Singapore, National University of Singapore, Singapore.
Yangyang SongCancer Science Institute of Singapore, National University of Singapore, Singapore.
Leilei ChenCancer Science Institute of Singapore, National University of Singapore, Singapore.
Dora Lai-Wan KwongDepartment of Clinical Oncology, Li Ka Shing Faculty of Medicine, the University of Hong Kong, Hong Kong.
Xin-Yuan GuanDepartment of Clinical Oncology, Li Ka Shing Faculty of Medicine, the University of Hong Kong, Hong Kong.
University of Hong Kong · HKNational University of Singapore · SGChinese University of Hong Kong · CNGuangzhou Medical University · CNNational University Cancer Institute, Singapore · SGSouthern University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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 α-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-κB. In summary, we found that AKR7A3 functions as a tumor suppressor gene in HCC through attenuating c-Jun, ERK and NF-κB signaling pathways.

Indexed as

AKR7A3chemoresistanceHCCmethylationtumor suppressor

Identifiers

PMID29137357
PMCPMC5663529
OpenAlexW2534088339

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.