Evidence map›Paper›PMID 32924268›Full record

ArticleJournal of cellular and molecular medicine2020

Pseudogene AKR1B10P1 enhances tumorigenicity and regulates epithelial-mesenchymal transition in hepatocellular carcinoma via stabilizing SOX4.

Fengjie Hao, Xiaochun Fei, Xinping Ren, Joanna Xi Xiao, Yongjun Chen, Junqing Wang

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. 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
1.7field-weighted citation impact, top 18% 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, 23 citations in OpenAlex.

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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

6 authors at 1 institution in 1 country.

Fengjie HaoDepartment of General Surgery, Hepatobiliary Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.
Xiaochun FeiDepartment of Pathology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.
Xinping RenDepartment of Ultrasound, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.
Joanna Xi XiaoDepartment of Ultrasound, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.
Yongjun ChenDepartment of General Surgery, Hepatobiliary Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.
Junqing WangDepartment of General Surgery, Hepatobiliary Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.ORCID 0000-0003-1219-639X
Shanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pseudogenes exert potential functions in tumorigenicity and tumour process in human beings. In our previous research on oncogene AKR1B10 in hepatocellular carcinoma (HCC), its pseudogene, AKR1B10P1, was preliminarily noticed being anomalistic transcribed, whereas whether AKR1B10P1 plays any specific function in HCC is poorly understood. By using shRNA transfection and lentiviral infection, we regulated the expression of ARK1B10P1 transcript and the relative targets in two ways. As we discovered, pathological transcription of AKR1B10P1 in HCC cells significantly promotes cell growth and motility either in vitro or in vivo. AKR1B10P1 was correlated with relatively dismal features of HCC. The epithelial-mesenchymal transition (EMT) was enhanced by up-regulating AKR1B10P1. And, a potential sequence of AKR1B10P1 transcript was discovered directly interacting with miR-138. SOX4, a pivotal promotor of EMT, was validated as the down-streaming target of miR-138. Mechanistically, degradation of SOX4 mRNA induced by miR-138 was effectively abrogated by AKR1B10P1. In conclusion, pseudogene AKR1B10P1 exerts stabilizing effect on SOX4 in HCC, associated EMT process, by directly sponging miR-138, which post-transcriptionally modulates SOX4's regulating gene.

Indexed as

PseudogenesAnimalsApoptosisBase SequenceCarcinogenesisCarcinoma, HepatocellularCell CycleCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionHumansLiver NeoplasmsMaleMice, Inbred BALB CMice, NudeMicroRNAsMIRN138 microRNA, humanRNA, MessengerSOX4 protein, humanSOXC Transcription FactorsAKR1B10P1hepatocellular carcinomametastasismiR-138SOX4

Identifiers

PMID32924268
PMCPMC7579691
OpenAlexW3084720105

What OpenQuestion holds

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Registered trials

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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.