Evidence map›Paper›PMID 35030977›Full record

ArticleBioengineered2022

Enabled homolog (ENAH) regulated by RNA binding protein splicing factor 3b subunit 4 (SF3B4) exacerbates the proliferation, invasion and migration of hepatocellular carcinoma cells via Notch signaling pathway.

Guoming Deng, Yufeng Luo, Yaoming Zhang, Jinfeng Zhang, Zongyun He

Open access · goldAbstract readVideo-Audio Media
In one paragraph

Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

12 citing papers in PubMed, 22 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

5 authors at 1 institution in 1 country.

Guoming DengThe 2nd Department of Hepatobiliary Surgery, Meizhou People's Hospital, Meizhou, China.
Yufeng LuoThe 2nd Department of Hepatobiliary Surgery, Meizhou People's Hospital, Meizhou, China.
Yaoming ZhangThe 2nd Department of Hepatobiliary Surgery, Meizhou People's Hospital, Meizhou, China.
Jinfeng ZhangGuangdong Provincial Key Laboratory of Precision Medicine and Clinical Translational Research of Hakka Population, Meizhou, China.
Zongyun HeGuangdong Provincial Key Laboratory of Precision Medicine and Clinical Translational Research of Hakka Population, Meizhou, China.
Meizhou City People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Enabled homolog (ENAH) is an actin-binding protein that implicated in multiple malignant tumors. High ENAH expression has been verified to be associated with poor prognosis in hepatocellular carcinoma (HCC). We aimed to reveal the role of ENAH in HCC and the potential mechanism. ENAH expression in HCC tissues and the prognostic correlation were analyzed by GEPIA2 database. RT-qPCR and Western blot were used to test ENAH expression in HCC cells. Following ENAH silencing, cell proliferation was estimated by CCK-8 and colony formation assays. Transwell and wound healing assays were to assess cell invasion and migration. ENCORI database was to analyze the correlation between ENAH and splicing factor 3b subunit 4 (SF3B4) in HCC tissues, which was then verified by RIP and actinomycin D assay. Then, the expression of Notch signaling-related proteins was detected by Western blotting after ENAH knockdown. Afterward, Notch1 was overexpressed to validate whether ENAH impacted the biological events of HCC cells through mediating Notch signaling. Results revealed that ENAH expression was elevated in HCC tissues and cells and associated with poor prognosis. ENAH deficiency mitigated proliferation, invasion and migration of HCC cells. Mechanistically, ENAH was positively correlated with SF3B4 in HCC tissues. SF3B4 could bind to ENAH mRNA and stabilized ENAH. Besides, ENAH activated Notch signaling. Notch1 up-regulation reversed the influence of ENAH knockdown on biological events of HCC cells. Collectively, ENAH regulated by SF3B4 promoted the development of HCC through activating Notch signaling, which identified ENAH as a potent molecular target for HCC therapy and prognosis.

Indexed as

Signal TransductionCarcinoma, HepatocellularCell Line, TumorHumansLiver NeoplasmsMicrofilament ProteinsReceptors, NotchRNA Splicing FactorsEnah protein, humanMicrofilament ProteinsReceptors, NotchRNA Splicing FactorsSF3B4 protein, humanENAHHepatocellular carcinomaNotch signaling pathwaySF3B4

Identifiers

PMID35030977
PMCPMC8973836
OpenAlexW4205816714

What OpenQuestion holds

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LicenceCC BY
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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.