Evidence map›Paper›PMID 35328513›Full record

ArticleInternational journal of molecular sciences2022

PRP4 Induces Epithelial-Mesenchymal Transition and Drug Resistance in Colon Cancer Cells via Activation of p53.

Salman Ul Islam, Muhammad Bilal Ahmed, Jong-Kyung Sonn, Eun-Jung Jin, Young-Sup Lee

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.2field-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

15 citing papers in PubMed, 16 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 2 institutions in 2 countries.

Salman Ul IslamDepartment of Pharmacy, Cecos University, Hayatabad, Peshawar 25000, Pakistan.
Muhammad Bilal AhmedSchool of Life Sciences, College of Natural Sciences, Kyungpook National University, Daegu 41566, Korea.
Jong-Kyung SonnDepartment of Biology, College of Natural Sciences, Kyungpook National University, Daegu 41566, Korea.
Eun-Jung JinDepartment of Biological Science, College of Natural Science, Wonkwang University, Iksan 54538, Korea.ORCID 0000-0002-6874-3017
Young-Sup LeeSchool of Life Sciences, College of Natural Sciences, Kyungpook National University, Daegu 41566, Korea.ORCID 0000-0002-5841-6506
Kyungpook National University · KRWonkwang University · KR

Funding

National Research Foundation of Korea NRF- 2019R1A2C1003003
6 · The paper itself

Abstract

Pre-mRNA processing factor 4B (PRP4) promotes pre-mRNA splicing and signal transduction. Recent studies have shown that PRP4 modulates the assembly of actin cytoskeleton in cancer cells and induces epithelial-mesenchymal transition (EMT) and drug resistance. PRP4 displays kinase domain-like cyclin-dependent kinases and mitogen-activated protein kinases, making it capable of phosphorylating p53 and other target proteins. In the current study, we report that PRP4 induces drug resistance and EMT via direct binding to the p53 protein, inducing its phosphorylation. Moreover, PRP4 overexpression activates the transcription of miR-210 in a hypoxia-inducible factor 1α (HIF-1α)-dependent manner, which activates p53. The involvement of miR-210 in the activation of p53 was confirmed by utilizing si-miR210. si-miR210 blocked the PRP4-activated cell survival pathways and reversed the PRP4-induced EMT phenotype. Moreover, we used deferoxamine as a hypoxia-mimetic agent, and si-HIF to silence HIF-1α. This procedure demonstrated that PRP4-induced EMT and drug resistance emerged in response to consecutive activation of HIF-1α, miR-210, and p53 by PRP4 overexpression. Collectively, our findings suggest that the PRP4 contributes to EMT and drug resistance induction via direct interactions with p53 and actions that promote upregulation of HIF-1α and miR-210. We conclude that PRP4 is an essential factor promoting cancer development and progression. Specific PRP4 inhibition could benefit patients with colon cancer.

Indexed as

Colonic NeoplasmsMicroRNAsCell Line, TumorDrug ResistanceEpithelial-Mesenchymal TransitionHumansHypoxiaHypoxia-Inducible Factor 1, alpha SubunitProtein Serine-Threonine KinasesRibonucleoprotein, U4-U6 Small NuclearRNA PrecursorsTumor Suppressor Protein p53Hypoxia-Inducible Factor 1, alpha SubunitMicroRNAsProtein Serine-Threonine KinasesPRPF4B protein, humanRibonucleoprotein, U4-U6 Small NuclearRNA PrecursorsTumor Suppressor Protein p53drug resistanceEMTHCT116miR-210p53PRP4

Identifiers

PMID35328513
PMCPMC8955441
OpenAlexW4220694775

What OpenQuestion holds

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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.