Evidence map›Paper›PMID 34768932›Full record

ArticleInternational journal of molecular sciences2021

Dual Knockdown of Musashi RNA-Binding Proteins MSI-1 and MSI-2 Attenuates Putative Cancer Stem Cell Characteristics and Therapy Resistance in Ovarian Cancer Cells.

Maria T Löblein, Isabel Falke, Hans Theodor Eich, Burkhard Greve, Martin Götte, Fabian M Troschel

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

22 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Ro 08-2750 increases radiation-induced cytotoxicity in DLBCL by dysregulating the DNA damage response.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2026
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  16. Role of the RNA-binding protein family in gynecologic cancers.American journal of cancer research · 2023
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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.

Maria T LöbleinDepartment of Radiation Oncology, University Hospital Münster, 48149 Münster, Germany.ORCID 0000-0002-3173-2664
Isabel FalkeDepartment of Radiation Oncology, University Hospital Münster, 48149 Münster, Germany.ORCID 0000-0001-7845-6284
Hans Theodor EichDepartment of Radiation Oncology, University Hospital Münster, 48149 Münster, Germany.
Burkhard GreveDepartment of Radiation Oncology, University Hospital Münster, 48149 Münster, Germany.
Martin GötteDepartment of Gynecology and Obstetrics, University Hospital Münster, 48149 Münster, Germany.ORCID 0000-0003-2360-2496
Fabian M TroschelDepartment of Radiation Oncology, University Hospital Münster, 48149 Münster, Germany.ORCID 0000-0001-5066-6650
University Hospital Münster · DE

Funding

Medical Faculty, Münster University n/aMünster University Open Access Publication Fund n/a
6 · The paper itself

Abstract

In ovarian cancer, therapy resistance mechanisms complicate cancer cell eradication. Targeting Musashi RNA-binding proteins (MSI) may increase therapeutic efficacy. Database analyses were performed to identify gene expression associations between MSI proteins and key therapy resistance and cancer stem cell (CSC) genes. Then, ovarian cancer cells were subjected to siRNA-based dual knockdown of MSI-1 and MSI-2. CSC and cell cycle gene expression was investigated using quantitative polymerase chain reaction (qPCR), western blots, and flow cytometry. Metabolic activity and chemoresistance were assessed by MTT assay. Clonogenic assays were used to quantify cell survival post-irradiation. Database analyses demonstrated positive associations between MSI proteins and putative CSC markers NOTCH, MYC, and ALDH4A1 and negative associations with NOTCH inhibitor NUMB. MSI-2 expression was negatively associated with the apoptosis regulator p21. MSI-1 and MSI-2 were positively correlated, informing subsequent dual knockdown experiments. After MSI silencing, CSC genes were downregulated, while cell cycle progression was reduced. Metabolic activity was decreased in some cancer cells. Both chemo- and radioresistance were reduced after dual knockdown, suggesting therapeutic potential. Dual knockdown of MSI proteins is a promising venue to impede tumor growth and sensitize ovarian cancer cells to irradiation and chemotherapy.

Indexed as

1-Pyrroline-5-Carboxylate DehydrogenaseApoptosisCarcinoma, Ovarian EpithelialCell CycleCell Line, TumorCell ProliferationCyclin-Dependent Kinase Inhibitor p21Down-RegulationDrug Resistance, NeoplasmFemaleGene Expression Regulation, NeoplasticHumansNeoplastic Stem CellsNerve Tissue ProteinsOvarian NeoplasmsOvary1-Pyrroline-5-Carboxylate DehydrogenaseALDH4A1 protein, humanCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21MSI1 protein, humanMSI2 protein, humanMYC protein, humanNerve Tissue ProteinsProto-Oncogene Proteins c-mycReceptors, NotchRNA-Binding ProteinsRNA, Small Interferingcancer stem cellcell cycleMusashinotchovarian cancerproliferationradioresistancetherapy resistance

Identifiers

PMID34768932
PMCPMC8584030
OpenAlexW3210615301

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.