Evidence map›Paper›PMID 33763472›Full record

ArticleBioMed research international2021

Therapeutic Potential of RTA 404 in Human Brain Malignant Glioma Cell Lines via Cell Cycle Arrest via p21/AKT Signaling.

Tai-Hsin Tsai, Ann-Shung Lieu, Yi-Wen Wang, Sheau-Fang Yang, Yi-Chiang Hsu, Chih-Lung Lin

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

  1. Trial
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  3. SoloxoloneFrontiers in pharmacology · 2024
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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 2 institutions in 1 country.

Tai-Hsin TsaiDivision of Neurosurgery, Department of Surgery, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan.ORCID https://orcid.org/0000-0002-1956-4311
Ann-Shung LieuDivision of Neurosurgery, Department of Surgery, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan.
Yi-Wen WangDepartment of Nursing, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan.
Sheau-Fang YangDepartment of Pathology, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan.
Yi-Chiang HsuSchool of Medicine, I-Shou University, Kaohsiung, Taiwan.ORCID https://orcid.org/0000-0002-6256-9521
Chih-Lung LinDivision of Neurosurgery, Department of Surgery, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan.ORCID https://orcid.org/0000-0002-6716-2771
Kaohsiung Medical University · TWI-Shou University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGlioblastoma multiforme (GBM) is the most common malignant brain tumor in the world. Despite advances in surgical resection, radiotherapy, and chemotherapy, GBM continues to have a poor overall survival. CDDO (2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid), a synthetic triterpenoid, is an Nrf2 activator used to inhibit proliferation and induce differentiation and apoptosis in various cancer cells. One new trifluoroethylamide derivative of CDDO, RTA 404, has been found to have increased ability to cross the blood-brain barrier. However, it is not clear what effect it may have on tumorigenesis in GBM.

methodsThis in vitro study evaluated the effects of RTA 404 on GBM cells. To do this, we treated GBM840 and U87 MG cell lines with RTA 404 and assessed apoptosis, cell cycle, cell locomotion, and senescence. DNA content and induction of apoptosis were analyzed by flow cytometry and protein expression by Western blot analysis.

resultsRTA 404 significantly inhibited the proliferation of tumor cells at concentrations higher than 100 nM (

conclusionRTA404 can inhibit proliferation, cell locomotion, cell cycle progression, and induce apoptosis in GBM cells in vitro, possibly through its inhibition of N-cadherin and E-cadherin expression via its inhibition of the AKT pathway.

Indexed as

Brain NeoplasmsGliomaAntineoplastic AgentsCell Cycle CheckpointsCell Line, TumorCyclin-Dependent Kinase Inhibitor p21Drug Screening Assays, AntitumorHumansProto-Oncogene Proteins c-aktSignal TransductionAntineoplastic AgentsCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21Proto-Oncogene Proteins c-akt

Identifiers

PMID33763472
PMCPMC7963900
OpenAlexW3134302409

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.