Evidence map›Paper›PMID 34075570›Full record

ArticleNeuromolecular medicine2022

Receptor-Interacting Protein 140 Enhanced Temozolomide-Induced Cellular Apoptosis Through Regulation of E2F1 in Human Glioma Cell Lines.

Hong-Chieh Tsai, Kuo-Chen Wei, Pin-Yuan Chen, Chiung-Yin Huang, Ko-Ting Chen, Ya-Jui Lin, Hsiao-Wei Cheng, Chun-Hao Huang, Hsiang-Tsui Wang

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Neuromolecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.2field-weighted citation impact, top 52% 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

0 citing papers in PubMed, 2 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 1 country.

Hong-Chieh TsaiDepartment of Neurosurgery, Linkou Chang Gung Memorial Hospital, Taoyuan, 333, Taiwan.
Kuo-Chen WeiDepartment of Neurosurgery, New Taipei Municipal TuCheng Hospital, Chang Gung Memorial Hospital, New Taipei Municipal, Taipei, 236, Taiwan.
Pin-Yuan ChenDepartment of Neurosurgery, Keelung Chang Gung Memorial Hospital, Keelung, 204, Taiwan.
Chiung-Yin HuangDepartment of Neurosurgery, Linkou Chang Gung Memorial Hospital, Taoyuan, 333, Taiwan.
Ko-Ting ChenDepartment of Neurosurgery, Linkou Chang Gung Memorial Hospital, Taoyuan, 333, Taiwan.
Ya-Jui LinDepartment of Neurosurgery, Linkou Chang Gung Memorial Hospital, Taoyuan, 333, Taiwan.
Hsiao-Wei ChengDepartment of Neurosurgery, Linkou Chang Gung Memorial Hospital, Taoyuan, 333, Taiwan.
Chun-Hao HuangDepartment of Pharmacology, National Yang Ming Chiao Tung University, Taipei, 112, Taiwan.
Hsiang-Tsui WangDepartment of Pharmacology, National Yang Ming Chiao Tung University, Taipei, 112, Taiwan. htwang01@nycu.edu.tw.ORCID 0000-0003-4443-0670
Chang Gung University · TWNational Yang Ming Chiao Tung University · TWChang Gung Memorial Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma (GBM), a grade IV glioma, is responsible for the highest years of potential life lost among cancers. The poor prognosis is attributable to its high recurrence rate, caused in part by the development of resistance to chemotherapy. Receptor-interacting protein 140 (RIP140) is a very versatile coregulator of nuclear receptors and transcription factors. Although many of the pathways regulated by RIP140 contribute significantly to cancer progression, the function of RIP140 in GBM remains to be determined. In this study, we found that higher RIP140 expression was associated with prolonged survival in patients with newly diagnosed GBM. Intracellular RIP140 levels were increased after E2F1 activation following temozolomide (TMZ) treatment, which in turn modulated the expression of E2F1-targeted apoptosis-related genes. Overexpression of RIP140 reduced glioma cell proliferation and migration, induced cellular apoptosis, and sensitized GBM cells to TMZ. Conversely, knockdown of RIP140 increased TMZ resistance. Taken together, our results suggest that RIP140 prolongs the survival of patients with GBM both by inhibiting tumor cell proliferation and migration and by increasing cellular sensitivity to chemotherapy. This study helps improve our understanding of glioma recurrence and may facilitate the development of more effective treatments.

Indexed as

Brain NeoplasmsGlioblastomaGliomaNuclear Receptor Co-Repressor 1TemozolomideApoptosisCell Line, TumorDrug Resistance, NeoplasmE2F1 Transcription FactorGene Expression Regulation, NeoplasticHumansNuclear Receptor Interacting Protein 1E2F1 protein, humanE2F1 Transcription FactorNRIP1 protein, humanNuclear Receptor Co-Repressor 1Nuclear Receptor Interacting Protein 1TemozolomideApoptosisE2F1Glioblastoma multiformeReceptor-interacting protein 140Temozolomide

Identifiers

PMID34075570
OpenAlexW3165476786

What OpenQuestion holds

Textmetadata
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.