Evidence map›Paper›PMID 34469035›Full record

ArticleJournal of cellular and molecular medicine2021

Imipramine impedes glioma progression by inhibiting YAP as a Hippo pathway independent manner and synergizes with temozolomide.

Yan Wang, Xiang Wang, Xu Wang, Di Wu, Ji Qi, Yu Zhang, Kai Wang, Ding Zhou, Qing-Ming Meng, Er Nie and 3 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 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

13 authors at 2 institutions in 1 country.

Yan WangInsititute of Nervous System Diseases, Xuzhou Medical University, Xuzhou, China.
Xiang WangInsititute of Nervous System Diseases, Xuzhou Medical University, Xuzhou, China.
Xu WangInsititute of Nervous System Diseases, Xuzhou Medical University, Xuzhou, China.
Di WuPathological Diagnosis Center, Xuzhou Central Hospital, Xuzhou, China.
Ji QiInsititute of Nervous System Diseases, Xuzhou Medical University, Xuzhou, China.
Yu ZhangInsititute of Nervous System Diseases, Xuzhou Medical University, Xuzhou, China.
Kai WangInsititute of Nervous System Diseases, Xuzhou Medical University, Xuzhou, China.
Ding ZhouInsititute of Nervous System Diseases, Xuzhou Medical University, Xuzhou, China.
Qing-Ming MengInsititute of Nervous System Diseases, Xuzhou Medical University, Xuzhou, China.
Er NieDepartment of Neurosurgery, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, China.
Qiang WangDepartment of Neurosurgery, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, China.
Ru-Tong YuInsititute of Nervous System Diseases, Xuzhou Medical University, Xuzhou, China.
Xiu-Ping ZhouInsititute of Nervous System Diseases, Xuzhou Medical University, Xuzhou, China.ORCID 0000-0002-6663-8168
Xuzhou Medical College · CNXuzhou Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Patients with malignant glioma often suffered from depression, which leads to an increased risk of detrimental outcomes. Imipramine, an FDA-approved tricyclic antidepressant, has been commonly used to relieve depressive symptoms in the clinic. Recently, imipramine has been reported to participate in the suppression of tumour progression in several human cancers, including prostate cancer, colon cancer and lymphomas. However, the effect of imipramine on malignant glioma is largely unclear. Here, we show that imipramine significantly retarded proliferation of immortalized and primary glioma cells. Mechanistically, imipramine suppressed tumour proliferation by inhibiting yes-associated protein (YAP), a recognized oncogene in glioma, independent of Hippo pathway. In addition to inhibiting YAP transcription, imipramine also promoted the subcellular translocation of YAP from nucleus into cytoplasm. Consistently, imipramine administration significantly reduced orthotopic tumour progression and prolonged survival of tumour-bearing mice. Moreover, exogenous overexpression of YAP partially restored the inhibitory effect of imipramine on glioma progression. Most importantly, compared with imipramine or temozolomide (TMZ) monotherapy, combination therapy with imipramine and TMZ exhibited enhanced inhibitory effect on glioma growth both in vitro and in vivo, suggesting the synergism of both agents. In conclusion, we found that tricyclic antidepressant imipramine impedes glioma progression by inhibiting YAP. In addition, combination therapy with imipramine and TMZ may potentially serve as promising anti-glioma regimens, thus predicting a broad prospect of clinical application.

Indexed as

AnimalsAntineoplastic AgentsCell Cycle ProteinsCell Line, TumorCell ProliferationDisease Models, AnimalDose-Response Relationship, DrugDrug SynergismGliomaHippo KinasesHumansImipramineIntracellular Signaling Peptides and ProteinsMicePrognosisProtein Serine-Threonine KinasesAntineoplastic AgentsCell Cycle ProteinsHippo KinasesImipramineIntracellular Signaling Peptides and ProteinsProtein Serine-Threonine KinasesSTK4 protein, humanTemozolomideTranscription FactorsYY1AP1 protein, humangliomaimipramineproliferationtemozolomideYAP

Identifiers

PMID34469035
PMCPMC8500960
OpenAlexW3196415878

What Socratic holds

Textmetadata
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 Socratic graph.