Evidence map›Paper›PMID 34926694›Full record

ArticleBioMed research international2021

Aprepitant Promotes Caspase-Dependent Apoptotic Cell Death and G2/M Arrest through PI3K/Akt/NF-

Hossein Javid, Amir R Afshari, Farnaz Zahedi Avval, Jahanbakhsh Asadi, Seyed Isaac Hashemy

RetractedOpen access · hybridAbstract readRetracted Publication
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. It has been retracted, and should not be counted. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 1 country.

Hossein JavidDepartment of Clinical Biochemistry, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.ORCID https://orcid.org/0000-0002-2248-7708
Amir R AfshariDepartment of Physiology and Pharmacology, Faculty of Medicine, North Khorasan University of Medical Sciences, Bojnurd, Iran.ORCID https://orcid.org/0000-0001-9989-9818
Farnaz Zahedi AvvalDepartment of Clinical Biochemistry, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.ORCID https://orcid.org/0000-0001-8915-3596
Jahanbakhsh AsadiDepartment of Clinical Biochemistry, Faculty of Medicine, Golestan University of Medical Sciences, Gorgan, Iran.ORCID https://orcid.org/0000-0002-7068-2970
Seyed Isaac HashemyDepartment of Clinical Biochemistry, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.ORCID https://orcid.org/0000-0002-1323-5250
Mashhad University of Medical Sciences · IRGolestan University · IRNorth Khorasan University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The antagonists of the neurokinin-1 receptor (NK1R) are known for their anti-inflammatory, anxiolytic, antiemetic, and anticancer activities. Aprepitant, a nonpeptide NK1R antagonist, is used in nausea and vomiting, the most common side effects of cancer chemotherapy in patients. It has been established that NK1R activation by substance P (SP), which links cancer promotion and progression to a neurokinin-mediated environment, became one mechanism that corresponds to the mitogenesis of tumor cells. Therefore, this study is aimed at explaining and evaluating the anticancer impacts of aprepitant on esophageal squamous cancer cell (ESCC) spheres by using in vitro experiments, such as resazurin, ROS, annexin-V binding, RT-PCR, and Western blot analysis. As a result, we showed that aprepitant had strong antiproliferative and cytotoxic effects on ESCC cell spheres. Also, aprepitant caused significant G2-M cell cycle arrest depending on concentration increase. Further, exposure of cells to this agent resulted in caspase -8/-9-dependent apoptotic pathway activation by modifying the expression of genes involved in apoptosis. Besides, treatment of the cells by aprepitant abrogates of the PI3K/Akt pathway, as shown by reducing the level of Akt, induces apoptotic cell death. In summary, pharmacological inhibition of NK1R with aprepitant seems to have a significant chance of treating ESCC as a single agent or in conjunction with other chemotherapeutic drugs.

Indexed as

Antineoplastic AgentsApoptosisAprepitantCaspasesCell DeathCell Line, TumorEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaG2 Phase Cell Cycle CheckpointsHumansM Phase Cell Cycle CheckpointsNF-kappa BPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, Neurokinin-1Signal TransductionAntineoplastic AgentsAprepitantCaspasesNF-kappa BPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, Neurokinin-1

Identifiers

PMID34926694
PMCPMC8677400
OpenAlexW4200137064

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.