Evidence map›Paper›PMID 34766230›Full record

ArticleMolecular biology reports2022

Potential in vitro therapeutic effects of targeting SP/NK1R system in cervical cancer.

Mahtab Mozafari, Safieh Ebrahimi, Reza Assaran Darban, Seyed Isaac Hashemy

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Article in Molecular biology reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

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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

14 citing papers in PubMed, 34 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

4 authors at 2 institutions in 1 country.

Mahtab MozafariDepartment of Biology, Faculty of Sciences, Mashhad Branch, Islamic Azad University, Mashhad, Iran.
Safieh EbrahimiDepartment of Clinical Biochemistry, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Reza Assaran DarbanDepartment of Biology, Faculty of Sciences, Mashhad Branch, Islamic Azad University, Mashhad, Iran. assaran@mshdiau.ac.ir.ORCID https://orcid.org/0000-0001-9126-5618
Seyed Isaac HashemyDepartment of Clinical Biochemistry, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. hashemyi@mums.ac.ir.ORCID http://orcid.org/0000-0002-1323-5250
Islamic Azad University, Mashhad · IRMashhad University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCervical cancer, an aggressive gynecological cancer, seriously threatens women's health worldwide. It is recently reported that neuropeptide substance P (SP) regulates many tumor-associated processes through neurokinin-1 receptor (NK1R). Therefore, we used cervical cancer cell line (HeLa) to investigate the functional relevance of the SP/NK1R system in cervical cancer pathogenesis.

methodsCellular proliferation and cytotoxicity were analyzed by colorimetric MTT assay. Quantitative real-time PCR (qRT-PCR) was used to measure mRNA expression levels of desired genes. Cell cycle distribution and apoptosis were evaluated by flow cytometry. A wound-healing assay was employed to assess migration ability.

resultsWe found that the truncated isoform of NK1R(NK1R-Tr) is the dominantly expressed form of the receptor in Hela cells. We also indicated that that SP increased HeLa cell proliferation while treatment with NK1R antagonist, aprepitant, inhibited HeLa cell viability in a dose and time-dependent manner. SP also alters the levels of cell cycle regulators (up-regulation of cyclin B1 along with downregulation of p21) and apoptosis-related genes (up-regulation of Bcl-2 along with downregulation of Bax) while aprepitant reversed these effects. Aprepitant also induced arrest within the G2 phase of the cell cycle and subsequent apoptosis. Furthermore, SP promoted the migrative phenotype of HeLa cells and increased MMP-2 and MMP-9 expression while aprepitant exposure significantly reversed these effects.

conclusionCollectively, our results indicate the importance of the SP / NK1R system in promoting both proliferative and migrative phenotypes of cervical cancer cells and suggest that aprepitant may be developed as a novel treatment for combating cervical cancer.

Indexed as

ApoptosisAprepitantCell Line, TumorCell ProliferationFemaleGene ExpressionGene Expression Regulation, NeoplasticHeLa CellsHumansMatrix Metalloproteinase 2Matrix Metalloproteinase 9Neurokinin-1 Receptor AntagonistsReceptors, Neurokinin-1Signal TransductionSubstance PUterine Cervical NeoplasmsAprepitantMatrix Metalloproteinase 2Matrix Metalloproteinase 9MMP2 protein, humanMMP9 protein, humanNeurokinin-1 Receptor AntagonistsReceptors, Neurokinin-1Substance PTACR1 protein, humanAprepitantCervical cancerNeurokinin-1 receptorSubstance P

Identifiers

PMID34766230
OpenAlexW3213751760

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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.