Evidence map›Paper›PMID 31993929›Full record

ArticleMolecular and cellular biochemistry2020

The influence of conjugated linoleic acid on the expression of peroxisome proliferator-activated receptor-γ and selected apoptotic genes in non-small cell lung cancer.

Bartosz Kazimierz Słowikowski, Hanna Drzewiecka, Michał Malesza, Ida Mądry, Karolina Sterzyńska, Paweł Piotr Jagodziński

Open access · hybridAbstract read
In one paragraph

Article in Molecular and cellular biochemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

15 citing papers in PubMed, 35 citations in OpenAlex.

  1. Trial
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  4. Article
  5. The Phytochemical Profile of the Petroleum Ether Extract ofInternational journal of molecular sciences · 2024
    Article
  6. Article
  7. Production of Conjugated Linoleic Acid (CLA) byFoods (Basel, Switzerland) · 2024
    Review
  8. Article
  9. Article
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  11. Article
  12. Review
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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 1 institution in 1 country.

Bartosz Kazimierz Słowikowski *Department of Biochemistry and Molecular Biology, Poznan University of Medical Sciences, Święcickiego 6 Street, 60-781, Poznan, Poland. slowikowski.bartek@gmail.com.ORCID http://orcid.org/0000-0002-6547-486X
Hanna Drzewiecka *Department of Biochemistry and Molecular Biology, Poznan University of Medical Sciences, Święcickiego 6 Street, 60-781, Poznan, Poland.
Michał MaleszaDepartment of Biochemistry and Molecular Biology, Poznan University of Medical Sciences, Święcickiego 6 Street, 60-781, Poznan, Poland.
Ida MądryDepartment of Biochemistry and Molecular Biology, Poznan University of Medical Sciences, Święcickiego 6 Street, 60-781, Poznan, Poland.
Karolina SterzyńskaDepartment of Histology and Embryology, Poznan University of Medical Sciences, Święcickiego 6 Street, 60-781, Poznan, Poland.
Paweł Piotr JagodzińskiDepartment of Biochemistry and Molecular Biology, Poznan University of Medical Sciences, Święcickiego 6 Street, 60-781, Poznan, Poland.
Poznan University of Medical Sciences · PL

Funding

Uniwersytet Medyczny im. Karola Marcinkowskiego w Poznaniu 502-05-01124182-10482
6 · The paper itself

Abstract

In recent years, peroxisome proliferator-activated receptor-γ (PPARγ) has been intensively studied. Because its activation is often associated with changes in the expression level of various apoptotic genes, many studies have emphasized the role of PPARγ as an important anticancer agent. However, in different types of cancer, different genes are influenced by PPARγ action. Previous studies showed that conjugated linoleic acid (CLA) was able to induce apoptosis, upregulate PPARG gene expression and activate PPARγ protein in certain human cancer cell lines. Moreover, some PPARγ agonists inhibited the growth of human lung cancer cells through the induction of apoptosis. Nevertheless, the impact of CLA on PPARγ mRNA and protein levels in non-small cell lung cancer (NSCLC) cell lines has not been investigated thus far. Therefore, in our study, we analysed the influence of the c9,t11 linoleic acid isomer on the expression of PPARG and other genes involved in the apoptotic response (BCL-2, BAX, and CDKN1A) in two NSCLC cell lines of different histological origin (A549 and Calu-1) and in normal human bronchial epithelial Beas-2B cells. Cells were treated with several doses of c9,t11 CLA, followed by RNA and protein isolation, cDNA synthesis, real-time quantitative PCR (RT-qPCR) and Western blot analysis. We showed that the investigated CLA isomer was able to enhance the expression of PPARγ in the examined cell lines and alter the mRNA and protein levels of genes involved in apoptosis. Fluorescent staining and MMT assay revealed the antiproliferative potential of CLA as well as its ability to activate pathways that lead to cell death.

Indexed as

A549 CellsApoptosisApoptosis Regulatory ProteinsCarcinoma, Non-Small-Cell LungGene Expression RegulationHumansLinoleic Acids, ConjugatedLung NeoplasmsPPAR gammaApoptosis Regulatory ProteinsLinoleic Acids, ConjugatedPPAR gammaPPARG protein, humanApoptosisCLANon-small cell lung cancerPpar-gamma

Identifiers

PMID31993929
PMCPMC7028827
OpenAlexW3004309075

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Registered trials

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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.