Evidence map›Paper›PMID 36658296›Full record

ArticleEndocrine2023

Visfatin induces ovarian cancer resistance to anoikis by regulating mitochondrial activity.

Justyna Gogola-Mruk, Wacław Tworzydło, Kinga Krawczyk, Weronika Marynowicz, Anna Ptak

Open access · hybridAbstract read
In one paragraph

Article in Endocrine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

13 citing papers in PubMed, 16 citations in OpenAlex.

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  8. Breast cancer shares many epidemiological, lifestyle, and local hormonal and metabolic underpinnings with endometrial and ovarian cancer: a narrative review.Translational breast cancer research : a journal focusing on translational research in breast cancer · 2025
    Review
  9. Mechanisms by which obesity regulates inflammation and anti-tumor immunity in cancer.Biochemical and biophysical research communications · 2024
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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

5 authors at 1 institution in 1 country.

Justyna Gogola-MrukLaboratory of Physiology and Toxicology of Reproduction, Institute of Zoology and Biomedical Research, Jagiellonian University, Krakow, Poland. justyna.gogola@uj.edu.pl.ORCID 0000-0001-7290-1009
Wacław TworzydłoDepartment of Developmental Biology and Invertebrate Morphology, Institute of Zoology and Biomedical Research, Jagiellonian University, Krakow, Poland.
Kinga KrawczykLaboratory of Physiology and Toxicology of Reproduction, Institute of Zoology and Biomedical Research, Jagiellonian University, Krakow, Poland.
Weronika MarynowiczLaboratory of Physiology and Toxicology of Reproduction, Institute of Zoology and Biomedical Research, Jagiellonian University, Krakow, Poland.
Anna PtakLaboratory of Physiology and Toxicology of Reproduction, Institute of Zoology and Biomedical Research, Jagiellonian University, Krakow, Poland.
Jagiellonian University · PL

Funding

Narodowe Centrum Nauki 2019/33/N/NZ5/00471
6 · The paper itself

Abstract

purposeOvarian cancer is characterized by recurrent peritoneal and distant metastasis. To survive in a non-adherent state, floating ovarian cancer spheroids develop mechanisms to resist anoikis. Moreover, ascitic fluid from ovarian cancer patients contains high levels of visfatin with anti-apoptotic properties. However, the mechanism by which visfatin induces anoikis resistance in ovarian cancer spheroids remains unknown. Here, we aimed to assess wheather visfatin which possess anti-apoptotic properties can induce resistance of anoikis in ovarian cancer spheroids.

methodsVisfatin synthesis were examined using a commercial human visfatin ELISA Kit. Spheroid were exposed to visfatin and cell viability and caspase 3/7 activity were measured using CellTiter-Glo 3D cell viability assay and Caspase-Glo® 3/7 Assay System. mRNA and protein expression were analyzed by Real-time PCR and Western Blot analysis, respectively. Analysis of mitochondrial activity was estimated by JC-1 staining.

resultsFirst, our results suggested higher expression and secretion of visfatin by epithelial than by granulosa ovarian cells, and in non-cancer tissues versus cancer tissues. Interestingly, visfatin increased the proliferation/apoptosis ratio in ovarian cancer spheroids. Specifically, both the intrinsic and extrinsic pathways of anoikis were regulated by visfatin. Moreover, the effect of the visfatin inhibitor (FK866) was opposite to that of visfatin. Furthermore, both NAMPT and FK866 affected mitochondrial activity in ovarian cancer cells.

conclusionIn conclusion, visfatin acts as an anti-apoptotic factor by regulating mitochondrial activity, leading to anoikis resistance in ovarian cancer spheroids. The finding suggest visfatin as a potential novel therapeutic target for the treatment of ovarian carcinoma with peritoneal dissemination.

Indexed as

AnoikisNicotinamide PhosphoribosyltransferaseOvarian NeoplasmsCell Line, TumorCytokinesFemaleHumansCytokinesNicotinamide Phosphoribosyltransferasenicotinamide phosphoribosyltransferase, humanAnoikisFK866Mitochondrial activityOvarian cancerVisfatin

Identifiers

PMID36658296
PMCPMC10140008
OpenAlexW4317496083

What OpenQuestion holds

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LicenceCC BY
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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.