Evidence map›Paper›PMID 37048170›Full record

ArticleCells2023

The αMSH-Dependent PI3K Pathway Supports Energy Metabolism, via Glucose Uptake, in Melanoma Cells.

Giorgia Cardinali, Daniela Kovacs, Sarah Mosca, Barbara Bellei, Enrica Flori, Aldo Morrone, Anna Maria Mileo, Vittoria Maresca

Open access · goldAbstract read
In one paragraph

Article in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 44% 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

2 citing papers in PubMed, 1 citations in OpenAlex.

  1. Review
  2. Article
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

8 authors at 2 institutions in 1 country.

Giorgia CardinaliLaboratory of Cutaneous Physiopathology, San Gallicano Dermatological Institute, IRCCS, 00144 Rome, Italy.ORCID 0000-0002-7527-9451
Daniela KovacsLaboratory of Cutaneous Physiopathology, San Gallicano Dermatological Institute, IRCCS, 00144 Rome, Italy.
Sarah MoscaLaboratory of Cutaneous Physiopathology, San Gallicano Dermatological Institute, IRCCS, 00144 Rome, Italy.ORCID 0000-0002-6468-200X
Barbara BelleiLaboratory of Cutaneous Physiopathology, San Gallicano Dermatological Institute, IRCCS, 00144 Rome, Italy.ORCID 0000-0002-3883-5500
Enrica FloriLaboratory of Cutaneous Physiopathology, San Gallicano Dermatological Institute, IRCCS, 00144 Rome, Italy.ORCID 0000-0002-9275-1041
Aldo MorroneLaboratory of Cutaneous Physiopathology, San Gallicano Dermatological Institute, IRCCS, 00144 Rome, Italy.
Anna Maria MileoTumor Immunology and Immunotherapy Unit, Department of Research Advanced Diagnostic and Technological Innovation, Regina Elena National Cancer Institute, IRCCS, 00144 Rome, Italy.ORCID 0000-0002-1970-3297
Vittoria MarescaLaboratory of Cutaneous Physiopathology, San Gallicano Dermatological Institute, IRCCS, 00144 Rome, Italy.
San Gallicano Hospital · ITIstituti di Ricovero e Cura a Carattere Scientifico · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Stimulation of melanocytes and murine melanoma cells with αMSH plus the PI3K inhibitor LY294002 resulted in ROS increase, oxidative DNA damage, and pigment retention. We performed cellular and molecular biology assays (Western blot, FACS, immunofluorescence analysis, scratch assay) on murine and human melanoma cells. Treatment with αMSH plus LY294002 altered cortical actin architecture. Given that cytoskeleton integrity requires energy, we next evaluated ATP levels and we observed a drop in ATP after exposure to αMSH plus LY294002. To evaluate if the αMSH-activated PI3K pathway could modulate energy metabolism, we focused on glucose uptake by analyzing the expression of the Glut-1 glucose translocator. Compared with cells treated with αMSH alone, those exposed to combined treatment showed a reduction of Glut-1 on the plasma membrane. This metabolic alteration was associated with changes in mitochondrial mass. A significant decrease of the cell migratory potential was also observed. We demonstrated that the αMSH-dependent PI3K pathway acts as a regulator of energy metabolism via glucose uptake, influencing the actin cytoskeleton, which is involved in melanosome release and cell motility. Hence, these results could constitute the basis for innovative therapeutical strategies.

Indexed as

MelanomaPhosphatidylinositol 3-KinasesAdenosine Triphosphatealpha-MSHAnimalsEnergy MetabolismGlucoseHumansMiceAdenosine Triphosphatealpha-MSHGlucosePhosphatidylinositol 3-Kinasesenergy metabolismglucose uptakemelanomaPI3K pathwayαMSH

Identifiers

PMID37048170
PMCPMC10093374
OpenAlexW4362701085

What OpenQuestion 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 OpenQuestion graph.