Caloric restriction and metformin selectively improved LKB1-mutated NSCLC tumor response to chemo- and chemo-immunotherapy.

Caloric restriction Cancer metabolism KRAS LKB1 Metformin NSCLC

Journal

Journal of experimental & clinical cancer research : CR
ISSN: 1756-9966
Titre abrégé: J Exp Clin Cancer Res
Pays: England
ID NLM: 8308647

Informations de publication

Date de publication:
02 Jan 2024
Historique:
received: 07 09 2023
accepted: 11 12 2023
medline: 2 1 2024
pubmed: 2 1 2024
entrez: 2 1 2024
Statut: epublish

Résumé

About 10% of NSCLCs are mutated in KRAS and impaired in STK11/LKB1, a genetic background associated with poor prognosis, caused by an increase in metastatic burden and resistance to standard therapy. LKB1 is a protein involved in a number of biological processes and is particularly important for its role in the regulation of cell metabolism. LKB1 alterations lead to protein loss that causes mitochondria and metabolic dysfunction that makes cells unable to respond to metabolic stress. Different studies have shown how it is possible to interfere with cancer metabolism using metformin and caloric restriction (CR) and both modify the tumor microenvironment (TME), stimulating the switch from "cold" to "hot". Given the poor therapeutic response of KRAS Mouse cell lines were derived from lung nodules of transgenic mice carrying KRAS Our preclinical results indicate that in NSCLC KRAS Our in vitro and in vivo preliminary studies confirm our hypothesis that the addition of metformin and CR is able to improve the antitumor activity of chemo and chemoimmunotherapy in LKB1 impaired tumors, exploiting their inability to overcome metabolic stress.

Sections du résumé

BACKGROUND BACKGROUND
About 10% of NSCLCs are mutated in KRAS and impaired in STK11/LKB1, a genetic background associated with poor prognosis, caused by an increase in metastatic burden and resistance to standard therapy. LKB1 is a protein involved in a number of biological processes and is particularly important for its role in the regulation of cell metabolism. LKB1 alterations lead to protein loss that causes mitochondria and metabolic dysfunction that makes cells unable to respond to metabolic stress. Different studies have shown how it is possible to interfere with cancer metabolism using metformin and caloric restriction (CR) and both modify the tumor microenvironment (TME), stimulating the switch from "cold" to "hot". Given the poor therapeutic response of KRAS
METHODS METHODS
Mouse cell lines were derived from lung nodules of transgenic mice carrying KRAS
RESULTS RESULTS
Our preclinical results indicate that in NSCLC KRAS
CONCLUSION CONCLUSIONS
Our in vitro and in vivo preliminary studies confirm our hypothesis that the addition of metformin and CR is able to improve the antitumor activity of chemo and chemoimmunotherapy in LKB1 impaired tumors, exploiting their inability to overcome metabolic stress.

Identifiants

pubmed: 38163906
doi: 10.1186/s13046-023-02933-5
pii: 10.1186/s13046-023-02933-5
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

6

Subventions

Organisme : Fondazione AIRC per la ricerca sul cancro ETS
ID : IG 2017-20085
Organisme : Fondazione AIRC per la ricerca sul cancro ETS
ID : IG 2020-24347

Informations de copyright

© 2023. The Author(s).

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Auteurs

Gloriana Ndembe (G)

Laboratory of Molecular Pharmacology, Department of Experimental Oncology, Istituto Di Ricerche Farmacologiche Mario Negri IRCCS, Milan, Italy.

Ilenia Intini (I)

Laboratory of Molecular Pharmacology, Department of Experimental Oncology, Istituto Di Ricerche Farmacologiche Mario Negri IRCCS, Milan, Italy.

Massimo Moro (M)

Tumor Genomics Unit, Department of Experimental Oncology and Molecular Medicine, Fondazione IRCCS Istituto Nazionale Dei Tumori, Milan, Italy.

Chiara Grasselli (C)

Immunopharmacology Unit, Department of Experimental Oncology, Istituto Di Ricerche Farmacologiche Mario Negri IRCCS, Milan, Italy.

Andrea Panfili (A)

Immunopharmacology Unit, Department of Experimental Oncology, Istituto Di Ricerche Farmacologiche Mario Negri IRCCS, Milan, Italy.

Nicolò Panini (N)

Immunopharmacology Unit, Department of Experimental Oncology, Istituto Di Ricerche Farmacologiche Mario Negri IRCCS, Milan, Italy.

Augusto Bleve (A)

Immunopharmacology Unit, Department of Experimental Oncology, Istituto Di Ricerche Farmacologiche Mario Negri IRCCS, Milan, Italy.

Mario Occhipinti (M)

Thoracic Unit, Medical Oncology Department, Fondazione IRCCS Istituto Nazionale Dei Tumori, Milan, Italy.

Cristina Borzi (C)

Tumor Genomics Unit, Department of Experimental Oncology and Molecular Medicine, Fondazione IRCCS Istituto Nazionale Dei Tumori, Milan, Italy.

Marina Chiara Garassino (MC)

Thoracic Unit, Medical Oncology Department, Fondazione IRCCS Istituto Nazionale Dei Tumori, Milan, Italy.

Mirko Marabese (M)

Laboratory of Molecular Pharmacology, Department of Experimental Oncology, Istituto Di Ricerche Farmacologiche Mario Negri IRCCS, Milan, Italy.

Simone Canesi (S)

Mouse & Animal Pathology Lab, Fondazione Filarete, Milan, Italy.
Department of Veterinary Medicine, University of Milan, Milan, Italy.

Eugenio Scanziani (E)

Mouse & Animal Pathology Lab, Fondazione Filarete, Milan, Italy.
Department of Veterinary Medicine, University of Milan, Milan, Italy.

Gabriella Sozzi (G)

Tumor Genomics Unit, Department of Experimental Oncology and Molecular Medicine, Fondazione IRCCS Istituto Nazionale Dei Tumori, Milan, Italy.

Massimo Broggini (M)

Laboratory of Molecular Pharmacology, Department of Experimental Oncology, Istituto Di Ricerche Farmacologiche Mario Negri IRCCS, Milan, Italy. massimo.broggini@marionegri.it.

Monica Ganzinelli (M)

Thoracic Unit, Medical Oncology Department, Fondazione IRCCS Istituto Nazionale Dei Tumori, Milan, Italy.

Classifications MeSH