ArticleJournal of experimental & clinical cancer research : CR2024
Caloric restriction and metformin selectively improved LKB1-mutated NSCLC tumor response to chemo- and chemo-immunotherapy.
Article in Journal of experimental & clinical cancer research : CR, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 17 citations in OpenAlex.
- Molecular insights and therapeutic implications for the tumor suppressor role of LKB1 in non-small cell lung cancer.Cancer letters · 2026Review
- Lipid metabolic reprogramming of tumor-associated macrophages drives resistance to immune checkpoint blockade in lung cancer: a narrative review of mechanisms and therapeutic strategies.Translational lung cancer research · 2026Review
- Targeting non-small cell lung cancer: Molecular mechanisms and clinical studies (Review).Oncology letters · 2026Review
- Nutritional modulation of metabolic signaling within the tumor microenvironment for cancer therapy.Molecular and cellular biochemistry · 2026Review
- Exploratory evaluation of immunotherapy response and medication use in endometrial and cervical carcinoma.Gynecologic oncology reports · 2025Article
- Targeting LKB1/STK11-mutant cancer: distinct metabolism, microenvironment, and therapeutic resistance.Trends in pharmacological sciences · 2025Review
- Early molecular changes predict cancer cachexia in LKB1-deleted mouse models of NSCLC.Clinical and translational medicine · 2025Article
- Establishment of a mouse lung cancer organoid model and its applications for therapeutic screening.Biological procedures online · 2025Article
- The Research Progress of Metformin Regulation of Metabolic Reprogramming in Malignant Tumors.Pharmaceutical research · 2024Review
- Current advances in cancer energy metabolism under dietary restriction: a mini review.Medical oncology (Northwood, London, England) · 2024Review
- LKB1 biology: assessing the therapeutic relevancy of LKB1 inhibitors.Cell communication and signaling : CCS · 2024Review
- Immune checkpoint blockade resistance in lung cancer: emerging mechanisms and therapeutic opportunities.Trends in pharmacological sciences · 2024Review
- Metformin is a potential therapeutic for COVID-19/LUAD by regulating glucose metabolism.Scientific reports · 2024Article
- Metformin promotes anti-tumor immunity inOncology research · 2024Article
- Detection of aberrant locomotor activity in a mouse model of lung cancer via home cage monitoring.Frontiers in oncology · 2024Article
Corrections and comments
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Authors and funding
16 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundAbout 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
methodsMouse cell lines were derived from lung nodules of transgenic mice carrying KRAS
resultsOur preclinical results indicate that in NSCLC KRAS
conclusionOur 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.
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Registered trials
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.