ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2022
A Novel Metabolic Reprogramming Strategy for the Treatment of Diabetes-Associated Breast Cancer.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2022. 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, 22 citations in OpenAlex.
- Identifying PLAU as a shared pathogenic gene in type 2 diabetes and bladder urothelial carcinoma through integrated transcriptomic analysis and machine learning for diagnostic and therapeutic value.Clinical and experimental medicine · 2026Article
- An 8-gene diabetes-related signature predicts survival and immunotherapy response in breast cancer.Clinics (Sao Paulo, Brazil) · 2026Article
- Methylglyoxal-derived glycated albumin enhances the stemness potential of invasive ductal carcinoma-derived breast cancer stem-like cell line KAIMRC1.Oncology letters · 2026Article
- Bi-Polar Bioenergetic Intervention via a Pathology Self-Adaptive Single-Atom Nanocatalyst for Diabetic Tumor Postoperative Management.Nano-micro letters · 2026Article
- Solute Carrier transporters in tumor metabolism and immune modulation: implications for therapy.Journal of translational medicine · 2026Review
- Syrosingopine and UK5099 synergistically suppress non-small cell lung cancer by activating the integrated stress response.Cell death & disease · 2024Article
- MCT4-driven CAF-mediated metabolic reprogramming in breast cancer microenvironment is a vulnerability targetable by miR-425-5p.Cell death discovery · 2024Article
- Trabectedin and Lurbinectedin Modulate the Interplay between Cells in the Tumour Microenvironment-Progresses in Their Use in Combined Cancer Therapy.Molecules (Basel, Switzerland) · 2024Review
- Harnessing glucose metabolism with nanomedicine for cancer treatment.Theranostics · 2024Review
- Advancements in small molecule drug design: A structural perspective.Drug discovery today · 2023Review
- FGF1 supports glycolytic metabolism through the estrogen receptor in endocrine-resistant and obesity-associated breast cancer.Breast cancer research : BCR · 2023Article
- Drug Repurposing of FDA Compounds against α-Glucosidase for the Treatment of Type 2 Diabetes: Insights from Molecular Docking and Molecular Dynamics Simulations.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Potential Therapies Targeting the Metabolic Reprogramming of Diabetes-Associated Breast Cancer.Journal of personalized medicine · 2023Review
- Tumor-targeted dual-starvation therapy based on redox-responsive micelle nanosystem with co-loaded LND and BPTES.Materials today. Bio · 2022Article
- A Novel Metabolic Reprogramming Strategy for the Treatment of Diabetes-Associated Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
Corrections and comments
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Authors and funding
14 authors at 7 institutions in 3 countries.
Funding
Abstract
Diabetes is directly related to the risk of breast cancer (BC) occurrence and worsened BC prognosis. Currently, there are no specific treatments for diabetes-associated BC. This paper aims to understand the fundamental mechanisms of diabetes-induced BC progression and to develop personalized treatments. It reports a metabolic reprogramming strategy (MRS) that pharmaceutical induction of glucose import and glycolysis with metformin and NF-κB inhibitor (NF-κBi) while blocking the export of excessive lactate via inhibiting monocarboxylate transporter 4 (MCT4) leads to a metabolic crisis within the cancer cells. It demonstrates that the MRS shifts the metabolism of BC cells toward higher production of lactate, blocks lactate secretion, prompts intracellular acidification and induces significant cytotoxicity. Moreover, a novel MCT4 inhibitor CB-2 has been identified by structure-based virtual screening. A triple combination of metformin, CB-2, and trabectedin, a drug that impedes NF-κB signaling, strongly inhibits BC cells. Compared to normal glucose condition, MRS elicits more potent cancer cell-killing effects under high glucose condition. Animal model studies show that diabetic conditions promote the proliferation and progression of BC xenografts in nude mice and that MRS treatment significantly inhibits HG-induced BC progression. Therefore, inhibition of MCT4 combined with metformin/NF-κBi is a promising cancer therapy, especially for diabetes-associated BC.
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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.