SynthesisAging2024
Overexpression of MTFR1 promotes cancer progression and drug-resistance on cisplatin and is related to the immune microenvironment in lung adenocarcinoma.
Synthesis in Aging, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 3 citations in OpenAlex.
- Integrating single-cell transcriptomics and machine learning to predict breast cancer prognosis and immunotherapy sensitivity: a study based on proliferating T cells.World journal of surgical oncology · 2026Article
- A robust multiplex-DIA workflow profiles protein turnover regulations associated with cisplatin resistance and aneuploidy.Nature communications · 2025Article
- Analysis of shared pathogenic mechanisms and drug targets in myocardial infarction and gastric cancer based on transcriptomics and machine learning.Frontiers in immunology · 2025Article
- Revealing the mechanisms of RAC3 in tumor aggressiveness, the immunotherapy response, and drug resistance in bladder cancer.Frontiers in oncology · 2024Article
- Identification of MTFR1 as a Novel Prognostic Biomarker and Putative Oncogene for Breast Cancer: A Multi-Omics Analysis and in Vitro Experimental Validation.IET systems biologyArticle
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThe roles of MTFR1 in the drug resistance of lung adenocarcinoma (LAC) to cisplatin remain unexplored. In this study, the expression, clinical values and mechanisms of MTFR1 were explored, and the relationship between MTFR1 expression and immune microenvironment was investigated in LAC using bioinformatics analysis, cell experiments, and meta-analysis.
methodsMTFR1 expression and clinical values, and the relationship between MTFR1 expression and immunity were explored, through bioinformatics analysis. The effects of MTFR1 on the growth, migration and cisplatin sensitivity of LAC cells were identified using cell counting kit-8, wound healing and Transwell experiments. Additionally, the mechanisms of drug resistance of LAC cells involving MTFR1 were investigated using western blotting.
resultsMTFR1 was elevated in LAC tissues. MTFR1 overexpression was associated with sex, age, primary therapy outcome, smoking, T stage, unfavourable prognosis and diagnostic value and considered an independent risk factor for an unfavourable prognosis in patients with LAC. MTFR1 co-expressed genes involved in the cell cycle, oocyte meiosis, DNA replication and others. Moreover, interfering with MTFR1 expression inhibited the proliferation, migration and invasion of A549 and A549/DDP cells and promoted cell sensitivity to cisplatin, which was related to the inhibition of p-AKT, p-P38 and p-ERK protein expression. MTFR1 overexpression was associated with stromal, immune and estimate scores along with natural killer cells, pDC, iDC and others in LAC.
conclusionsMTFR1 overexpression was related to the unfavourable prognosis, diagnostic value and immunity in LAC. MTFR1 also participated in cell growth and migration and promoted the drug resistance of LAC cells to cisplatin via the p-AKT and p-ERK/P38 signalling pathways.
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