ReviewInternational journal of molecular sciences2023
The Nexus of Inflammation-Induced Epithelial-Mesenchymal Transition and Lung Cancer Progression: A Roadmap to Pentacyclic Triterpenoid-Based Therapies.
Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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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.
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Who cites it
14 citing papers in PubMed, 18 citations in OpenAlex.
- E-cigarette aerosol exposure modulates crystalline silica-induced fibrotic responses in the lungs.Archives of toxicology · 2026Article
- Machine learning prioritization identifies PANX1 as an inflammation-associated candidate regulator in lung adenocarcinoma.Frontiers in genetics · 2026Article
- Molecular mechanisms of therapeutic resistance in areca nut-associated oral squamous cell carcinoma: the interplay of chronic inflammation and epithelial-mesenchymal transition.Frontiers in oncology · 2026Review
- Correlation analysis of serum amyloid A, neutrophil-lymphocyte ratio, platelet-lymphocyte ratio, and systemic immune-inflammation index with neoadjuvant therapy efficacy and prognosis in breast cancer.Frontiers in oncology · 2026Article
- Novel Cross-Cancer Hub Genes in Doxorubicin Resistance Identified by Transcriptional Mapping.Biomedicines · 2025Article
- Transcriptomic-Driven Drug Repurposing Reveals SP600125 as a Promising Drug Candidate for the Treatment of Glial-Mesenchymal Transition in Glioblastoma.International journal of molecular sciences · 2025Article
- Deciphering the Tenascin-C Nexus: A Comprehensive Review of Its Involvement in Chronic Respiratory Diseases.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025Review
- Cancer Development and Progression Through a Vicious Cycle of DNA Damage and Inflammation.International journal of molecular sciences · 2025Review
- Advances in research on the effects of medicinal and edible substances on lung cancer: an updated review.Frontiers in pharmacology · 2025Review
- Multiple signaling pathways in the frontiers of lung cancer progression.Frontiers in immunology · 2025Review
- Impact of asthma and/or chronic obstructive pulmonary disease on the survival of patients with lung adenocarcinoma.Therapeutic advances in medical oncology · 2025Article
- Morphine promotes non-small cell lung cancer progression by downregulating E-cadherin via the PI3K/AKT/mTOR pathway.Scientific reports · 2024Article
- Pulmonary mucinous adenocarcinoma: An overview of pathophysiology and advancements in treatment.Heliyon · 2024Review
- PCSK9 inhibitor alleviates experimental pulmonary fibrosis-induced pulmonary hypertension via attenuating epithelial-mesenchymal transition by suppressing Wnt/β-catenin signalingFrontiers in medicine · 2024Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Lung cancer is the leading cause of cancer-related death worldwide. Its high mortality is partly due to chronic inflammation that accompanies the disease and stimulates cancer progression. In this review, we analyzed recent studies and highlighted the role of the epithelial-mesenchymal transition (EMT) as a link between inflammation and lung cancer. In the inflammatory tumor microenvironment (iTME), fibroblasts, macrophages, granulocytes, and lymphocytes produce inflammatory mediators, some of which can induce EMT. This leads to increased invasiveness of tumor cells and self-renewal of cancer stem cells (CSCs), which are associated with metastasis and tumor recurrence, respectively. Based on published data, we propose that inflammation-induced EMT may be a potential therapeutic target for the treatment of lung cancer. This prospect is partially realized in the development of EMT inhibitors based on pentacyclic triterpenoids (PTs), described in the second part of our study. PTs reduce the metastatic potential and stemness of tumor cells, making PTs promising candidates for lung cancer therapy. We emphasize that the high diversity of molecular mechanisms underlying inflammation-induced EMT far exceeds those that have been implicated in drug development. Therefore, analysis of information on the relationship between the iTME and EMT is of great interest and may provide ideas for novel treatment approaches for lung cancer.
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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.