Related Experiment Video
Updated: Aug 9, 2025
Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
LncRNA H19 promotes tumor angiogenesis in smokers by targeting anti-angiogenic miRNAs
1Infectious & Tropical Diseases Research Center, Tabriz University of Medical Sciences, Tabriz, 15731, Iran.
Abstract:
A key concept in drug discovery is the identification of candidate therapeutic targets such as long noncoding RNAs (lncRNAs) because of their extensive involvement in neoplasms, and impressionability by smoking. Induced by exposure to cigarette smoke, lncRNA H19 targets and inactivates miR-29, miR-30a, miR-107, miR-140, miR-148b, miR-199a and miR-200, which control the rate of angiogenesis by inhibiting BiP, DLL4, FGF7, HIF1A, HIF1B, HIF2A, PDGFB, PDGFRA, VEGFA, VEGFB, VEGFC, VEGFR1, VEGFR2 and VEGFR3. Nevertheless, these miRNAs are often dysregulated in bladder cancer, breast cancer, colorectal cancer, glioma, gastric adenocarcinoma, hepatocellular carcinoma, meningioma, non-small-cell lung carcinoma, oral squamous cell carcinoma, ovarian cancer, prostate adenocarcinoma and renal cell carcinoma. As such, the present perspective article seeks to establish an evidence-based hypothetical model of how a smoking-related lncRNA known as H19 might aggravate angiogenesis by interfering with miRNAs that would otherwise regulate angiogenesis in a nonsmoking individual.
Insights
Smoking-induced H19 long noncoding RNA (lncRNA) may worsen angiogenesis by inactivating specific microRNAs (miRNAs). This disruption is implicated in various cancers where these miRNAs normally regulate blood vessel formation.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Long noncoding RNAs (lncRNAs) are increasingly recognized as key players in cancer development and progression.
- Cigarette smoke exposure is a significant risk factor for numerous cancers and can influence gene expression, including lncRNAs.
- Angiogenesis, the formation of new blood vessels, is crucial for tumor growth and metastasis and is tightly regulated by various molecular factors.
Purpose of the Study:
- To propose a hypothetical model explaining how smoking-induced H19 lncRNA exacerbates angiogenesis.
- To investigate the role of H19 in targeting and inactivating specific microRNAs (miRNAs) involved in angiogenesis regulation.
- To highlight the potential implications of this mechanism in various smoking-associated cancers.
Main Methods:
- This is a perspective article, presenting a hypothetical model based on existing literature.
- The model focuses on the interaction between H19 lncRNA, specific miRNAs (miR-29, miR-30a, miR-107, miR-140, miR-148b, miR-199a, miR-200), and angiogenesis-related genes.
- The study reviews the dysregulation of these miRNAs in multiple cancer types.
Main Results:
- H19 lncRNA, induced by cigarette smoke, targets and inactivates a panel of miRNAs that normally inhibit angiogenesis.
- These miRNAs regulate key angiogenesis factors including BiP, DLL4, FGF7, HIF1A, HIF1B, HIF2A, PDGFB, PDGFRA, VEGFA, VEGFB, VEGFC, VEGFR1, VEGFR2, and VEGFR3.
- The dysregulation of these miRNAs by H19 is proposed as a mechanism contributing to enhanced angiogenesis in smokers.
Conclusions:
- H19 lncRNA plays a critical role in smoking-induced angiogenesis by interfering with miRNA-mediated regulation.
- The inactivation of angiogenesis-inhibiting miRNAs by H19 represents a potential therapeutic target for smoking-related cancers.
- Understanding this molecular interplay is crucial for developing novel anti-angiogenic strategies in oncology.
Related Concept Videos
02:39lncRNA - Long Non-coding RNAs
01:22MicroRNAs
01:24Regulation of Angiogenesis and Blood Supply
01:10Mechanism of Angiogenesis
02:23Abnormal Proliferation
01:12Loss of Tumor Suppressor Gene Functions
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...