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Published on: March 30, 2019
Dual mechanism of Let-7i in tumor progression
Jiapei Zhou1, Hongjie Xiang2, Zhiqun Cao1
1First Clinical Medical College, Shandong University of Traditional Chinese Medicine, Jinan, China.
Abstract:
Let-7i regulates tumors primarily by binding to the 3' untranslated region (3' UTR) of mRNA, which indirectly regulates post-transcriptional gene expression. Let-7i also has an epigenetic function via modulating DNA methylation to directly regulate gene expression. Let-7i performs a dual role by inducing both the promotion and inhibition of various malignancies, depending on its target. The mechanism of Let-7i action involves cancer cell proliferation, migration, invasion, apoptosis, epithelial-mesenchymal transition, EV transmission, angiogenesis, autophagy, and drug resistance sensitization. Let-7i is closely related to cancer, and hence, is a potential biomarker for the diagnosis and prognosis of various cancers. Therapeutically, it can be used to promote an anti-cancer immune response by modifying exosomes, thus exerting a tumor-suppressive effect.
Insights
Let-7i microRNA plays a dual role in cancer, regulating gene expression epigenetically and post-transcriptionally. It shows potential as a cancer biomarker and therapeutic target, influencing tumor progression and drug resistance.
Area of Science:
- Molecular Biology
- Genetics
- Oncology
Background:
- MicroRNAs (miRNAs) are key regulators of gene expression.
- Let-7i, a specific miRNA, has been implicated in various biological processes.
- Understanding Let-7i's role in cancer is crucial for developing new diagnostics and therapeutics.
Purpose of the Study:
- To elucidate the multifaceted regulatory mechanisms of Let-7i in tumorigenesis.
- To explore Let-7i's potential as a diagnostic and prognostic biomarker for cancer.
- To investigate the therapeutic implications of Let-7i in cancer treatment.
Main Methods:
- Analysis of Let-7i binding to mRNA 3' untranslated regions (3' UTRs) for post-transcriptional regulation.
- Investigation of Let-7i's epigenetic function through DNA methylation modulation.
- Assessment of Let-7i's impact on key cancer hallmarks including proliferation, migration, invasion, apoptosis, EMT, EV transmission, angiogenesis, autophagy, and drug resistance.
Main Results:
- Let-7i exhibits a dual role in cancer, promoting or inhibiting malignancies based on its specific targets.
- Let-7i influences critical cancer cell behaviors, affecting proliferation, migration, invasion, apoptosis, EMT, EV transmission, angiogenesis, autophagy, and drug resistance.
- Let-7i is identified as a potential biomarker for cancer diagnosis and prognosis.
Conclusions:
- Let-7i is a significant regulator in cancer, acting through both post-transcriptional and epigenetic mechanisms.
- Let-7i's complex role highlights its potential as a versatile biomarker and therapeutic target.
- Modulating Let-7i, potentially via exosome modification, could promote anti-cancer immune responses and exert tumor-suppressive effects.
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