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Published on: May 18, 2020
[Molecular mechanism and related influence factors of Lin28/Let-7 axsis]
Abstract:
There are 13 members of the Let -7 miRNAs family which is regarded as tumor suppressor gene, locating in nine different chromosome loci. Lin28 acts as negative regulatory factor of miRNA biological recurrence. By selectively blocking the processing synthesis of the Let-7 miRNAs family, Lin28 block the inhibition effect of miRNA of proto-oncogenes and interact with RNA helicase to enhance gene translation at the same time. By not quite clear mechanism, an up-regulation of Let-7 inhibits the expression and function of Lin28. In more and more studies of human tumor, Lin28/Let-7 axsis was proved to be important significance of the tumor's occurrence and development. In this paper, we research briefly the recent progress of the molecular mechanism and related influence factors of ILin28/Let-7 axsis.
Insights
The Lin28/Let-7 axis, a key regulator in human tumors, involves Lin28 protein inhibiting Let-7 microRNAs (miRNAs) and promoting cancer. Understanding this axis is crucial for cancer research.
Area of Science:
- Molecular Biology
- Oncology
- Genetics
Background:
- The Let-7 microRNA (miRNA) family, comprising 13 members across nine loci, functions as a tumor suppressor.
- Lin28 protein negatively regulates miRNA biogenesis by inhibiting Let-7 miRNA processing.
- The Lin28/Let-7 axis plays a significant role in the development and progression of human tumors.
Purpose of the Study:
- To review the molecular mechanisms governing the Lin28/Let-7 axis.
- To explore factors influencing the Lin28/Let-7 axis in the context of cancer.
Main Methods:
- Literature review of recent studies on the Lin28/Let-7 axis.
- Analysis of molecular interactions between Lin28 and Let-7 miRNAs.
- Investigation of regulatory feedback loops and oncogenic pathways.
Main Results:
- Lin28 selectively blocks Let-7 miRNA synthesis, thereby diminishing miRNA-mediated inhibition of proto-oncogenes.
- Lin28 interacts with RNA helicases to concurrently enhance oncogene translation.
- An incompletely understood mechanism shows Let-7 upregulation inhibits Lin28 expression and function.
Conclusions:
- The Lin28/Let-7 axis is a critical regulatory pathway in tumorigenesis.
- Further research into the molecular intricacies of this axis may reveal novel therapeutic targets for cancer treatment.
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