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Updated: Mar 20, 2026
Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
Bioinformatic Studies to Predict MicroRNAs with the Potential of Uncoupling RECK Expression from
Zhipeng Wang1, Ryusuke Murakami2, Kanako Yuki1
1Laboratory for Malignancy Control Research, Medical Innovation Center, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Abstract:
RECK is downregulated in many tumors, and forced RECK expression in tumor cells often results in suppression of malignant phenotypes. Recent findings suggest that RECK is upregulated after epithelial-mesenchymal transition (EMT) in normal epithelium-derived cells but not in cancer cells. Since several microRNAs (miRs) are known to target RECK mRNA, we hypothesized that certain miR(s) may be involved in this suppression of RECK upregulation after EMT in cancer cells. To test this hypothesis, we used three approaches: (1) text mining to find miRs relevant to EMT in cancer cells, (2) predicting miR targets using four algorithms, and (3) comparing miR-seq data and RECK mRNA data using a novel non-parametric method. These approaches identified the miR-183-96-182 cluster as a strong candidate. We also looked for transcription factors and signaling molecules that may promote cancer EMT, miR-183-96-182 upregulation, and RECK downregulation. Here we describe our methods, findings, and a testable hypothesis on how RECK expression could be regulated in cancer cells after EMT.
Insights
Researchers identified the miR-183-96-182 cluster as a key regulator suppressing RECK (Reversion-Inducing Cysteine-Rich Proteinous Endogenous Kinase) upregulation during cancer cell epithelial-mesenchymal transition (EMT). This finding offers insights into cancer progression mechanisms.
Area of Science:
- Oncology
- Molecular Biology
- Gene Regulation
Background:
- RECK (Reversion-Inducing Cysteine-Rich Proteinous Endogenous Kinase) is frequently downregulated in tumors, and its restoration can suppress malignant phenotypes.
- While RECK is upregulated after epithelial-mesenchymal transition (EMT) in normal cells, this upregulation is often suppressed in cancer cells.
Purpose of the Study:
- To investigate the role of microRNAs (miRs) in suppressing RECK upregulation during cancer cell EMT.
- To identify specific miRs and regulatory pathways involved in RECK downregulation in the context of cancer EMT.
Main Methods:
- Utilized text mining to identify miRs associated with EMT in cancer.
- Employed four algorithms for predicting miR targets on RECK mRNA.
- Applied a novel non-parametric method to compare miR sequencing and RECK mRNA expression data.
Main Results:
- The miR-183-96-182 cluster was identified as a strong candidate responsible for targeting RECK mRNA.
- Evidence suggests this miR cluster contributes to the suppression of RECK upregulation post-EMT in cancer cells.
- Identified potential transcription factors and signaling molecules involved in promoting cancer EMT, miR-183-96-182 upregulation, and RECK downregulation.
Conclusions:
- The miR-183-96-182 cluster plays a significant role in regulating RECK expression during cancer EMT.
- This study proposes a testable hypothesis for the intricate regulation of RECK in cancer cells following EMT.
- Findings contribute to understanding the molecular mechanisms underlying cancer progression and potential therapeutic targets.
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