Related Experiment Video
Updated: Jan 4, 2026

Genome-wide Screen for miRNA Targets Using the MISSION Target ID Library
Published on: April 6, 2012
miR-128 Functions as an OncomiR for the Downregulation of HIC1 in Breast Cancer
Yan Li1, Ying Wang2, Xiabo Shen3
1Department of Medical Oncology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
Abstract:
Hypermethylated in cancer 1 (HIC1) is continually decreased in breast cancer. However, the underlying molecular basis of the upstream regulation of HIC1 remains elusive. Here, we showed that HIC1 was downregulated in breast cancer tissues. Bioinformatics analysis identified that miR-128 might potentially target HIC1. HIC1 was proved as the target gene of miR-128 by overexpressing or knocking down miR-128. Additionally, we observed that HIC1 suppression by miR-128 increased cell invasion, proliferation, and reduced apoptosis. Lastly, we found that miR-128 accelerated tumor growth in xenograft mice by inhibiting HIC1. Altogether, this study presents the first evidence that miR-128 suppresses the expression of HIC1 to accelerate breast cancerogenesis.
Insights
MicroRNA-128 (miR-128) downregulates Hypermethylated in cancer 1 (HIC1) in breast cancer. This mechanism promotes tumor growth, invasion, and proliferation, highlighting a new target for breast cancer therapy.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Hypermethylated in cancer 1 (HIC1) expression is decreased in breast cancer tissues.
- The regulatory mechanisms controlling HIC1 levels in breast cancer are not fully understood.
Purpose of the Study:
- To investigate the role of microRNA-128 (miR-128) in regulating HIC1 expression in breast cancer.
- To elucidate the functional consequences of HIC1 suppression by miR-128 on breast cancer progression.
Main Methods:
- Bioinformatic analysis to predict miR-128 targeting of HIC1.
- Experimental validation of HIC1 as a direct target of miR-128 through overexpression and knockdown studies.
- Assessment of cell invasion, proliferation, and apoptosis in response to miR-128 modulation.
- In vivo studies using xenograft mouse models to evaluate tumor growth.
Main Results:
- HIC1 was confirmed as a direct target gene of miR-128.
- Suppression of HIC1 by miR-128 led to increased breast cancer cell invasion and proliferation.
- miR-128-mediated HIC1 inhibition resulted in reduced apoptosis.
- In vivo, miR-128 accelerated tumor growth by downregulating HIC1.
Conclusions:
- This study establishes miR-128 as a key regulator that suppresses HIC1 expression in breast cancer.
- The miR-128/HIC1 axis plays a significant role in promoting breast cancerogenesis.
- Targeting the miR-128/HIC1 pathway may offer a novel therapeutic strategy for breast cancer.
More Related Videos
Related Concept Videos
MicroRNAs
MicroRNAs
Hedgehog Signaling Pathway
Receptor Downregulation in MVBs
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR...
lncRNA - Long Non-coding RNAs
mTOR Signaling and Cancer Progression
The mTOR pathway or the...

