Related Experiment Video
Updated: Jun 13, 2025

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
LncRNA HAND2-AS1 Inhibited Colon Cancer Progression By Regulating miR-3118/ZG16 Axis
Ling Hu1, Linfeng Xie2, Shan Huang3
1Department of Gastroenterology, WUHAN ASIA GENERAL HOSPITAI, Wuhan, 430050, Hubei, China.
Abstract:
LncRNA HAND2-AS1 is a novel cancer regulator, but the role and mechanisms of HAND2-AS1 involved with colon cancer (CC) progression remains unknown. The purpose of this research was to figure out how HAND2-AS1 regulates the progression of CC. Using qRT-PCR, we studied expression levels of miR-3118, HAND2-AS1, and ZG16 in CC tissues and cells. Protein levels of apoptosis-related proteins (Bax and Bcl-2) and ZG16 were quantified by western blotting. In vitro function analysis referred to western blotting, wound healing assay and CCK-8. The binding association among miR-3118, HAND2-AS1, and ZG16 was investigated using luciferase reporter and RIP assays. The functional role of HAND2-AS1 was analyzed using xenograft tumor models in vivo. In tissues and cells of CC, HAND2-AS1 was downregulated. We observed that HAND2-AS1 overexpression declined CC cell proliferation and migration while facilitating apoptosis. We further verified that when HAND2-AS1 is overexpressed it reduced CC tumor development in vivo. In CC cells and tissues, miR-3118 competed with HAND2-AS1 and was elevated. Further it was noted that the HAND2-AS1 when overexpressed, lessened the survival of CC cells, however overexpression of miR-3118 restored these changes. ZG16 was shown to be a target of miR-3118, it was found that ZG16 was downregulated in CC tissue and cells. We observed, high expression of ZG16 partially restored the enhanced malignant phenotype caused by miR-3118 overexpression. HAND2-AS1 inhibited CC progression by upregulating ZG16 expression through sponging miR-3118. Hence, HAND2-AS1/miR-3118/ZG16 axis could be a possible new target for CC treatment.
Insights
Long non-coding RNA HAND2-AS1 inhibits colon cancer (CC) progression by upregulating ZG16 via sponging miR-3118. This HAND2-AS1/miR-3118/ZG16 pathway presents a potential therapeutic target for CC treatment.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Long non-coding RNAs (lncRNAs) are increasingly recognized as crucial regulators in cancer development.
- The specific role and underlying mechanisms of lncRNA HAND2-AS1 in colon cancer (CC) progression are not well understood.
Purpose of the Study:
- To elucidate the regulatory role and molecular mechanisms of HAND2-AS1 in colon cancer progression.
- To investigate the potential of the HAND2-AS1/miR-3118/ZG16 axis as a therapeutic target for CC.
Main Methods:
- Quantitative reverse transcription polymerase chain reaction (qRT-PCR) to assess gene expression.
- Western blotting to quantify protein levels.
- In vitro functional assays (wound healing, CCK-8) and in vivo xenograft models.
- Luciferase reporter and RNA immunoprecipitation (RIP) assays to confirm molecular interactions.
Main Results:
- HAND2-AS1 was found to be downregulated in CC tissues and cells.
- Overexpression of HAND2-AS1 suppressed CC cell proliferation, migration, and tumor growth in vivo, while promoting apoptosis.
- HAND2-AS1 inhibited CC progression by upregulating ZG16 expression through sponging miR-3118.
Conclusions:
- The HAND2-AS1/miR-3118/ZG16 axis plays a significant role in regulating colon cancer progression.
- HAND2-AS1 functions as a tumor suppressor in CC by modulating the miR-3118/ZG16 pathway.
- This axis represents a promising novel therapeutic target for colon cancer treatment.
Related Concept Videos
lncRNA - Long Non-coding RNAs
MicroRNAs
Targeted Cancer Therapies
There are several types of targeted therapies against...
Role Of Notch Signalling In Intestinal Stem Cell Renewal
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
Canonical Wnt Signaling Pathway
Abnormal Proliferation

