Related Experiment Video
Updated: Sep 11, 2025

In Vitro Cultivation Techniques for Modeling Liver Organogenesis, Building Assembloids, and Designing Synthetic Tissues using Human Cell Lines
Published on: April 18, 2025
HOPX regulates the invasion and migration abilities of hepatocellular carcinoma by targeting SNAIL
Rong Wang1, Haizhou Xu2, Changhuan Hu2
1Department of Gastrointestinal Surgery, The Affiliated Qingyuan Hospital (Qingyuan People' Hospital), Guangzhou Medical University, Qingyuan, 511500, China.
Abstract:
HOPX acts as a tumor suppressor in certain cancers, but the function of HOPX, as well as its mechanism of action in hepatocellular carcinoma (HCC) has not been fully elucidated. In this study, using in vitro and in vivo animal models, the effect of HOPX on the development of HCC was explored. In our study, the HOPX expression at both protein and mRNA level were found to be downregulated in HCC cells and tumor tissues. Restoration of HOPX expression was found to inhibit HCC cell invasion and migration capabilities, but produced no effect on growth. Moreover, HOPX prevented metastasis in an HCC cell metastatic mouse model. Further investigations showed that HOPX could suppress HCC cell epithelial-to-mesenchymal transition (EMT) by inhibiting SNAIL, an EMT transcription factor that is required for the metastasis-inhibition activity of HOPX to proceed. Our study identified HOPX as a suppressor of the development of HCC, which implies that HOPX suppresses HCC cells invasion and migration by inhibiting SNAIL.
Insights
The HOPX gene suppresses hepatocellular carcinoma (HCC) development by inhibiting cancer cell invasion and migration. Restoring HOPX expression reduces metastasis by downregulating SNAIL, an epithelial-to-mesenchymal transition factor.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- The tumor suppressor role of HOPX is known in some cancers, but its function and mechanism in hepatocellular carcinoma (HCC) remain unclear.
- Understanding HOPX's role is crucial for developing targeted therapies against HCC, a significant global health concern.
Purpose of the Study:
- To investigate the effect of HOPX on hepatocellular carcinoma (HCC) development and elucidate its mechanism of action.
- To determine if HOPX can inhibit HCC cell invasion, migration, and metastasis.
Main Methods:
- Utilized in vitro and in vivo animal models to study HOPX's effect on HCC.
- Analyzed HOPX protein and mRNA expression levels in HCC cells and tissues.
- Investigated the impact of HOPX restoration on HCC cell behavior and metastasis in a mouse model.
- Examined the interaction between HOPX and SNAIL, a key transcription factor in epithelial-to-mesenchymal transition (EMT).
Main Results:
- HOPX expression was significantly downregulated at both protein and mRNA levels in HCC cells and tumor tissues.
- Restoring HOPX expression inhibited HCC cell invasion and migration but did not affect cell growth.
- HOPX administration prevented metastasis in a mouse model of HCC.
- HOPX suppressed HCC cell epithelial-to-mesenchymal transition (EMT) by inhibiting SNAIL expression.
Conclusions:
- HOPX functions as a tumor suppressor in hepatocellular carcinoma (HCC).
- HOPX inhibits HCC cell invasion and migration by downregulating the transcription factor SNAIL, thereby suppressing metastasis.
- Targeting HOPX may offer a novel therapeutic strategy for preventing HCC progression and metastasis.
More Related Videos
07:47Non-Invasive PET/MR Imaging in an Orthotopic Mouse Model of Hepatocellular Carcinoma
Published on: August 31, 2022
06:38An Oncogenic Hepatocyte-Induced Orthotopic Mouse Model of Hepatocellular Cancer Arising in the Setting of Hepatic Inflammation and Fibrosis
Published on: September 12, 2019
Related Concept Videos
Cancer Cell Migration through Invadopodia
Hedgehog Signaling Pathway
Regulation of Angiogenesis and Blood Supply
Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal
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...
Metastasis
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...