Related Experiment Video
Updated: Nov 28, 2025

An Oncogenic Hepatocyte-Induced Orthotopic Mouse Model of Hepatocellular Cancer Arising in the Setting of Hepatic Inflammation and Fibrosis
Published on: September 12, 2019
FAM225A promotes sorafenib resistance in hepatocarcinoma cells through modulating miR-130a-5p-CCNG1 interaction
Yan Tong Liu1, Guo Qing Liu2, Jing Min Huang2
1Xi'an Medical University, Xi'an, China.
Abstract:
Chemotherapy resistance is still a key hurdle in current hepatocellular carcinoma (HCC) treatment. Therefore, clarifying the molecular mechanisms contributing to this acquired resistance is urgent for the effective treatment of liver cancer. In this research, we observed that lncRNA FAM225A expression is dramatically upregulated not only in hepatocellular carcinoma tissues and cell lines but also in sorafenib-resistant HepG2/SOR cells. Moreover, FAM225A knockdown significantly weakened HepG2/SOR cells resistance to sorafenib treatment by MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay. Similar results were obtained from the tumor xenograft model in mice. Further mechanistic researches revealed that the direct interaction between FAM225A and miR-130a-5p, while miR-130a-5p negatively modulated CCNG1 expression by targeting 3'UTR of CCNG1. MiR-130a-5p inhibition or CCNG1 overexpression could partially offset FAM225A knockdown-induced increased viability of HepG2/SOR cells in response to sorafenib challenge. Collectively, our findings provide evidence that FAM225A/miR-130a-5p/CCNG1 interaction network regulates the resistance of HCC cells to sorafenib treatment and could supply a possible strategy for restoring sorafenib sensitivity in HCC therapy.
Insights
Long non-coding RNA FAM225A promotes hepatocellular carcinoma resistance to sorafenib. Targeting the FAM225A/miR-130a-5p/CCNG1 network may restore sensitivity to this liver cancer therapy.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Hepatocellular carcinoma (HCC) treatment faces challenges due to chemotherapy resistance.
- Understanding molecular mechanisms of acquired resistance is crucial for effective liver cancer therapy.
Purpose of the Study:
- To investigate the role of lncRNA FAM225A in sorafenib resistance in HCC.
- To elucidate the molecular pathway involving FAM225A, miR-130a-5p, and CCNG1 in HCC drug resistance.
Main Methods:
- Quantitative analysis of FAM225A expression in HCC tissues and cell lines.
- FAM225A knockdown experiments in HepG2/SOR cells and in vivo tumor xenograft models.
- Assessment of cell viability using MTT assay.
- Investigation of interactions between FAM225A, miR-130a-5p, and CCNG1 using molecular biology techniques.
Main Results:
- FAM225A was significantly upregulated in HCC tissues, cell lines, and sorafenib-resistant cells.
- FAM225A knockdown reduced sorafenib resistance in HCC cells and tumor xenografts.
- FAM225A directly interacts with miR-130a-5p, which targets CCNG1, modulating sorafenib sensitivity.
Conclusions:
- The FAM225A/miR-130a-5p/CCNG1 network plays a key role in regulating sorafenib resistance in HCC.
- Targeting this network offers a potential strategy to re-sensitize HCC to sorafenib treatment.
More Related Videos
09:40Author Spotlight: Unveiling the Role of TMOD3 in Platinum Resistance and Immune Infiltration in Ovarian Cancer
Published on: August 2, 2024
13:18Network Pharmacology Prediction and Experimental Validation of Trichosanthes-Fritillaria thunbergii Action Mechanism Against Lung Adenocarcinoma
Published on: March 3, 2023
Related Concept Videos
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
Treatment Resistant Cancers