Related Experiment Video
Updated: Jun 12, 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
Kinesin Family Member C1: Function in liver hepatocellular carcinoma and potential target for chemotherapeutic
Lei Liu1, Fengyang Jing2, Jia Li1
1Department of General Surgery, Department of Emergency Surgery, Fuyang Hospital of Anhui Medical University, Fuyang, 236000, Anhui, China.
Abstract:
MiR-105 exerts inhibitory effects on the development and progression of various cancers, including breast cancer, lung cancer, and gastric cancer. Through GEO data analysis, we observed decreased expression of miR-105 in liver cancer tissues compared to adjacent tissues. Furthermore, miR-105 downregulates KIFC1 expression levels by targeting its 3' UTR. KIFC1 (Kinesin Family Member C1), a Protein Coding gene, may play a role in mitotic metaphase plate polymerization and mitotic spindle assembly. However, our findings suggest that this gene could serve as a potential chemotherapeutic target for Liver hepatocellular carcinoma (LIHC). We obtained the LIHC dataset from the TCGA database and genotype Tissue Expression Project (GTEx) normal tissue data for differential analysis. Additionally, we utilized the cBioPortal database, tumor immune single-cell center (TISCH) database, gene set enrichment analysis (GSEA), and R software to investigate the possible functions and mechanisms of KIFC1. These findings were further validated through experiments such as immunohistochemistry and wound healing assays. Our results indicate that KIFC1 might be involved in DNA repair and cell cycle regulation in LIHC cells which subsequently impacts tumor cell proliferation; moreover, miR-105 influences hepatoma cell line proliferation via its interaction with KIFC1. Collectively, these results highlight the potential therapeutic significance of targeting KIFC1 for chemotherapy treatment in LIHC patients.
Insights
MicroRNA-105 (miR-105) inhibits liver cancer progression by downregulating Kinesin Family Member C1 (KIFC1). Targeting KIFC1 offers a potential new chemotherapy strategy for liver hepatocellular carcinoma (LIHC).
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- MicroRNA-105 (miR-105) demonstrates inhibitory roles in various cancers.
- Decreased miR-105 expression is observed in liver cancer tissues.
- Kinesin Family Member C1 (KIFC1) is implicated in cell division and may be a target in liver cancer.
Purpose of the Study:
- To investigate the role of miR-105 and its target KIFC1 in liver hepatocellular carcinoma (LIHC).
- To explore the potential of targeting KIFC1 as a chemotherapeutic strategy for LIHC.
Main Methods:
- Analysis of The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) databases for differential gene expression.
- Utilized cBioPortal, Tumor Immune Single-cell Center (TISCH) database, Gene Set Enrichment Analysis (GSEA), and R software.
- Experimental validation including immunohistochemistry and wound healing assays.
Main Results:
- MiR-105 directly downregulates KIFC1 expression in LIHC.
- KIFC1 is potentially involved in DNA repair and cell cycle regulation in LIHC cells, impacting proliferation.
- MiR-105 affects hepatoma cell proliferation through its interaction with KIFC1.
Conclusions:
- The miR-105/KIFC1 axis plays a significant role in LIHC development and progression.
- Targeting KIFC1 presents a promising therapeutic avenue for LIHC chemotherapy.
- Further research into this pathway could lead to novel treatment strategies for liver cancer.
Related Concept Videos
Targeted Cancer Therapies
There are several types of targeted therapies against...
Inhibition of Cdk Activity
Combination Therapies and Personalized Medicine
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...
M-Cdk Drives Transition Into Mitosis
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
Electron Transport Chain: Complex I and II
ROS generation is regulated and maintained at moderate levels necessary...

