Related Experiment Video
Updated: Sep 25, 2025

Intratibial Osteosarcoma Cell Injection to Generate Orthotopic Osteosarcoma and Lung Metastasis Mouse Models
Published on: October 28, 2021
The Roles of KIFC1 in the Development of Osteosarcoma: Characterization of Potential Therapeutic Targets
1Department of Intense Care Unit, Yantai Yuhuangding Hospital, No. 20 Yudong Road, Zhifu District, Yantai City, 264000 Shandong Province, China.
Background:
As an important member of the mitotic kinesin family, kinesin family member C1 (KIFC1) is abnormally expressed in a variety of tumors. However, the roles of KIFC1 in the development of osteosarcoma (OS) have never been elucidated.
Methods:
The expression of KIFC1 in OS tissues which was detected by immunohistochemistry (IHC) staining was further confirmed by Gene Expression Profiling Interactive Analysis 2 (GEPIA2) database. The relationship between KIFC1 and CDC20 was analyzed by clinical data, STRING database, and GEPIA2 database. Survival analysis was performed through GEPIA2 database. To elucidate the roles of KIFC1 in OS, MG-63 and U-2 OS cells were treated with short hairpin RNA (shRNA) to knock down KIFC1 expression, and the knockdown efficiency was validated with quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and western blotting (WB). Moreover, colony formation and Cell Counting Kit-8 (CCK-8) assays were utilized to evaluate cell proliferation.
Results:
According to IHC staining and GEPIA2 analysis, the expression of KIFC1 in OS tissues was significantly higher than that in adjacent normal tissues, which was inversely connected to the prognosis. These results were consistent with our clinical data. Besides, KIFC1 was positively correlated with CDC20. In addition, KIFC1 shRNA could effectively silence KIFC1 expression in MG-63 and U-2 OS cells. Furthermore, the knockdown of KIFC1 inhibited the cell proliferation ability with increased cell apoptosis in MG-63 and U-2 OS cells.
Conclusion:
KIFC1 was significantly upregulated in OS and promoted OS progression by cell proliferation. These findings offered new clues for OS diagnosis and prognosis, suggesting KIFC1 could be a potential therapeutic target for OS in further study.
Insights
Kinesin family member C1 (KIFC1) is upregulated in osteosarcoma (OS) and promotes tumor progression by increasing cell proliferation. This suggests KIFC1 is a potential therapeutic target for osteosarcoma.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Kinesin family member C1 (KIFC1) is implicated in various cancers.
- The role of KIFC1 in osteosarcoma (OS) development remains unclear.
Purpose of the Study:
- To investigate the expression and function of KIFC1 in osteosarcoma.
- To determine if KIFC1 could serve as a potential therapeutic target for OS.
Main Methods:
- KIFC1 expression was analyzed in OS tissues using immunohistochemistry (IHC) and the GEPIA2 database.
- KIFC1's correlation with CDC20 and patient prognosis was assessed.
- KIFC1 was knocked down using short hairpin RNA (shRNA) in OS cell lines (MG-63, U-2 OS).
- Cell proliferation and apoptosis were evaluated using CCK-8, colony formation, and apoptosis assays.
Main Results:
- KIFC1 expression was significantly elevated in OS tissues compared to normal tissues and inversely correlated with patient prognosis.
- KIFC1 expression was positively correlated with CDC20.
- KIFC1 knockdown effectively reduced KIFC1 expression and inhibited cell proliferation while increasing apoptosis in OS cells.
Conclusions:
- KIFC1 is upregulated in osteosarcoma and promotes tumor progression through enhanced cell proliferation.
- KIFC1 represents a potential diagnostic and prognostic biomarker for OS.
- KIFC1 inhibition may offer a novel therapeutic strategy for osteosarcoma treatment.
Related Concept Videos
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
Inhibition of Cdk Activity
NF-κB-dependent Signaling Pathway
NF-κB-dependent Signaling Mechanism
The...
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...
PI3K/mTOR/AKT Signaling Pathway
Targeted Cancer Therapies
There are several types of targeted therapies against...

