Related Experiment Video
Updated: Aug 24, 2025
Intratibial Osteosarcoma Cell Injection to Generate Orthotopic Osteosarcoma and Lung Metastasis Mouse Models
Published on: October 28, 2021
Apatinib Functioned as Tumor Suppressor of Synovial Sarcoma through Regulating miR-34a-5p/HOXA13 Axis
Qi Feng1, Donglai Wang1, Peng Guo1
1Department of Orthopedics, The Fourth Hospital of Hebei Medical University, Shijiazhuang, 050011 Hebei Province, China.
Objective:
Synovial sarcoma is a rare malignant tumor. The role of apatinib in synovial sarcoma remains unclear. In this study, we aimed to determine the biological functions and the potential molecular mechanism of action of apatinib in synovial sarcoma.
Methods:
SW982 cells were stimulated with apatinib. The relative expression of the genes was determined by performing qPCR. Protein levels were evaluated by western blot and immunohistochemistry assays. Proliferation, apoptosis, migration, and invasion of SW982 cells were determined by the CCK-8 assay, clone formation assay, flow cytometry, wound healing, and the transwell assay, respectively. Additionally, SW982 cells were injected into mice to induce synovial sarcoma.
Results:
Apatinib decreased the proliferation, migration, and invasion but increased the apoptosis of SW982 cells. Apatinib repressed tumor growth in vivo and elevated miR-34a-5p in SW982 cells. The inhibition of miR-34a-5p repressed the reduction of proliferation, migration, and invasion and also the elevation of apoptosis in apatinib-treated SW982 cells. The luciferase activity decreased after cotransfection of the miR-34a-5p mimic and the wild-type HOXA13 vector. Additionally, an increase in miR-34a-5p repressed the levels of HOXA13 mRNA and protein. Moreover, HOXA13 reversed these patterns caused by the inhibition of miR-34a-5p in apatinib-treated SW982 cells.
Conclusion:
Apatinib elevated miR-34a-5p and reduced HOXA13, leading to a significant decrease in proliferation, migration, and invasion, along with an enhancement of apoptosis in SW982 cells. Apatinib suppressed tumorigenesis and tumor growth in SW982 cells in vivo.
Insights
Apatinib inhibits synovial sarcoma cell growth by increasing miR-34a-5p and decreasing HOXA13. This targeted therapy suppresses tumor proliferation, migration, and invasion while enhancing apoptosis.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Synovial sarcoma is a rare and aggressive malignancy.
- The therapeutic potential of apatinib in synovial sarcoma is not well understood.
- Investigating novel therapeutic targets is crucial for improving patient outcomes.
Purpose of the Study:
- To elucidate the biological functions of apatinib in synovial sarcoma.
- To determine the molecular mechanism of action of apatinib.
- To evaluate apatinib's efficacy in preclinical models of synovial sarcoma.
Main Methods:
- SW982 synovial sarcoma cells were treated with apatinib.
- Gene and protein expression analyzed via qPCR, western blot, and immunohistochemistry.
- Cellular functions (proliferation, apoptosis, migration, invasion) assessed using various assays.
- Tumorigenesis and growth evaluated in a mouse xenograft model.
Main Results:
- Apatinib significantly reduced SW982 cell proliferation, migration, and invasion.
- Apatinib treatment increased apoptosis in SW982 cells.
- In vivo studies demonstrated that apatinib suppressed tumor growth and elevated miR-34a-5p levels.
- Apatinib's mechanism involves upregulating miR-34a-5p, which downregulates HOXA13 expression.
Conclusions:
- Apatinib exerts anti-cancer effects in synovial sarcoma by modulating the miR-34a-5p/HOXA13 axis.
- Apatinib effectively inhibits synovial sarcoma cell proliferation, migration, and invasion, while promoting apoptosis.
- Apatinib demonstrates significant potential as a therapeutic agent for synovial sarcoma.
Related Concept Videos
01:22PI3K/mTOR/AKT Signaling Pathway
01:05Cancer-Critical Genes II: Tumor Suppressor Genes
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
02:07Tumor Progression
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
02:53Adaptive Mechanisms in Cancer Cells
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
01:12Loss of Tumor Suppressor Gene Functions
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
02:57Targeted Cancer Therapies
There are several types of targeted therapies against...