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Updated: Oct 1, 2026
Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells
Published on: August 25, 2021
Semaphorin 3F gene from human 3p21.3 suppresses tumor formation in nude mice
RuiHua Xiang1, Albert R Davalos, Charles H Hensel
1Department of Cellular and Structural Biology, The University of Texas Health Science Center, San Antonio, Texas 78229-3900, USA.
Abstract:
Loss of heterozygosity on human chromosome 3p21.3 is a frequent occurrence in many tumor types. In a previous study, our laboratory demonstrated that an 80-kb P1 clone from chromosome 3 suppresses the tumorigenicity of the mouse fibrosarcoma cell line A9. Two cDNAs corresponding to genes encoded on this P1 clone, semaphorin 3F (SEMA3F) and N23, were tested for their effects on in vitro and in vivo growth characteristics after transfection into mouse A9 cells. Transfection of SEMA3F cDNA resulted in complete loss of tumorigenicity in nude mice, whereas transfection of N23 had no effect. Moreover, SEMA3F also functioned to block apoptosis of transfected A9 cells treated with Taxol or Adriamycin. The human ovarian adenocarcinoma cell line HEY showed a similar result as A9 cells, but the small cell lung cancer line GLC45 was unaffected by expression of SEMA3F.
Insights
Semaphorin 3F (SEMA3F) gene expression suppressed tumor growth in mouse models. SEMA3F also protected cancer cells from chemotherapy-induced apoptosis, suggesting its potential as a tumor suppressor.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Loss of heterozygosity on chromosome 3p21.3 is common in various cancers.
- Previous research identified a chromosome 3 P1 clone that suppresses tumorigenicity in mouse fibrosarcoma cells.
Purpose of the Study:
- To investigate the tumor-suppressive potential of two genes, semaphorin 3F (SEMA3F) and N23, located on chromosome 3p21.3.
- To determine the effect of SEMA3F and N23 expression on cancer cell growth and apoptosis.
Main Methods:
- Transfection of mouse fibrosarcoma A9 cells with SEMA3F and N23 cDNAs.
- In vitro and in vivo assessment of tumor growth characteristics in transfected cells.
- Evaluation of apoptosis in transfected cells treated with chemotherapeutic agents (Taxol, Adriamycin).
Main Results:
- SEMA3F cDNA transfection led to a complete loss of tumorigenicity in nude mice.
- SEMA3F expression inhibited apoptosis in A9 cells treated with Taxol or Adriamycin.
- N23 cDNA transfection had no significant effect on tumor growth or apoptosis.
- Similar tumor suppression was observed in human ovarian adenocarcinoma HEY cells, but not in small cell lung cancer GLC45 cells.
Conclusions:
- SEMA3F acts as a tumor suppressor gene, inhibiting cancer cell proliferation and promoting survival.
- The tumor-suppressive function of SEMA3F may be cell-type specific.
- SEMA3F warrants further investigation for its therapeutic potential in specific cancer types.
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