Related Experiment Video
Updated: Aug 26, 2026
Derivation of Thymic Lymphoma T-cell Lines from Atm-/- and p53-/- Mice
Published on: April 3, 2011
Tumorigenesis of murine erythroleukemia cell line transfected with exogenous p53 gene
Dagong Sun1, Jinhua Wang, Weijuan Yao
1Hemorheology Center, Department of Medical Physics, School of Basic medical Sciences, Peking University, Health Science Center, Beijing 100083, China.
Abstract:
Mutant p53 gene and wild-type p53 gene were introduced into murine erythroleukemia cell line (MEL). The MEL cells transfected with mutant p53 gene (MEL-M) and with wild-type p53 gene (MEL-W) were obtained by G418 selection. MEL, MEL-W and MEL-M were injected intraperitoneally into BALB/C mice. In the first week after injection, the signs of erythroleukemia were induced in all three groups. Abnormalities were mainly found in the spleen, bone marrow, liver and peripheral blood. There was an increase of proerythroblasts in the bone marrow. A large amount of normoblasts (early and intermediate erythroblasts) appeared in the spleen. In the peripheral blood, the white blood cells, reticulocyte and platelet counts increased and RBC count and hematocrit decreased. The degree of abnormalities in the MEL-W group was significantly lower than that in other two groups. Hemorheological measurements indicated that the deformability and orientation of RBCs in MEL and MEL-M groups were impaired, whereas those in MEL-W group did not change significantly. Micropipette aspiration measurement revealed that MEL-W had higher elastic modulus than MEL and MEL-M, indicating that it was more difficult for MEL-W to deform and migrate in vivo. The results of animal test and micropipette suggest that exogenous wild-type p53 gene could reduce the tumorigenesis of murine erythroleukemia cells.
Insights
Introducing wild-type p53 gene into murine erythroleukemia cells (MEL) reduced cancer development. This study found wild-type p53 mitigated MEL cell abnormalities and improved red blood cell function.
Area of Science:
- Oncology
- Molecular Biology
- Hematology
Background:
- The p53 gene plays a crucial role in tumor suppression.
- Mutations in p53 are common in various cancers, including leukemia.
- Understanding the role of wild-type p53 in erythroleukemia is essential for developing new therapies.
Purpose of the Study:
- To investigate the effect of introducing wild-type p53 gene into murine erythroleukemia (MEL) cells.
- To compare the tumorigenesis and hematological abnormalities induced by MEL cells with and without wild-type p53.
Main Methods:
- Murine erythroleukemia (MEL) cells were transfected with either mutant p53 or wild-type p53 genes.
- Transfected cells (MEL-M and MEL-W) and control MEL cells were injected into BALB/C mice.
- Hematological parameters, spleen, bone marrow, and peripheral blood were analyzed.
- Hemorheological measurements, including red blood cell deformability and micropipette aspiration, were performed.
Main Results:
- All groups developed signs of erythroleukemia, with abnormalities in spleen, bone marrow, liver, and peripheral blood.
- The MEL-W group (wild-type p53) showed significantly fewer abnormalities compared to MEL and MEL-M groups.
- Red blood cell deformability and orientation were impaired in MEL and MEL-M groups but not in MEL-W.
- MEL-W cells exhibited a higher elastic modulus, indicating reduced deformability.
Conclusions:
- Exogenous wild-type p53 gene introduction can reduce the tumorigenesis of murine erythroleukemia cells.
- Wild-type p53 expression appears to normalize red blood cell function and mitigate disease progression.
- These findings suggest a potential therapeutic role for wild-type p53 in treating erythroleukemia.
Related Concept Videos
02:23Abnormal Proliferation
02:43Mouse Models of Cancer Study
The development of transgenic, knockout, and knock-in mice has led to an exponential increase in their use as model organisms in research,...