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Published on: November 10, 2017
Knockdown of WISP1 inhibit proliferation and induce apoptosis in ALL Jurkat cells
Xiaomin Zhang1, Xi Chen1, Juan Liu1
1Department of Hematology, The Second Affiliated Hospital, Harbin Medical University Harbin 150086, Heilongjiang, China.
Abstract:
WISP1, a Wnt-induced secreted protein, has been found to have anticancer activity. ALL is a leading cause of death. Here we investigate the WISP1 effects on ALL Jurkat cells. Cell viability was assessed by CCK-8. Cell cycle and apoptosis were detected by flow cytometry. Mitochondrial membrane potential (MMP) was monitored using TMRM. Generation of reactive oxygen species (ROS) was quantified using DCFH-DA. Western blot was used to detect the expression of cell proliferation and apoptosis related genes. The results showed that knockdown of WISP1 significantly inhibited proliferation of Jurkat cells. Parallelly, cell cycle distribution was increased at G1 phase and apoptotic rate was induced after WISP1 knockdown. Furthermore, knockdown of WISP1 induced apoptosis of Jurkat cells was also associated with loss of MMP and generation of ROS. Western blot results showed that the protein expression p-AKT, PCNA, CDK1, P-ERK, CDK2, VEGF, VEGFR2 and Bcl2 were decreased, while the expression of Bax was up-regulated. In conclusion, WISP1 plays an important role in proliferation and apoptosis of Jurkat cells in mitochondria dependent pathway, the specific mechanisms need further study.
Insights
WISP1 knockdown inhibits proliferation and induces apoptosis in leukemia cells. This occurs via mitochondrial dysfunction and reactive oxygen species generation, impacting key cell cycle and survival proteins.
Area of Science:
- Oncology
- Cell Biology
- Biochemistry
Background:
- WISP1 (Wnt-induced secreted protein 1) exhibits anticancer properties.
- Acute Lymphoblastic Leukemia (ALL) remains a significant cause of mortality.
- Understanding WISP1's role in ALL is crucial for therapeutic development.
Purpose of the Study:
- To investigate the effects of WISP1 on Acute Lymphoblastic Leukemia (ALL) Jurkat cells.
- To elucidate the mechanisms underlying WISP1's influence on leukemia cell proliferation and apoptosis.
Main Methods:
- Cell viability assessed using CCK-8 assay.
- Cell cycle and apoptosis analyzed via flow cytometry.
- Mitochondrial membrane potential (MMP) and reactive oxygen species (ROS) quantified.
- Western blot used to detect protein expression of proliferation and apoptosis markers.
Main Results:
- WISP1 knockdown significantly inhibited Jurkat cell proliferation.
- WISP1 knockdown led to G1 phase arrest and increased apoptosis.
- Apoptosis induction was linked to loss of MMP and ROS generation.
- Key proteins (p-AKT, PCNA, CDK1, P-ERK, CDK2, VEGF, VEGFR2, Bcl2) decreased, while Bax increased.
Conclusions:
- WISP1 is integral to Jurkat cell proliferation and apoptosis.
- The observed effects involve a mitochondria-dependent pathway.
- Further research is needed to fully delineate WISP1's specific mechanisms in leukemia.
Related Concept Videos
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02:34Inhibition of CDK Activity
01:30Apoptosis