CD40L inhibits cell growth of THP-1 cells by suppressing the PI3K/Akt pathway
| Autor: | Zhongxin Feng, Zuguo Tian, Yuping Gong, Qi Chen, Mingqiang Ren |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
CD40 biology Cell growth Chemistry hemic and immune systems 03 medical and health sciences 030104 developmental biology 0302 clinical medicine Oncology Apoptosis Cell culture 030220 oncology & carcinogenesis Cancer cell biology.protein Cancer research PTEN Pharmacology (medical) Protein kinase B PI3K/AKT/mTOR pathway |
| Zdroj: | OncoTargets and Therapy. 12:3011-3017 |
| ISSN: | 1178-6930 |
| DOI: | 10.2147/ott.s175347 |
| Popis: | Introduction Acute myeloid leukemia (AML), the hematological malignant tumor with high mortality, is still difficult to treat. CD40L is a type II transmembrane protein, which has been reported to have the potential to inhibit growth of some cancer cells. Materials and methods In order to determine the role of CD40L on AML-M5 cell line THP-1, we overexpressed CD40L in the cells using a lentiviral vector system (pHBLV-CMVIE-Zs Green-T2A-puro vector); overexpression was confirmed by the detection of green fluorescent protein and CD40L protein expression. Results Cellular apoptosis, proliferation, and cycle assays showed that CD40L could promote the apoptosis of, suppress the proliferation of, and stimulate the arrest of the G1/S phase of THP-1 cells. Finally, the protein expression of P53, Bax/Bcl-2, cyclinD1, PCNA, PTEN, and p-Akt illustrated that CD40L may partly influence cell growth of THP-1 cells through those genes, which was confirmed by immunohistochemistry and a PI3K/Akt activator. Conclusion Taken together, CD40L could inhibit cell growth of THP-1 cells through the PI3K/Akt pathway, indicating that the overexpression of CD40L may be a potential target to treat the AML-M5 disease. |
| Databáze: | OpenAIRE |
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