Over expression of PTEN induces apoptosis and prevents cell proliferation in breast cancer cells.

Abstract

The phosphatase and tensin homolog (PTEN) is a tumor suppressor lipid phosphatase frequently mutated or deleted in breast cancer cells. Loss of PTEN is associated with aberrant activation of P13K/AKT signaling pathways, which are responsible for uncontrolled cell cycle, migration and prolonged survival. Therefore, stability and functional PTEN is essential for prevention of cancer growth and migration. In the present study, we have determined the effect of PTEN over expression in apoptosis induction and cell proliferation in breast cancer cells. We showed that PTEN over expression significantly declined the cell proliferation rate during logarithmic growth phase. Furthermore, the PTEN over expression leads to the activation of mitochondrial based intrinsic apoptosis pathways, which is confirmed by the activation and over expression of caspases 9 and caspases 3. In addition, the number of apoptotic cells are significantly more in PTEN over expressed cells, where they showed more apoptotic bodies in AO-EtBr and Hoechst 33344 staining. Finally, PTEN over expressed cells showed decreased chemo resistance as chemotherapeutic drugs kill them efficiently. Therefore, our findings suggest that tumor suppressive effect of PTEN is crucial for cancer prevention and thus PTEN might be a potential target for anti-cancer drugs.

• Authors: Jinfeng Wu, Hong Gao, Wanyu Ge, Jie He
• Journal: Acta biochimica Polonica (Acta Biochim Pol) Vol. 67 Issue 4 Pg. 515-519 (Dec 17 2020) ISSN: 1734-154X [Electronic] Poland
• PMID: 33332075 (Publication Type: Journal Article)

Chemical References

• Antineoplastic Agents
• BCL2 protein, human
• Proto-Oncogene Proteins c-bcl-2
• Docetaxel
• Doxorubicin
• Proto-Oncogene Proteins c-akt
• PTEN Phosphohydrolase
• PTEN protein, human
• CASP3 protein, human
• CASP9 protein, human
• Caspase 3
• Caspase 9
• Fluorouracil

Topics

• Antineoplastic Agents (pharmacology)
• Apoptosis (drug effects, genetics)
• Caspase 3 (genetics, metabolism)
• Caspase 9 (genetics, metabolism)
• Cell Proliferation (drug effects)
• Docetaxel (pharmacology)
• Doxorubicin (pharmacology)
• Enzyme Activation (drug effects)
• Female
• Fluorouracil (pharmacology)
• Gene Expression Regulation, Neoplastic
• Humans
• MCF-7 Cells
• PTEN Phosphohydrolase (genetics, metabolism)
• Phosphatidylinositol 3-Kinases (genetics, metabolism)
• Proto-Oncogene Proteins c-akt (genetics, metabolism)
• Proto-Oncogene Proteins c-bcl-2 (genetics, metabolism)
• Signal Transduction