PTEN, a Barrier for Proliferation and Metastasis of Gastric Cancer Cells: From Molecular Pathways to Targeting and Regulation

Cancer is one of the life-threatening disorders that, in spite of excellent advances in medicine and technology, there is no effective cure for. Surgery, chemotherapy, and radiotherapy are extensively applied in cancer therapy, but their efficacy in eradication of cancer cells, suppressing metastasi...

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Published in:Biomedicines 2020-08, Vol.8 (8), p.264
Main Authors: Ashrafizadeh, Milad, Najafi, Masoud, Ang, Hui Li, Moghadam, Ebrahim Rahmani, Mahabady, Mahmood Khaksary, Zabolian, Amirhossein, Jafaripour, Leila, Bejandi, Atefe Kazemzade, Hushmandi, Kiavash, Saleki, Hossein, Zarrabi, Ali, Kumar, Alan Prem
Format: Article
Language:English
Subjects:
1-Phosphatidylinositol 3-kinase
AKT protein
Antitumor agents
Biomarkers
Bladder cancer
Breast cancer
Cancer therapies
Cell activation
Cell cycle
Cell migration
Cell proliferation
Chemotherapy
Deoxyribonucleic acid
DNA
DNA methylation
DNA repair
Epigenetics
Experiments
Gastric cancer
Genes
growth
Immunotherapy
Medical prognosis
Metastases
Metastasis
miRNA
Mutation
Non-coding RNA
Phosphatase
phosphatase and tensin homolog (PTEN)
Phosphorylation
PI3K/Akt
Prostate
Proteins
PTEN protein
Radiation therapy
Review
Signal transduction
Studies
Surgery
Tensin
Tumorigenesis
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Summary:Cancer is one of the life-threatening disorders that, in spite of excellent advances in medicine and technology, there is no effective cure for. Surgery, chemotherapy, and radiotherapy are extensively applied in cancer therapy, but their efficacy in eradication of cancer cells, suppressing metastasis, and improving overall survival of patients is low. This is due to uncontrolled proliferation of cancer cells and their high migratory ability. Finding molecular pathways involved in malignant behavior of cancer cells can pave the road to effective cancer therapy. In the present review, we focus on phosphatase and tensin homolog (PTEN) signaling as a tumor-suppressor molecular pathway in gastric cancer (GC). PTEN inhibits the PI3K/Akt pathway from interfering with the migration and growth of GC cells. Its activation leads to better survival of patients with GC. Different upstream mediators of PTEN in GC have been identified that can regulate PTEN in suppressing growth and invasion of GC cells, such as microRNAs, long non-coding RNAs, and circular RNAs. It seems that antitumor agents enhance the expression of PTEN in overcoming GC. This review focuses on aforementioned topics to provide a new insight into involvement of PTEN and its downstream and upstream mediators in GC. This will direct further studies for evaluation of novel signaling networks and their targeting for suppressing GC progression.
ISSN:2227-9059
2227-9059
DOI:10.3390/biomedicines8080264