Yazar "Entezari, M." seçeneğine göre listele

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    AMPK signaling in diabetes mellitus, insulin resistance and diabetic complications: A pre-clinical and clinical investigation
    (Elsevier, 2022) Entezari, M.; Hashemi, D.; Taheriazam, A.; Zabolian, A.; Zabolian, A.; Fakhri, F.; Hashemi, M.; Hushmandi, K.; Ashrafizadeh, M.; Zarrabi, A.; Ertas, Y.N.; Mirzaei, S.
    Diabetes mellitus (DM) is considered as a main challenge in both developing and developed countries, as lifestyle has changed and its management seems to be vital. Type I and type II diabetes are the main kinds and they result in hyperglycemia in patients and related complications. The gene expression alteration can lead to development of DM and related complications. The AMP-activated protein kinase (AMPK) is an energy sensor with aberrant expression in various diseases including cancer, cardiovascular diseases and DM. The present review focuses on understanding AMPK role in DM. Inducing AMPK signaling promotes glucose in DM that is of importance for ameliorating hyperglycemia. Further investigation reveals the role of AMPK signaling in enhancing insulin sensitivity for treatment of diabetic patients. Furthermore, AMPK upregulation inhibits stress and cell death in ? cells that is of importance for preventing type I diabetes development. The clinical studies on diabetic patients have shown the role of AMPK signaling in improving diabetic complications such as brain disorders. Furthermore, AMPK can improve neuropathy, nephropathy, liver diseases and reproductive alterations occurring during DM. For exerting such protective impacts, AMPK signaling interacts with other molecular pathways such as PGC-1?, PI3K/Akt, NOX4 and NF-?B among others. Therefore, providing therapeutics based on AMPK targeting can be beneficial for amelioration of DM.
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    Molecular landscape of c-Myc signaling in prostate cancer: A roadmap to clinical translation
    (Elsevier GmbH, 2022) Faskhoudi, M.A.; Molaei, P.; Sadrkhanloo, M.; Orouei, S.; Hashemi, M.; Bokaie, S.; Rashidi, M.; Entezari, M.; Zarrabi, A.; Hushmandi, K.; Mirzaei, S.; Gholami, M.H.
    The c-Myc signaling is a new emerging target in cancer therapy. Activation of c-Myc signaling leads to cancer growth and invasion in vitro and in vivo. The stability of c-Myc can also mediate drug resistance and radioresistance in cancers. The apoptosis inhibition and enhancing cell cycle progression are mediated by c-Myc overexpression. On the other hand, prostate cancer (PC) is the most common cancer in men and causes high death. The present review focuses on c-Myc signaling in PC. The c-Myc overexpression is in favor of PC growth and migration. Upon c-Myc inhibition, apoptosis and cell cycle arrest (G0/G1 phase) occur in PC cells. The c-Myc induces glycolysis in enhancing PC growth. Besides, stability and overexpression of c-Myc can mediate resistance of PC cells to chemotherapy and radiotherapy. The inhibition of c-Myc by both anti-tumor agents and genetic tools suppress PC progression. The miRNAs, lncRNAs, circRNAs and other factors such as PI3K/Akt can act as upstream regulator of c-Myc signaling. The c-Myc can function as independent prognostic and diagnostic factor in PC patients. The c-Myc upregulation is associated with reduced overall survival, clinical stage, lymph node metastasis and undesirable prognosis of PC patients. © 2022 Elsevier GmbH
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    Transforming growth factor-beta (TGF-?) in prostate cancer: A dual function mediator?
    (Elsevier B.V., 2022) Mirzaei, S.; Paskeh, M.D.A.; Saghari, Y.; Zarrabi, A.; Hamblin, M.R.; Entezari, M.; Hashemi, M.; Aref, A.R.; Hushmandi, K.; Kumar, A.P.; Rabiee, N.; Ashrafizadeh, M.
    Transforming growth factor-beta (TGF-?) is a member of a family of secreted cytokines with vital biological functions in cells. The abnormal expression of TGF-? signaling is a common finding in pathological conditions, particularly cancer. Prostate cancer (PCa) is one of the leading causes of death among men. Several genetic and epigenetic alterations can result in PCa development, and govern its progression. The present review attempts to shed some light on the role of TGF-? signaling in PCa. TGF-? signaling can either stimulate or inhibit proliferation and viability of PCa cells, depending on the context. The metastasis of PCa cells is increased by TGF-? signaling via induction of EMT and MMPs. Furthermore, TGF-? signaling can induce drug resistance of PCa cells, and can lead to immune evasion via reducing the anti-tumor activity of cytotoxic T cells and stimulating regulatory T cells. Upstream mediators such as microRNAs and lncRNAs, can regulate TGF-? signaling in PCa. Furthermore, some pharmacological compounds such as thymoquinone and valproic acid can suppress TGF-? signaling for PCa therapy. TGF-? over-expression is associated with poor prognosis in PCa patients. Furthermore, TGF-? up-regulation before prostatectomy is associated with recurrence of PCa. Overall, current review discusses role of TGF-? signaling in proliferation, metastasis and therapy response of PCa cells and in order to improve knowledge towards its regulation, upstream mediators of TGF-? such as non-coding RNAs are described. Finally, TGF-? regulation and its clinical application are discussed. © 2022