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    Cervical cancer progression is regulated by SOX transcription factors: Revealing signaling networks and therapeutic strategies
    (Elsevier Science, 2021) Paskeh, Mahshid Deldar Abad; Mirzaei, Sepideh; Gholami, Mohammad Hossein; Zarrabi, Ali; Zabolian, Amirhossein; Hashemi, Mehrdad; Hushmandi, Kiavash
    Cervical cancer is the fourth common gynecologic cancer and is considered as second leading cause of death among women. Various strategies are applied in treatment of cervical cancer including radiotherapy, chemotherapy and surgery. However, cervical cancer cells demonstrate aggressive behavior in advanced phases, requiring novel strategies in their elimination. On the other hand, SOX proteins are transcription factors capable of regulating different molecular pathways and their expression varies during embryogenesis, disease development and carcinogenesis. In the present review, our aim is to reveal role of SOX transcription factors in cervical cancer. SOX transcription factors play like a double-edged sword in cancer. For instance, SOX9 possesses both tumor-suppressor and tumor-promoting role in cervical cancer. Therefore, exact role of each SOX members in cervical cancer has been discussed to direct further experiments for revealing other functions. SOX proteins can regulate proliferation and metastasis of cervical cancer cells. Furthermore, response of cervical cancer cells to chemotherapy and radiotherapy is tightly regulated by SOX transcription factors. Different downstream targets of SOX proteins such as Wnt signaling, EMT and Hedgehog have been identified. Besides, upstream mediators such as microRNAs, lncRNAs and circRNAs can regulate SOX expression in cervical cancer. In addition to pre-clinical studies, role of SOX transcription factors as prognostic and diagnostic tools in cervical cancer has been shown.
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    Emerging role of exosomes in cancer progression and tumor microenvironment remodeling
    (BioMed Central, 2022) Paskeh, Mahshid Deldar Abad; Entezari, Maliheh; Mirzaei, Sepideh; Zabolian, Amirhossein; Zarrabi, Ali
    Cancer is one of the leading causes of death worldwide, and the factors responsible for its progression need to be elucidated. Exosomes are structures with an average size of 100 nm that can transport proteins, lipids, and nucleic acids. This review focuses on the role of exosomes in cancer progression and therapy. We discuss how exosomes are able to modulate components of the tumor microenvironment and influence proliferation and migration rates of cancer cells. We also highlight that, depending on their cargo, exosomes can suppress or promote tumor cell progression and can enhance or reduce cancer cell response to radio- and chemo-therapies. In addition, we describe how exosomes can trigger chronic inflammation and lead to immune evasion and tumor progression by focusing on their ability to transfer non-coding RNAs between cells and modulate other molecular signaling pathways such as PTEN and PI3K/Akt in cancer. Subsequently, we discuss the use of exosomes as carriers of anti-tumor agents and genetic tools to control cancer progression. We then discuss the role of tumor-derived exosomes in carcinogenesis. Finally, we devote a section to the study of exosomes as diagnostic and prognostic tools in clinical courses that is important for the treatment of cancer patients. This review provides a comprehensive understanding of the role of exosomes in cancer therapy, focusing on their therapeutic value in cancer progression and remodeling of the tumor microenvironment. Graphical Abstract: [Figure not available: see fulltext.]. © 2022, The Author(s).
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    EZH2 as a new therapeutic target in brain tumors: Molecular landscape, therapeutic targeting and future prospects
    (Elsevier, 2022) Paskeh, Mahshid Deldar Abad; Mehrabi, Atefeh; Gholami, Mohammad Hossein; Zabolian, Amirhossein; Ranjbar, Ehsan; Zarrabi, Ali
    Brain tumors are responsible for high mortality and morbidity worldwide. The brain tumor treatment depends on identification of molecular pathways involved in progression and malignancy. Enhancer of zeste homolog 2 (EZH2) has obtained much attention in recent years in field of cancer therapy due to its aberrant expression and capacity in modulating expression of genes by binding to their promoter and affecting methylation status. The present review focuses on EZH2 signaling in brain tumors including glioma, glioblastoma, astrocytoma, ependymomas, medulloblastoma and brain rhabdoid tumors. EZH2 signaling mainly participates in increasing proliferation and invasion of cancer cells. However, in medulloblastoma, EZH2 demonstrates tumor-suppressor activity. Furthermore, EZH2 can regulate response of brain tumors to chemotherapy and radiotherapy. Various molecular pathways can function as upstream mediators of EZH2 in brain tumors including lncRNAs and miRNAs. Owing to its enzymatic activity, EZH2 can bind to promoter of target genes to induce methylation and affects their expression. EZH2 can be considered as an independent prognostic factor in brain tumors that its upregulation provides undesirable prognosis. Both anti-tumor agents and gene therapies such as siRNA have been developed for targeting EZH2 in cancer therapy.
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    Nanoliposomes as nonviral vectors in cancer gene therapy
    (John Wiley and Sons Inc, 2024) Yıldız, Safiye Nur; Entezari, Maliheh; Paskeh, Mahshid Deldar Abad; Mirzaei, Sepideh; Kalbasi, Alireza; Zabolian, Amirhossein; Hashemi, Farid; Hushmandi, Kiavash; Hashemi, Mehrdad; Raei, Mehdi; Goharrizi, Mohammad Ali Sheikh Beig; Aref, Amir Reza; Zarrabi, Ali; Ren, Jun; Orive, Gorka; Rabiee, Navid; Ertaş, Yavuz Nuri
    Nonviral vectors, such as liposomes, offer potential for targeted gene delivery in cancer therapy. Liposomes, composed of phospholipid vesicles, have demonstrated efficacy as nanocarriers for genetic tools, addressing the limitations of off-targeting and degradation commonly associated with traditional gene therapy approaches. Due to their biocompatibility, stability, and tunable physicochemical properties, they offer potential in overcoming the challenges associated with gene therapy, such as low transfection efficiency and poor stability in biological fluids. Despite these advancements, there remains a gap in understanding the optimal utilization of nanoliposomes for enhanced gene delivery in cancer treatment. This review delves into the present state of nanoliposomes as carriers for genetic tools in cancer therapy, sheds light on their potential to safeguard genetic payloads and facilitate cell internalization alongside the evolution of smart nanocarriers for targeted delivery. The challenges linked to their biocompatibility and the factors that restrict their effectiveness in gene delivery are also discussed along with exploring the potential of nanoliposomes in cancer gene therapy strategies by analyzing recent advancements and offering future directions. © 2024 The Author(s). MedComm published by Sichuan International Medical Exchange & Promotion Association (SCIMEA) and John Wiley & Sons Australia, Ltd.
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    Targeted regulation of autophagy using nanoparticles: New insight into cancer therapy
    (Elsevier, 2022) Paskeh, Mahshid Deldar Abad; Entezari, Maliheh; Clark, Courtney; Zabolian, Amirhossein; Ranjbar, Ehsan; Zarrabi, Ali
    Normal cells depend on autophagy to maintain cellular homeostasis by recycling damaged organelles and misfolded proteins and degrading toxic agents. Similar to apoptosis, targeting autophagy has been under attention in cancer therapy. However, autophagy has both pro-survival and pro-death functions in tumors, and its targeting requires further elucidation. The current review focuses on using nanoparticles for targeting autophagy in cancer treatment. Nanocarriers can deliver autophagy regulators along with chemotherapeutic agents leading to intracellular accumulation in cancer cells and synergistic cancer therapy. Furthermore, genetic tools such as siRNA and shRNA can be used for targeting molecular components that regulate autophagy, such as the ATG12-ATG5-ATG16L1 complex. A number of nanostructures, such as gold and zinc oxide nanoparticles, can be used to enhance oxidative stress-mediated apoptosis and autophagy, reducing cancer progression. Further, using nanoparticles to modulate autophagy potentiates the anti-tumor effects of cisplatin and gefitinib during chemotherapy. Polymeric nanoparticles, lipid-based nanostructures and carbon-based nanomaterials are among other nanoparticles capable of regulating autophagy in cancer cells. Of note, various regulatory components of autophagy such as ATGs, Beclin-1 and LC3-II can be affected by nanomaterials. Based on the role of nanomaterial-induced autophagy as pro-survival or pro-death, further targeting can potentiate the fight against cancer cells. © 2021 Elsevier B.V.
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    Targeting AMPK signaling in ischemic/reperfusion injury: From molecular mechanism to pharmacological interventions
    (2022) Paskeh, Mahshid Deldar Abad; Asadi, Ava; Mirzaei, Sepideh; Hashemi, Mehrdad; Entezari, Maliheh; Raesi, Rasoul; Hushmandi, Kiavash; Zarrabi, Ali; Ertas, Yavuz Nuri; Aref, Amir Reza; Samarghandian, Saeed; Reiter, Russel J; Ren, Jun
    Ischemia is a pathological process in which blood supply to a particular organ is temporarily interrupted resulting in disturbed biological function and homeostasis of local tissues. Following ischemia, reperfusion and reoxygenation may occur which further worsens oxidative stress-mediated damage in cells and tissues. The combined processes are referred to as ischemia/reperfusion (I/R) injury. Immediate management and treatment of I/R is of utmost importance for preventing irreversible and extensive cellular damage. Apoptosis, inflammation and oxidative stress are the most validated pathologies associated with I/R. AMP-activated protein kinase (AMPK) modulates energy metabolism in cells and its activation occurs in response to elevated AMP and ADP levels. Aberrant levels of AMPK are noted in various pathological settings such as diabetes mellitus, cancer and neurological diseases. This review emphasizes AMPK signaling, its related molecular pathways and therapeutic utility during I/R. Activation of AMPK through phosphorylation prevents apoptosis and reduces oxidative stress and inflammation upon I/R. Inducing AMPK signaling normalizes mitochondrial function to inhibit cell death. Autophagy as a cytoprotective mechanism undergoes activation by AMPK/mTOR and AMPK/ULK1 pathways. AMPK reinforces the antioxidant defense capacity via Nrf2 signaling to counteract oxidative stress in I/R. Protective compounds including phytochemicals activate AMPK to alleviate I/R injury.
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    Targeting cancer stem cells by dietary agents: an important therapeutic strategy against human malignancies
    (MDPI, 2021) Paskeh, Mahshid Deldar Abad; Asadi, Shafagh; Zabolian, Amirhossein; Saleki, Hossein; Khoshbakht, Mohammad Amin; Zarrabi, Ali
    As a multifactorial disease, treatment of cancer depends on understanding unique mechanisms involved in its progression. The cancer stem cells (CSCs) are responsible for tumor stemness and by enhancing colony formation, proliferation as well as metastasis, and these cells can also mediate resistance to therapy. Furthermore, the presence of CSCs leads to cancer recurrence and therefore their complete eradication can have immense therapeutic benefits. The present review focuses on targeting CSCs by natural products in cancer therapy. The growth and colony formation capacities of CSCs have been reported can be attenuated by the dietary agents. These compounds can induce apoptosis in CSCs and reduce tumor migration and invasion via EMT inhibition. A variety of molecular pathways including STAT3, Wnt/?-catenin, Sonic Hedgehog, Gli1 and NF-?B undergo down-regulation by dietary agents in suppressing CSC features. Upon exposure to natural agents, a significant decrease occurs in levels of CSC markers including CD44, CD133, ALDH1, Oct4 and Nanog to impair cancer stemness. Furthermore, CSC suppression by dietary agents can enhance sensitivity of tumors to chemotherapy and radiotherapy. In addition to in vitro studies, as well as experiments on the different preclinical models have shown capacity of natural products in suppressing cancer stemness. Furthermore, use of nanostructures for improving therapeutic impact of dietary agents is recommended to rapidly translate preclinical findings for clinical use. © 2021 by the authors. Licensee MDPI, Basel, Switzerland.