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Öğe Long non-coding RNAs and exosomal incRNAs: Potential functions in lung cancer progression, drug resistance and tumor microenvironment remodeling(Elsevier Science, 2022) Entezari, Maliheh; Ghanbarirad, Maryam; Taheriazam, Afshin; Sadrkhanloo, Mehrdokht; Zabolian, Amirhossein; Shekhi Beig Goharrizi, Mohammad Ali; Hushmandi, Kiavash; Aref, Amir Reza; Ashrafizadeh, Milad; Zarrabi, Ali; Nabavi, Noushin; Rabiee, Navid; Hashemi, Mehrdad; Samarghandian, SaeedAmong the different kinds of tumors threatening human life, lung cancer is one that is commonly observed in both males and females. The aggressive behavior of lung cancer and interactions occurring in tumor microenvironment enhances the malignancy of this tumor. The lung tumor cells have demonstrated capacity in developing chemo- and radio-resistance. LncRNAs are a category of non-coding RNAs that do not encode proteins, but their aberrant expression is responsible for tumor development, especially lung cancer. In the present review, we focus on both lncRNAs and exosomal lncRNAs in lung cancer, and their ability in regulating proliferation and metastasis. Cell cycle progression and molecular mechanisms related to lung cancer metastasis such as EMT and MMPs are regulated by lncRNAs. LncRNAs interact with miRNAs, STAT, Wnt, EZH2, PTEN and PI3K/Akt signaling pathways to affect progression of lung cancer cells. LncRNAs demonstrate both tumor-suppressor and tumor-promoting functions in lung cancer. They can be considered as biomarkers in lung cancer and especially exosomal lncRNAs present in body fluids are potential tools for minimally invasive diagnosis. Furthermore, weÖğe Long non-coding RNAs and exosomal lncRNAs: Potential functions in lung cancer progression, drug resistance and tumor microenvironment remodeling(Elsevier, 2022) Entezari, Maliheh; Ghanbarirad, Maryam; Taheriazam, Afshin; Sadrkhanloo, Mehrdokht; Zabolian, Amirhossein; Goharrizi, Mohammad Ali Shekhi Beig; Hushmandi, Kiavash; Aref, Amir Reza; Ashrafizadeh, Milad; Zarrabi, Ali; Nabavi, Noushin; Rabiee, Navid; Hashemi, Mehrdad; Samarghandian, SaeedAmong the different kinds of tumors threatening human life, lung cancer is one that is commonly observed in both males and females. The aggressive behavior of lung cancer and interactions occurring in tumor microenvironment enhances the malignancy of this tumor. The lung tumor cells have demonstrated capacity in developing chemo- and radio-resistance. LncRNAs are a category of non-coding RNAs that do not encode proteins, but their aberrant expression is responsible for tumor development, especially lung cancer. In the present review, we focus on both lncRNAs and exosomal lncRNAs in lung cancer, and their ability in regulating proliferation and metastasis. Cell cycle progression and molecular mechanisms related to lung cancer metastasis such as EMT and MMPs are regulated by lncRNAs. LncRNAs interact with miRNAs, STAT, Wnt, EZH2, PTEN and PI3K/Akt signaling pathways to affect progression of lung cancer cells. LncRNAs demonstrate both tumor-suppressor and tumor-promoting functions in lung cancer. They can be considered as biomarkers in lung cancer and especially exosomal lncRNAs present in body fluids are potential tools for minimally invasive diagnosis. Furthermore, we discuss regulation of lncRNAs by anti-cancer drugs and genetic tools as well as the role of these factors in therapy response of lung cancer cells.Öğe Non-coding RNAs and macrophage interaction in tumor progression(Elsevier Ireland Ltd, 2022) Entezari, Maliheh; Sadrkhanloo, Mehrdokht; Rashidi, Mohsen; Asnaf, Sholeh Etehad; Taheriazam, Afshin; Hashemi, Mehrdad; Ashrafizadeh, Milad; Zarrabi, Ali; Rabiee, Navid; Hushmandi, Kiavash; Mirzaei, Sepideh; Sethi, GautamThe macrophages are abundantly found in TME and their M2 polarization is in favor of tumor malignancy. On the other hand, non-coding RNAs (ncRNAs) can modulate macrophage polarization in TME to affect cancer progression. The miRNAs can dually induce/suppress M2 polarization of macrophages and by affecting various molecular pathways, they modulate tumor progression and therapy response. The lncRNAs can affect miRNAs via sponging and other molecular pathways to modulate macrophage polarization. A few experiments have also examined role of circRNAs in targeting signaling networks and affecting macrophages. The therapeutic targeting of these ncRNAs can mediate TME remodeling and affect macrophage polarization. Furthermore, exosomal ncRNAs derived from tumor cells or macrophages can modulate polarization and TME remodeling. Suppressing biogenesis and secretion of exosomes can inhibit ncRNA-mediated M2 polarization of macrophages and prevent tumor progression. The ncRNAs, especially exosomal ncRNAs can be considered as non-invasive biomarkers for tumor diagnosis. © 2022 Elsevier B.V.Öğe Targeting Nrf2 in ischemia-reperfusion alleviation: From signaling networks to therapeutic targeting(Elsevier Inc., 2022) Sadrkhanloo, Mehrdokht; Entezari, Maliheh; Orouei, Sima; Zabolian, Amirhossein; Mirzaie, Amirreza; Maghsoudloo, Amin; Raesi, Rasoul; Asadi, Neda; Hashemi, Mehrdad; Zarrabi, Ali; Khan, Haroon; Mirzaei, Sepideh; Samarghandian, SaeedThe nuclear factor erythroid 2-related factor 2 (Nrf2) is a master regulator of redox balance and it responds to various cell stresses that oxidative stress is the most well-known one. The Nrf2 should undergo nuclear translocation to exert its protective impacts and decrease ROS production. On the other hand, ischemic/reperfusion (I/R) injury is a pathological event resulting from low blood flow to an organ and followed by reperfusion. The I/R induces cell injury and organ dysfunction. The present review focuses on Nrf2 function in alleviation of I/R injury. Stimulating of Nrf2 signaling ameliorates I/R injury in various organs including lung, liver, brain, testis and heart. The Nrf2 enhances activity of antioxidant enzymes to reduce ROS production and prevent oxidative stress-mediated cell death. Besides, Nrf2 reduces inflammation via decreasing levels of pro-inflammatory factors including IL-6, IL-1? and TNF-?. Nrf2 signaling is beneficial in preventing apoptosis and increasing cell viability. Nrf2 induces autophagy to prevent apoptosis during I/R injury. Furthermore, it can interact with other molecular pathways including PI3K/Akt, NF-?B, miRNAs, lncRNAs and GSK-3? among others, to ameliorate I/R injury. The therapeutic agents, most of them are phytochemicals such as resveratrol, berberine and curcumin, induce Nrf2 signaling in I/R injury alleviation. © 2022
