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Background: Lung cancer has the first place among cancer-related deaths worldwide and demands novel strategies in the treatment of this life-threatening disorder. The aim of this review is to explore the regulation of epithelial-to-mesenchymal transition (EMT) by long non-coding RNAs (lncRNAs) in lung cancer. Introduction: LncRNAs can be considered as potential factors for targeting in cancer therapy, since they regulate a bunch of biological processes, e.g. cell proliferation, differentiation and apoptosis. The abnormal expression of lncRNAs occurs in different cancer cells. On the other hand, epithelial-to-mesenchymal transition (EMT) is a critical mechanism participating in migration and metastasis of cancer cells. Method: Different databases, including Google Scholar, Pubmed and Science direct, were searched for collecting articles using keywords such as “LncRNA”, “EMT”, and “Lung cancer”. Results: There are tumor-suppressing lncRNAs that can suppress EMT and metastasis of lung cancer cells. Expression of such lncRNAs undergoes down-regulation in lung cancer progression and restoring their expression is of importance in suppressing lung cancer migration. There are tumor- promoting lncRNAs triggering EMT in lung cancer and enhancing their migration. Conclusion: LncRNAs are potential regulators of EMT in lung cancer, and targeting them, both pharmacologically and genetically, can be of importance in controlling the migration of lung cancer cells.

Brain tumors are responsible for high morbidity and mortality worldwide. Several factors such as the presence of blood-brain barrier (BBB), sensitive location in the brain, and unique biological features challenge the treatment of brain tumors. The conventional drugs are no longer effective in the treatment of brain tumors, and scientists are trying to find novel therapeutics for brain tumors. In this way, identification of molecular pathways can facilitate finding an effective treatment. c-Myc is an oncogene signaling pathway capable of regulation of biological processes such as apoptotic cell death, proliferation, survival, differentiation, and so on. These pleiotropic effects of c-Myc have resulted in much fascination with its role in different cancers, particularly brain tumors. In the present review, we aim to demonstrate the upstream and down-stream mediators of c-Myc in brain tumors such as glioma, glioblastoma, astrocytoma, and medulloblastoma. The capacity of c-Myc as a prognostic factor in brain tumors will be investigated. Our goal is to define an axis in which the c-Myc signaling pathway plays a crucial role and to provide direction for therapeutic targeting in these signaling networks in brain tumors.

Prostate cancer (PCa) is one of the leading causes of death worldwide. A variety of strategies, including surgery, chemotherapy, radiotherapy, and immunotherapy, are applied for PCa treatment. PCa cells are responsive towards therapy at early stages, but they can obtain resistance in the advanced stage. Furthermore, their migratory ability is high in advanced stages. It seems that genetic and epigenetic factors play an important role in this case. Zinc finger E-box-binding homeobox (ZEB) is a family of transcription with two key members, including ZEB1 and ZEB2. ZEB family members are known due to their involvement in promoting cancer metastasis via EMT induction. Recent studies have shown their role in cancer proliferation and inducing therapy resistance. In the current review, we focus on revealing the role of ZEB1 and ZEB2 in PCa. ZEB family members are able to significantly promote the proliferation and viability of cancer cells. ZEB1 and ZEB2 enhance migration and invasion of PCa cells via EMT induction. Overexpression of ZEB1 and ZEB2 is associated with a poor prognosis of PCa. ZEB1 and ZEB2 upregulation occurs during PCa progression and can provide therapy resistance to cancer cells. PRMT1, Smad2, and non-coding RNAs can function as upstream mediators of the ZEB family. Besides, Bax, Bcl-2, MRP1, Ncadherin, and E-cadherin can be considered as downstream targets of the ZEB family in PCa.