No abstract

In addition to aberrant alternation of transcriptome, it is now suggested that dysregulation of the non-coding transcripts, particularly long non-coding RNAs (lncRNAs), which comprise the majority of the genome, is contributed to cancer initiation and progression. As the result of recent huge efforts, the possible roles of numerous lncRNAs in the human cancers were characterized, as well as various strategies with inhibitory effects to target these transcripts on the transformed cells. Moreover, DNA damage response (DDR) pathway is a complex regulatory network responsible for the identification of disruptions in DNA structure, integrity and stability-it is reported to be associated with the upregulation and down-regulation of lncRNAs. This review explores the involvement of the various lncRNAs in different human cancers, afterwards discusses the association of the lncRNAs expression with the DDR and oxidative stress, which are implicated in a myriad pathophysiological and physiological intra-and extracellular damages.

Breast cancer is one of the most lethal malignancies in women in the world. Various factors are involved in the development and promotion of the malignancy; most of them involve changes in the expression of certain genes, such as microRNAs (miRNAs). MiRNAs can regulate signaling pathways negatively or positively, thereby affecting tumorigenesis and various aspects of cancer progression, particularly breast cancer. Besides, accumulating data demonstrated that miRNAs are a novel tool for prognosis and diagnosis of breast cancer patients. Herein, we will review the roles of these RNA molecules in several important signaling pathways, such as transforming growth factor, Wnt, Notch, nuclear factor‐κ B, phosphoinositide‐3‐kinase/Akt, and extracellular‐signal‐regulated kinase/mitogen activated protein kinase signaling pathways in breast cancer.

Different factors influence the development and control of ageing. It is well known that progressive telomere shorting is one of the molecular mechanisms underlying ageing. The shelterin complex consists of six telomere-specific proteins which are involved in the protection of chromosome ends. More particularly, this vital complex protects the telomeres from degradation, prevents from activation of unwanted repair systems, regulates the activity of telomerase, and has a crucial role in cellular senescent and ageing-related pathologies. This review explores the organization and function of telomeric DNA along with the mechanism of telomeres during ageing, followed by a discussion of the critical role of shelterin components and their changes during ageing.

DNA damage response (DDR) is a regulatory system responsible for maintaining genome integrity and stability, which can sense and transduce DNA damage signals. The severity of damage appears to determine DDRs, which can include damage repair, cell‐cycle arrest, and apoptosis. Furthermore, defective components in DNA damage and repair machinery are an underlying cause for the development and progression of various types of cancers. Increasing evidence indicates that there is an association between trace elements and DDR/repair mechanisms. In fact, trace elements seem to affect mediators of DDR. Besides, it has been revealed that oxidative stress (OS) and trace elements are associated with cancer development. In this review, we discuss the role of some critical trace elements in the risk of cancer. In addition, we provide a brief introduction on DDR and OS in cancer. Finally, we will further review the interactions between some important trace elements including selenium, zinc, chromium, cadmium, and arsenic, and DDR, and OS in cancer.