The Cyclin-dependent kinase (CDK) class of serine/threonine kinases has crucial roles in the regulation of cell cycle transition and is mainly involved in the pathogenesis of cancers. The expression of CDKs is controlled by a complex regulatory network comprised of genetic and epigenetic mechanisms, which are dysregulated during the progression of cancer. The abnormal activation of CDKs results in uncontrolled cancer cell proliferation and the induction of cancer stem cell characteristics. The levels of CDKs can be utilized to predict the prognosis and treatment response of cancer patients, and further understanding of the function and underlying mechanisms of CDKs in human tumors would pave the way for future cancer therapies that effectively target CDKs. Defects in the regulation of cell cycle and mutations in the genes coding cell-cycle regulatory proteins lead to unrestrained proliferation of cells leading to formation of tumors. A number of treatment modalities have been designed to combat dysregulation of cell cycle through affecting expression or activity of CDKs. However, effective application of these methods in the clinical settings requires recognition of the role of CDKs in the progression of each type of cancer, their partners, their interactions with signaling pathways and the effects of suppression of these kinases on malignant features. Thus, we designed this literature search to summarize these findings at cellular level, as well as in vivo and clinical levels.

Fibrosis is the endpoint of pathological remodeling. This process contributes to the pathogenesis of several chronic disorders and aging-associated organ damage. Different molecular cascades contribute to this process. TGF-β, WNT, and YAP/TAZ signaling pathways have prominent roles in this process. A number of long non-coding RNAs and microRNAs have been found to regulate organ fibrosis through modulation of the activity of related signaling pathways. miR-144-3p, miR-451, miR-200b, and miR-328 are among microRNAs that participate in the pathology of cardiac fibrosis. Meanwhile, miR-34a, miR-17-5p, miR-122, miR-146a, and miR-350 contribute to liver fibrosis in different situations. PVT1, MALAT1, GAS5, NRON, PFL, MIAT, HULC, ANRIL, and H19 are among long non-coding RNAs that participate in organ fibrosis. We review the impact of long non-coding RNAs and microRNAs in organ fibrosis and aging-related pathologies.

Recent studies have revealed the impact of microRNAs (miRNAs) in the carcinogenic process. miR-424 is a miRNA whose role in this process is being to be identified. Experiments in the ovarian cancer, cervical cancer, hepatocellular carcinoma, neuroblastoma, breast cancer, osteosarcoma, intrahepatic cholangiocarcinoma, prostate cancer, endometrial cancer, non-small cell lung cancer, hemangioma and gastric cancer have reported down-regulation of miR-424. On the other hand, this miRNA has been found to be up-regulated in melanoma, laryngeal and esophageal squamous cell carcinomas, glioma, multiple myeloma and thyroid cancer. Expression of this miRNA is regulated by methylation status of its promoter. Besides, LINC00641, CCAT2, PVT1, LIN00657, LINC00511 and NNT-AS1 are among lncRNAs that act as molecular sponges for miR-424, thus regulating its expression. Moreover, several members of SNHG family of lncRNAs have been found to regulate expression of miR-424. This miRNA is also involved in the regulation of E2F transcription factors. The current review aims at summarization of the role of miR-424 in the process of cancer evolution and its impact on clinical outcome of patients in order to find appropriate markers for malignancies.

Exosomes are an important group of extracellular vesicles that transfer several kinds of biomolecules and facilitate cell-cell communication. The content of exosomes, particularly the amounts of microRNA (miRNAs) inside these vesicles, demonstrates a disease-specific pattern reflecting pathogenic processes and may be employed as a diagnostic and prognostic marker. miRNAs may enter recipient cells through exosomes and generate a RISC complex that can cause degradation of the target mRNAs or block translation of their corresponding proteins. Therefore, exosome-derived miRNAs constitute an important mechanism of gene regulation in recipient cells. The miRNA content of exosomes can be used as an important tool in the detection of diverse disorders, particularly cancers. This research field has an important situation in cancer diagnosis. In addition, exosomal microRNAs offer a great deal of promise in the treatment of human disorders. However, there are still certain challenges to be resolved. The most important challenges are as follow: the detection of exosomal miRNAs should be standardized, exosomal miRNAs-associated studies should be conducted in large number of clinical samples, and experiment settings and detection criteria should be consistent across different labs. The goal of this article is to present an overview of the effects of exosome-derived microRNAs on a variety of diseases, including gastrointestinal, pulmonary, neurological, and cardiovascular diseases, with a particular emphasis on malignancies.

PTENP1 is a long non-coding RNA which has been regarded as a pseudogene of thePTENtumor suppressor gene. However, it has been shown to be a biologically active transcript that can function as a competing endogenous RNA and enhance expression of PTEN protein. This lncRNA has two transcripts, namely PTENP1-202 and PTENP1-202 with sizes of 3996 and 1215 bps, respectively. PTENP1 acts as a sponge for some PETN-targeting miRNAs, such as miR-17, miR-20a, miR-19b, miR-106b, miR-200c, miR-193a-3p, miR-499-5p and miR-214. Besides, it can affect miR-20a/PDCD4, miR-27a-3p/EGR1, miR-17‐5p/SOCS6 and miR-19b/TSC1 axes. This long non-coding RNA participates in the pathoetiology of several types of cancers as well as non-malignant conditions such as alcohol-induced osteopenia, insulin resistance, osteoporosis, sepsis-associated cardiac dysfunction and spinal cord injury. In the current review, we elucidate the role of PTENP1 in human disorders, particularly malignant conditions based on evidence acquired from cell line assays, animal studies and investigations on human samples.