The role of miRNA-424 and miR-631 in various cancers: Focusing on drug resistance and sensitivity.

BACKGROUND: However, advanced technologies have been developed in the treatment of various cancers, but the mortality rate from cancer is still very high. Drug resistance is a major problem for patients with cancer, which causes the treatment process to fail. In addition to inhibiting drug resistance, targeted therapy is also very important in treatment. MAIN BODY: Nowadays, miRNAs have gained increasing interest as they play a major role in both drug resistance and targeted therapy. MicroRNA (miRNA) is an important part of non-coding RNA that regulates gene expression at a post-transcriptional level. The prevailing studies about miRNA expression have been expanded into a variety of neoplasms. MiR-424 and miR-631 targets genes involved in various cellular processes and can participate in proliferation, differentiation, apoptosis, invasion, angiogenesis, and drug resistance and sensitivity. CONCLUSION: In this study, we focus on the role of miR-424 and miR-631 in many cancer types by displaying the potential target genes associated with each cancer, as well as briefly describing the clinical uses of miR-424 and miR-631 as a diagnostic and predictive tool in malignancies.

Cell cycle involvement in cancer therapy; WEE1 kinase, a potential target as therapeutic strategy.

Mitosis is the process of cell division and is regulated by checkpoints in the cell cycle. G1-S, S, and G2-M are the three main checkpoints that prevent initiation of the next phase of the cell cycle phase until previous phase has completed. DNA damage leads to activation of the G2-M checkpoint, which can trigger a downstream DNA damage response (DDR) pathway to induce cell cycle arrest while the damage is repaired. If the DNA damage cannot be repaired, the replication stress response (RSR) pathway finally leads to cell death by apoptosis, in this case called mitotic catastrophe. Many cancer treatments (chemotherapy and radiotherapy) cause DNA damages based on SSBs (single strand breaks) or DSBs (double strand breaks), which cause cell death through mitotic catastrophe. However, damaged cells can activate WEE1 kinase (as a part of the DDR and RSR pathways), which prevents apoptosis and cell death by inducing cell cycle arrest at G2 phase. Therefore, inhibition of WEE1 kinase could sensitize cancer cells to chemotherapeutic drugs. This review focuses on the role of WEE1 kinase (as a biological macromolecule which has a molecular mass of 96 kDa) in the cell cycle, and its interactions with other regulatory pathways. In addition, we discuss the potential of WEE1 inhibition as a new therapeutic approach in the treatment of various cancers, such as melanoma, breast cancer, pancreatic cancer, cervical cancer, etc.