Ovarian cancer is known as a serious malignancy that affects women’s reproductive tract and can considerably threat their health. A wide range of molecular mechanisms and genetic modifications have been involved in ovarian cancer pathogenesis making it difficult to develop effective therapeutic platforms. Hence, discovery and developing new therapeutic approaches are required. Medicinal plants, as a new source of drugs, could potentially be used alone or in combination with other medicines in the treatment of various cancers such as ovarian cancer. Among various natural compounds, quercetin has shown great anti-cancer and anti-inflammatory properties. In vitro and in vivo experiments have revealed that quercetin possesses a cytotoxic impact on ovarian cancer cells. Despite obtaining good results both in vitro and in vivo, few clinical studies have assessed the anti-cancer effects of quercetin particularly in the ovarian cancer. Therefore, it seems that further clinical studies may introduce quercetin as therapeutic agent alone or in combination with other chemotherapy drugs to the clinical setting. Here, we not only summarize the anti-cancer effects of quercetin but also highlight the therapeutic effects of quercetin in the ovarian cancer.
Circular RNAs (circRNAs) are a class of long non-coding RNAs (lncRNAs) which have a circular and closed loop structure. They are ubiquitous, stable, conserved and diverse RNA molecules with a range of activities such as translation and splicing regulation, which are able to interacting with RNA-binding proteins and specially miRNA sponge. The expression patterns of the circRNAs exhibited tissue specificity and also, step and stage specificity. Accumulating evidences approved the critical role of circular RNAs in many cancers such as ovarian cancer. Given that these molecules exert their effects through multiple cellular and molecular mechanisms (i.e., angiogenesis, apoptosis, growth, and metastasis) which are involved in cancer pathogenesis, circular RNAs, in particular, act by controlling cell proliferation in ovarian cancer, so that, it has been shown that the deregulation of these molecules is associated with initiation and progression of ovarian cancer. Therefore, they are attractive molecules which have introduced them as cancer biomarkers. Moreover, they could be used as new therapeutic candidates for developing novel treatment strategies. Here, for first time, we have provided a comprehensive review on the recent knowledge of circular RNAs and their pathological roles in the ovarian cancer.
: Long noncoding RNAs (lncRNAs) constitute large portions of the mammalian transcriptome which appeared as a fundamental player, regulating various cellular mechanisms. LncRNAs do not encode proteins, have mRNA-like transcripts and frequently processed similar to the mRNAs. Many investigations have determined that lncRNAs interact with DNA, RNA molecules or proteins and play a significant regulatory function in several biological processes, such as genomic imprinting, epigenetic regulation, cell cycle regulation, apoptosis, and differentiation. LncRNAs can modulate gene expression on three levels: chromatin remodeling, transcription, and post-transcriptional processing. The majority of the identified lncRNAs seem to be transcribed by the RNA polymerase II. Recent evidence has illustrated that dysregulation of lncRNAs can lead to many human diseases, in particular, cancer. The aberrant expression of lncRNAs in malignancies contributes to the dysregulation of proliferation and differentiation process. Consequently, lncRNAs can be useful to the diagnosis, treatment, and prognosis, and have been characterized as potential cancer markers as well. In this review, we highlighted the role and molecular mechanisms of lncRNAs and their correlation with some of the cancers.
Precursor B-cell acute lymphoblastic leukemia (B-ALL) is the most prevalent pediatric cancer. DNA methylation and changes in the microRNAs (miRNAs) expression are known to be important causes of B-ALL. Decitabine as a DNA methyltransferase inhibitor agent is able to induce hypomethylation in several tumor suppressor genes. Much evidence has proven BTG2, PPP1CA, and PTEN act as tumor suppressor genes in many malignancies. In this case control study, the messenger RNA (mRNA) expression of PPP1CA, BTG2, and PTEN genes using quantitative real-time polymerase chain reaction (rRT-PCR) in Nalm6 cell line and five patients suffer from ALL with mean age 5.6 years were determined in compare with seven normal healthy donors age and sex matched. qRT-PCR analysis revealed that the expression levels of PPP1CA, BTG2, and PTEN genes were significantly decreased in Nalm6 ([FC] = 0.46, [FC] = 0.046, [FC] = 0.54) and according to the Methylation-specific PCR (MSP) analysis, these genes were hypermethylated in Nalm6. In next step, the effects of decitabine treatment on the methylation and expression of these genes in association with changes in miR-125b, miR-17, and miR-181b expression levels were evaluated in optimal concentration 2.5 µM of decitabine. Our data showed that decitabine is able to restore the expression levels of aforementioned genes and downregulate expression levels of oncomiRs; including miR-125b, miR-17, and miR-181b in Nalm6 cell line. Therefore, it seems that decitabine can be used as a potential drug for the first line treatment of patients with B-ALL, but further in vivo investigation is necessary. K E Y W O R D S B-ALL, decitabine, DNA methylation, microRNA, NALM6 J Cell Biochem. 2019;120:13156-13167. wileyonlinelibrary.com/journal/jcb 13156 |
Background: Breast cancer is the most prevalent type of cancer among the female population, and about 15% to 20% of patients with breast cancer is human epidermal growth factor receptor 2 (HER2)-positive. The current cancer treatment methods such as surgery, radiation, and chemotherapy are not sufficiently effective in decreasing mortality rates; however, immunotherapy is a novel approach in the treatment of cancer that is more efficient and less harmful to the body. Anti-cancer immunotoxins are chimeric molecules containing two parts, namely the immuno part, which is an antibody or a binding segment of antibody, and toxin part, which is a killer toxin molecule. Objectives: In this study, we sought to design a novel immunotoxin, including the anti-HER2 receptor, trastuzumab, derived from a single-chain variable fragment (scFv) with a connection to the functional part of Campylobacter jejuni cytolethal distending toxin (Cj-CdtB). Methods: The chimeric protein's physicochemical properties, solubility, and secondary structure were analyzed, using ProtParam, PROSO II, and GORV, respectively. A three-dimensional (3D) model was built, using I-TASSER and refined, using GalaxyRefine. The model's structure was evaluated before and after refinement, using PROCHECK and RAMPAGE. The AlgPred server was employed to predict immunotoxin allergenicity, and mRNA stability was evaluated by RNAfold. Finally, the immunotoxin and HER2 were docked, using ZDOCK. Results: Analysis showed that the chimeric protein could be a stable and soluble protein and the secondary structure of its parts would not change and the protein had a robust 3D structure that might have a stable mRNA structure and could bind to HER2 receptor. Conclusions: The designed immunotoxin was a stable and soluble protein with the ability to bind to HER2 receptors, making it an appropriate immunotoxin candidate for breast cancer treatment. The results of the current work could be useful for future experimental studies.
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