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Gastric cancer (GC) is the third leading reason of death in men and the fourth in women. Studies have documented an inhibitory function of melatonin on the proliferation, progression and invasion of GC cells. MicroRNAs (miRNAs) are small, non-coding RNAs that play an important function in regulation of biological processes and gene expression of the cells. Some studies reported that melatonin can suppress the progression of GC by regulating the exosomal miRNAs. Thus, melatonin represents a promising potential therapeutic agent for subjects with GC. Herein, we evaluate the existing data of both in vivo and in vitro studies to clarify the molecular processes involved in the therapeutic effects of melatonin in GC. The data emphasize the critical function of melatonin in several signaling ways by which it may inhibit cancer cell proliferation, decrease chemo-resistance, induce apoptosis as well as limit invasion, angiogenesis, and metastasis. This review provides a resource that identifies some of the mechanisms by which melatonin controls GC enlargement. In light of the findings, melatonin should be considered a novel and testable therapeutic mediator for GC treatment.

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Intrauterine growth restriction (IUGR) or intrauterine growth retardation is a condition that the fetus does not grow as expected. And the biometric profile does not match with the age of fetus. This condition is associated with increased mortality and morbidity of the neonates along with increased risk of cardiovascular, lung, and central nervous system damage. Despite close monitoring of high-risk mothers and the development of new therapeutic approaches, the optimal outcome has not been achieved yet that it indicates the importance of investigations on new therapeutic approaches. Melatonin (MLT) is a neurohormone mainly produced by the pineal gland and has a wide range of effects on different organs due to the broad dispersion of its receptors. Moreover, melatonin is produced by the placenta and also its receptors have been found on the surface of this organ. Not only studies showed the importance of this neurohormone on growth and development of fetus but also they proved its highly anti-oxidant properties. As in IUGR the oxidative stress and inflammation increased melatonin could counteract these changes and improved organ's function. In this study, we found that use of MLT could be a good clinical approach for the treatment of IUGR as its high anti-oxidant activity and vasodilation could dampen the mechanisms lead to the IUGR development.

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Combination chemotherapy appears to be a preferable option for some cancer patients, especially when the medications target multiple pathways of oncogenesis; individuals treated with combination treatments may have a better prognosis than those treated with single agent chemotherapy. However, research has revealed that this is not always the case, and that this technique may just enhance toxicity while having little effect on boosting the anticancer effects of the medications. Cisplatin (CDDP) is a chemotherapeutic medicine that is commonly used to treat many forms of cancer. However, it has major adverse effects such as cardiotoxicity, skin necrosis, testicular toxicity, and nephrotoxicity. Many research have been conducted to investigate the effectiveness of melatonin (MLT) as an anticancer medication. MLT operates in a variety of ways, including decreasing cancer cell growth, causing apoptosis, and preventing metastasis. We review the literature on the role of MLT as an adjuvant in CDDP-based chemotherapies and discuss how MLT may enhance CDDP's antitumor effects (e.g., by inducing apoptosis and suppressing metastasis) while protecting other organs from its adverse effects, such as cardio- and nephrotoxicity.

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Different cancer types have been shown to have down-regulated expression levels of miR-195 as an anti-tumor agent. MiR-195 family members can inhibit cancer cell proliferation, angiogenesis, epithelial-mesenchymal transition and metastases, immunosuppression, glycolysis, drug resistance, and cancer stem cell development by targeting the 3'-UTR of the mRNA of different pro-tumor genes. MiR-195 identified as a tumor suppressor miR in a variety of cancers, most notably gynecological malignancies such as cervical, endometrial, and ovarian carcinoma. As a result, restoring miR-195 expression should be regarded as a potential therapy for either prevention or treatment of gynecological cancers. This review will present the most recent data about miR-195-mediated anti-tumor effects in gynecological malignancies, emphasizing its downstream signaling pathways and target genes, as well as prospective treatment techniques.

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Due to their high prevalence, gastrointestinal cancers are one of the key causes of cancer-related death globally. The development of drug-resistant cancer cell populations is a major factor in the high mortality rate, and it affects about half of all cancer patients. Because of advances in our understanding of cancer molecular biology, non-coding RNAs (ncRNAs) have emerged as critical factors in the initiation and development of gastrointestinal cancers. Gene expression can be controlled in several ways by ncRNAs, including through epigenetic changes, interactions between microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) and proteins, and the function of lncRNAs as miRNA precursors or pseudogenes. As lncRNAs may be detected in the blood, circulating ncRNAs have emerged as a promising new class of non-invasive cancer biomarkers for use in the detection, staging, and prognosis of gastrointestinal cancers, as well as in the prediction of therapy efficacy. In this review, we assessed the role lncRNAs play in the progression, and maintenance of colorectal cancer, and how they might be used as therapeutic targets in the future.

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Inflammation is a general term for a wide variety of both physiological and pathophysiological processes in the body which primarily prevents the body from diseases and helps to remove dead tissues. It has a crucial part in the body immune system. Tissue damage can recruit inflammatory cells and cytokines and induce inflammation. Inflammation can be classified as acute, sub-acute, and chronic. If it remained unresolved and lasted for prolonged periods, it would be considered as chronic inflammation (CI), which consequently exacerbates tissue damage in different organs. CI is the main pathophysiological cause of many disorders such as obesity, diabetes, arthritis, myocardial infarction, and cancer. Thus, it is critical to investigate different mechanisms involved in CI to understand its processes and to find proper anti-inflammatory therapeutic approaches for it. Animal models are one of the most useful tools for study about different diseases and mechanisms in the body, and are important in pharmacological studies to find proper treatments. In this study, we discussed the various experimental animal models that have been used to recreate CI which can help us to enhance the understanding of CI mechanisms in human and contribute to the development of potent new therapies.

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Autophagy is known as a conserved self-eating mechanism that contributes to cells to degrade different intracellular components (i.e., macromolecular complexes, aggregated proteins, soluble proteins, organelles, and foreign bodies). Autophagy needs formation of a double-membrane structure, which is composed of the sequestered cytoplasmic contents, called autophagosome. There are a variety of internal and external factors involved in initiation and progression of autophagy process. Viruses as external factors are one of the particles that could be associated with different stages of this process. Viruses exert their functions via activation and/or inhibition of a wide range of cellular and molecular targets, which are involved in autophagy process. Besides viruses, a variety of cellular and molecular pathways that are activated and inhibited by several factors (e.g., genetics, epigenetics, and environment factors) are related to beginning and developing of autophagy mechanism. Exosomes and microRNAs have been emerged as novel and effective players anticipated in various stages of autophagy. More knowledge in these pathways and identification of accurate roles of them could help to provide better therapeutic approaches in several diseases such as cancer. We highlighted the roles of viruses, exosomes, and microRNAs in the autophagy processes.

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A wide range of microRNAs (miRNAs) are coded for in the human genome and contribute to the regulation of gene expression. MiRNAs are able to degrade mRNAs and/or prevent the RNA transcript from being translated through complementary binding of the miRNA seed region (nucleotide 2-8) to the 3'-untranslated regions of many mRNAs. Although miRNAs are involved in almost all processes of normal human cells, they are also involved in the abnormal functions of cancer cells. MiRNAs can play dual regulatory roles in cancer, acting either as tumor suppressors or as tumor promoters, depending on the target, tumor type, and stage. In the current review, we discuss the present status of miRNA modulation in the setting of lysophosphatidic acid (LPA) signaling. LPA is produced from lysophosphatidylcholine by the enzyme autotaxin and signals via a range of G protein-coupled receptors to affect cellular processes, which ultimately causes changes in cell morphology, survival, proliferation, differentiation, migration, and adhesion. Several studies have identified miRNAs that are over-expressed in response to stimulation by LPA, but their functional roles have not yet been fully clarified. Since RNA-based treatments hold tremendous promise in the area of personalized medicne, many efforts have been made to bring miRNAs into clinical trials, and this field is evolving at an increasing pace.