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The clustered regularly interspaced short palindromic repeats system, called CRISPR, as one of the major technological advances, allows geneticists and researchers to perform genome editing. This remarkable technology is quickly eclipsing zinc-finger nucleases (ZFNs) and other editing tools, and its ease of use and accuracy have thus far revolutionized genome editing, from fundamental science projects to medical research and treatment options. This system consists of two key components: a CRISPR-associated (Cas) nuclease, which binds and cuts deoxyribonucleic acid (DNA) and a guide ribonucleic acid (gRNA) sequence, directing the Cas nuclease to its target site. In the research arena, CRISPR has been up to now exploited in various ways alongside gene editing, such as epigenome modifications, genome-wide screening, targeted cancer therapies, and so on. This article reviews the current perceptions of the CRISPR/Cas systems with special attention to studies reflecting on the relationship between the CRISPR/Cas systems and their role in cancer therapy., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Today, there is a growing interest nowadays in the use of herbal substances as cancer therapeutic agents. Over recent years, Xanthohumol (XTL) has been brought out as a prenylated chalcone that is found in hops (Humulus lupulus) and beer. XTL is being investigated for its potential properties, and it has been found to have various biological effects, including anti-microbial, anti-viral, and immunomodulatory. Other than these biological effects, it has also been found that XTL exerts anti-tumor effects. In the beginning, XTL, by modulating cell signaling pathways, including ERK, AKT, NF-κB, AMPK, Wnt/β-catenin, and Notch signaling in cancer cells, inhibits tumor cell functions. Moreover, XTL, by inducing apoptotic pathways, either intrinsic or extrinsic, promotes cancer cell death and arrests the cell cycle. Furthermore, XTL inhibits metastasis, angiogenesis, cancer stemness, drug resistance, cell respiration, etc., which results in tumor aggressiveness inhibition. XTL has low solubility in water, and it has been hypothesized that some modifications, including biotinylation, can improve its pharmacogenetic characteristics. Additionally, XTL derivates such as dihydroXTL and tetrahydroXTL can be helpful for more anti-tumor activities. Using XTL with other anti-tumor agents is another approach to overcome tumor cell resistance. XTL or its derivatives, it is believed, might provide novel chemotherapeutic methods in future cancer therapy., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

Today, herbal-derived compounds are being increasingly studied in cancer treatment. Over the past decade, Arctigenin has been introduced as a bioactive dibenzylbutyrolactone lignan which is found in Chinese herbal medicines. In addition to anti-microbial, anti-inflammatory, immune-modulatory functions, Arctigenin has attracted growing attention due to its anti-tumor capabilities. It has been shown that Arctigenin can induce apoptosis and necrosis and abolish drug resistance in tumor cells by inducing apoptotic signaling pathways, caspases, cell cycle arrest, and the modulating proteasome. Moreover, Arctigenin mediates other anti-tumor functions through several mechanisms. It has been demonstrated that Arctigenin can act as an anti-inflammatory compound to inhibit inflammation in the tumor microenvironment. It also downregulates factors involved in tumor metastasis and angiogenesis, such as matrix metalloproteinases, N-cadherin, TGF-β, and VEGF. Additionally, Arctigenin, through modulation of MAPK signaling pathways and stress-related proteins, is able to abolish tumor cell growth in nutrient-deprived conditions. Due to the limited solubility of Arctigenin in water, it is suggested that modification of this compound through amino acid esterification can improve its pharmacogenetic properties. Collectively, it is hoped that using Arctigenin or its derivates might introduce new chemotherapeutic approaches in future treatment., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Cancer is one of the healthcare problems that affect many communities around the world. Many factors contribute to cancer development. Besides, these factors are counted as the main impediment in cancer immunotherapy. Myeloid-derived suppressor cells (MDSCs) are one of these impediments. MDSCs inhibit the immune responses through various mechanisms such as inhibitory cytokine release and nitric oxide metabolite production. Several factors are involved in forming these cells, including tumor secreted cytokine and chemokines, transcription factors, and non-coding RNA. In the meantime, micro-RNAs (miRNAs) and long non-coding RNAs (lncRNAs) are the vital gene regulatory elements that affect gene expression. In this study, we are going to discuss the role of miRNAs and lncRNAs in MDSCs development in a cancer situation. It is hoped that miRNA and lncRNAs targeting may prevent the growth and development of these inhibitory cells in the cancer environment., Competing Interests: Declaration of competing interest The authors state that the research was carried out in the absence of any potential conflict of interest., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

Cancer-associated fibroblasts (CAFs) are senescent fibroblasts in tumor nest, which trigger a signaling center to remodel a desmoplastic tumor niche. CAF's functions in cancer are closely similar to myofibroblasts during the wound healing process. They can produce cytokines, enzymes, and protein- or RNA-containing exosomes to alter the function of surrounding cells. Non-- coding RNAs, including microRNAs and long non-coding RNAs, modulate pathologic mechanisms in cancer. Dysregulation of these RNAs influences the formation and function of CAFs. Furthermore, it has been demonstrated that CAFs, by releasing non-coding RNAs-containing exosomes, affect the tumor cells' behavior. CAFs also secrete mediators such as chemokines to alter the expression of non-coding RNAs in the tumor microenvironment. This study aimed to discuss the role of non-coding RNAs in CAF development in cancer. Additionally, we have shed light on the therapeutic approaches to develop the strategies based on the alteration of non-coding RNAs in cancer., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

DNA damage usually happens in all cell types, which may originate from endogenous sources (i.e., DNA replication errors) or be emanated from radiations or chemicals. These damages range from changes in few nucleotides to significant structural abnormalities on chromosomes and, if not repaired, could disturb the cellular homeostasis or cause cell death. As the most significant response to DNA damage, DNA repair provides biological pathways by which DNA damages are corrected and returned into their natural circumstance. However, an aberration in the DNA repair mechanisms may result in genomic and chromosomal instability and the accumulation of mutations. The activation of oncogenes and/or inactivation of tumor suppressor genes is a serious consequence of genomic and chromosomal instability and may bring the cells into a cancerous phenotype. Therefore, genomic and chromosomal instability is usually considered a crucial factor in carcinogenesis and an important hallmark of various human malignancies. In the present study, we review our current understanding of the most updated mechanisms underlying genomic instability in cancer and discuss the potential promises of these mechanisms in finding new targets for the treatment of cancer., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)