MicroRNA (miRNA/miR) represents a category of endogenous, short-chain non-coding RNA molecules comprising ~22 nucleotides. Specifically, miR-325 is situated within the first sub-band of region 2 on the short arm of the X chromosome. Notably, aberrant expression of miR-325 has been observed across various tumor systems, spanning the nervous, endocrine, respiratory, reproductive and digestive systems. miR-325 exhibits the capacity to target a minimum of 20 protein-coding genes, thereby influencing diverse cellular processes, including cell proliferation, epithelial-mesenchymal transition, apoptosis, invasion and migration. Moreover, miR-325 serves a pivotal role in the formation of six competing endogenous RNA (ceRNA) regulatory axes, involving one circular RNA, four long non-coding RNA and one additional miRNA. By participating in various signaling pathways through gene targeting, the abnormal expression of miR-325 has been associated with clinicopathological conditions in diverse patients with cancer, significantly impacting both the clinicopathology and prognosis of affected individuals. Additionally, miR-325 has been associated with the development of resistance to oxaliplatin, cisplatin and doxorubicin in cancer cells. Its involvement in the anticancer molecular mechanisms of these agents underscores its potential significance in therapeutic contexts. However, it is noteworthy that the current study did not specifically address sex-based cell line selection. In conclusion, the present review provides a comprehensive summary of the relevant findings concerning miR-325, offering valuable insights for future research endeavors focused on determining the molecular mechanisms associated with this miRNA.

DNA methylation is one of the earliest and most significant epigenetic mechanisms discovered. DNA methylation refers, in general, to the addition of a methyl group to a specific base in the DNA sequence under the catalysis of DNA methyltransferase, with S‑adenosine methionine as the methyl donor, via covalent bonding and chemical modifications. DNA methylation is an important factor in inducing cancer. There are different types of DNA methylation, and methylation at different sites plays different roles. It is well known that the progression of colorectal cancer (CRC) is affected by the methylation of key genes. The present review did not only discuss the potential relationship between DNA methylation and CRC but also discussed how DNA methylation affects the development of CRC by affecting key genes. Furthermore, the clinical significance of DNA methylation in CRC was highlighted, including that of the therapeutic targets and biomarkers of methylation; and the importance of DNA methylation inhibitors was discussed as a novel strategy for treatment of CRC. The present review did not only focus upon the latest research findings, but earlier reviews were also cited as references to older literature.

UNASSIGNED: Focal adhesion kinase (FAK) is a cytoplasmic non-receptor tyrosine kinase over-expressed in various malignancies which is related to various cellular functions such as adhesion, metastasis and proliferation.
UNASSIGNED: There is growing evidence that FAK is a promising therapeutic target for designing inhibitors by regulating the downstream pathways of FAK. Some potential FAK inhibitors have entered clinical phase research.
UNASSIGNED: FAK could be an effective target in medicinal chemistry research and there were a variety of FAKIs have been patented recently. Here, we updated an overview of design, synthesis and structure-activity relationship of chemotherapeutic FAK inhibitors (FAKIs) from 2017 until now based on our previous work. We hope our efforts can broaden the understanding of FAKIs and provide new ideas and insights for future cancer treatment from medicinal chemistry point of view.

Transfer RNA-derived small RNAs (tsRNAs) are a class of small non-coding RNA (sncRNA) molecules derived from tRNA, including tRNA derived fragments (tRFs) and tRNA halfs (tiRNAs). tsRNAs can affect cell functions by participating in gene expression regulation, translation regulation, intercellular signal transduction, and immune response. They have been shown to play an important role in various human diseases, including cardiovascular diseases (CVDs). Targeted regulation of tsRNAs expression can affect the progression of CVDs. The tsRNAs induced by pathological conditions can be detected when released into the extracellular, giving them enormous potential as disease biomarkers. Here, we review the biogenesis, degradation process and related functional mechanisms of tsRNAs, and discuss the research progress and application prospects of tsRNAs in different CVDs, to provide a new perspective on the treatment of CVDs.

UNASSIGNED: The P2Y14 receptor (P2Y14R), a member of the G protein-coupled receptor family, is activated by extracellular nucleotides. Due to its involvement in inflammatory, immunological and other associated processes, P2Y14R has emerged as a promising therapeutic target. Despite lacking a determined three-dimensional crystal structure, the homology modeling technique based on closely related P2Y receptors\' crystallography has been extensively utilized for developing active compounds targeting P2Y14R. Recent discoveries have unveiled numerous highly effective and subtype-specific P2Y14R inhibitors. This study presents an overview of the latest advancements in P2Y14R inhibitors.
UNASSIGNED: This review presents an overview of the advancements in P2Y14R inhibitor research over the past five years, encompassing new patents, journal articles, and highlighting the therapeutic prospects inherent in these compounds.
UNASSIGNED: The recent revelation of the vast potential of P2Y14R inhibitors has led to the development of novel compounds that exhibit promising capabilities for the treatment of sterile inflammation of the kidney, potentially diabetes, and asthma. Despite being a relatively nascent class of compounds, certain members have already exhibited their capacity to surmount specific challenges posed by conventional P2Y14R inhibitors. Targeting P2Y14R through small molecules may present a promising therapeutic strategy for effectively managing diverse inflammatory diseases.

The cell cycle is tightly regulated to ensure controlled cell proliferation. Dysregulation of the cell cycle machinery is a hallmark of cancer that leads to unchecked growth. This review comprehensively analyzes key molecular regulators of the cell cycle and how they contribute to carcinogenesis when mutated or overexpressed. It focuses on cyclins, cyclin-dependent kinases (CDKs), CDK inhibitors, checkpoint kinases, and mitotic regulators as therapeutic targets. Promising strategies include CDK4/6 inhibitors like palbociclib, ribociclib, and abemaciclib for breast cancer treatment. Other possible targets include the anaphase-promoting complex/cyclosome (APC/C), Skp2, p21, and aurora kinase inhibitors. However, challenges with resistance have limited clinical successes so far. Future efforts should focus on combinatorial therapies, next-generation inhibitors, and biomarkers for patient selection. Targeting the cell cycle holds promise but further optimization is necessary to fully exploit it as an anti-cancer strategy across diverse malignancies.

Carcinoembryonic antigen-related cell adhesion molecule 6 (CEACAM6) is an immunoglobulin superfamily protein primarily expressed on epithelial surfaces and myeloid cells. It plays a significant role in cancer progression by inhibiting apoptosis, promoting drug resistance, and facilitating cancer cell invasion and metastasis. Overexpression of CEACAM6 has been observed in various cancers, including lung, breast, colorectal, and hepatocellular cancers, and is associated with poorer overall survival and disease-free survival. Its differential expression on tumor cell surfaces makes it a promising cancer marker. This review aims to provide a comprehensive summary of CEACAM6\'s role in different cancer types, its involvement in signaling pathways, and recent advancements in CEACAM6-targeted treatments.

Stroke is a severe neurological disease that is associated with high rates of morbidity and mortality, and the underlying pathological processes are complex. Ferroptosis fulfills a significant role in the progression and treatment of stroke. It is well established that ferroptosis is a type of programmed cell death that is distinct from other forms or types of cell death. The process of ferroptosis involves multiple signaling pathways and regulatory mechanisms that interact with mechanisms inherent to stroke development. Inducers and inhibitors of ferroptosis have been shown to exert a role in the onset of this cell death process. Furthermore, it has been shown that interfering with ferroptosis affects the occurrence of stroke, indicating that targeting ferroptosis may offer a promising therapeutic approach for treating patients of stroke. Hence, the present review aimed to summarize the latest progress that has been made in terms of using therapeutic interventions for ferroptosis as treatment targets in cases of stroke. It provides an overview of the relevant pathways and molecular mechanisms that have been investigated in recent years, highlighting the roles of inducers and inhibitors of ferroptosis in stroke. Additionally, the intervention potential of various types of Traditional Chinese Medicine is also summarized. In conclusion, the present review provides a comprehensive overview of the potential therapeutic targets afforded by ferroptosis‑associated pathways in stroke, offering new insights into how ferroptosis may be exploited in the treatment of stroke.

Long non-coding RNAs have emerged as important players in cancer biology. Increasing evidence has uncovered their potency in improving cancer management as they can be used as a credible prognostic and diagnostic biomarker. Recently, DARS-AS1 has gained significant attention for its involvement in facilitating tumor progression. So far, numerous research has been reported its upregulation in different malignancies of human body systems and revealed its association with cancer hallmarks as well as clinicopathological characteristics. Importantly, targeting DARS-AS1 holds promise in cancer therapy. In the current study, we provide an in-depth analysis of its expression status and explore the underlying mechanisms through which DARS-AS1 contributes to tumor initiation, growth, invasion, and metastasis. Additionally, we examine the correlation between DARS-AS1 expression and clinicopathological features of cancer patients, shedding light on its potential as a cancer biomarker. Furthermore, we discuss the therapeutic potential of targeting DARS-AS1 in cancer treatment, highlighting emerging strategies, such as RNA interference and small molecule inhibitors. Boosting the understanding of its functional role can open new avenues for precision medicine, thus resulting in better outcomes for cancer patients.

UNASSIGNED: Long non-coding RNAs (lncRNAs) are a group of non-coding RNAs consisting of more than 200 nucleotides that are widely involved in various physiological and pathobiological processes in the body. LncRNA plays a crucial role in tumorigenesis and development with its unique functions, such as playing a role in a variety of biological processes of malignant tumors as a cancer-promoting factor or a cancer-suppressor factor. Lysyl oxidase-like protein 1-antisense RNA1 (LOXL1-AS1) is a novel functional lncRNA recently reported. This article reviews the current findings on the role of LOXL1-AS1 in cancer, and discusses the potential clinical significance and application prospects, in order to provide a theoretical basis and reference for the clinical diagnosis, treatment and screening of prognostic markers for malignant tumors.
UNASSIGNED: The PubMed and Embase databases were searched using the keywords \"cancer\" or \"tumor\" or \"neoplasm\" and \"LOXL1-AS1\" for publications from 2018 to the present. The English literature was searched, with a focus on relevant articles. These articles validated the role and mechanism of LOXL1-AS1 in different cancers.
UNASSIGNED: LOXL1-AS1 is a recently reported novel lncRNA, which is abnormally expressed and upregulated in more than ten cancers, and is positively correlated with adverse clinical features and poor prognosis in cancer patients. LOXL1-AS1 competently binds to a variety of microRNAs to regulate the expression of downstream target genes and regulate related signaling pathways, including proliferation, migration, invasion and inhibition of malignant biological behaviors such as apoptosis.
UNASSIGNED: LOXL1-AS1 is expected to become a novel biomarker for cancer diagnosis and treatment, with great potential as an independent prognostic indicator.