Current Drug Targets - Current Issue
Volume 26, Issue 15, 2025
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The Emerging Landscape of LINC01123 in Cancer: Roles, Mechanisms, and Clinical Significance
More LessAuthors: Jingjie Yang, Fan Peng, Haodong He, Haoran Liu, Kexing Liu, Zhouya Xu, Yaqi Hu, Guihua Liao, Yan Cai and Chengfu YuanIntroductionLong intergenic non-coding RNA 01123 (LINC01123) is a lncRNA located on the human chromosome 2q13. It is upregulated in various cancers and has been identified as an oncogene. Its expression is associated with the risk and poor prognosis of multiple cancers.
MethodsA systematic literature search was conducted in PubMed, Web of Science, and Google Scholar databases using “LINC01123” as the search term. The retrieved studies were reviewed to analyze the expression patterns, oncogenic mechanisms, and clinical significance of LINC01123 in cancers.
ResultsLINC01123 is activated by transcription factors such as c-Myc, ZEB1, and FOXC1. It promotes cancer progression, metastasis, and drug resistance by acting as a “molecular sponge” for miRNAs, activating signaling pathways, or interacting with proteins. Its upregulation correlates with adverse clinicopathological features and poor prognosis in multiple cancers.
DiscussionThe findings suggest that LINC01123 plays a multifaceted role in cancer biology. Its ability to regulate gene expression through various mechanisms highlights its potential as both a prognostic biomarker and a therapeutic target. However, further research is needed to elucidate its mechanisms fully and to explore its clinical applications across different cancer types.
ConclusionLINC01123 has potential as a novel prognostic biomarker and therapeutic target for cancer. Further research is needed to elucidate its mechanisms and clinical applications fully.
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Personalised Transdermal Therapy for Chronic Pain with Digital Twin Technology
More LessDigital twin technology has emerged as a breakthrough development in healthcare, providing personalised transdermal drug delivery systems for chronic pain treatment. Digital twins provide accurate, customised therapy to enhance therapeutic outcomes and reduce risks by combining patient-specific computational models. This article aims to explore the applicability of digital twin technology in improving the transdermal delivery of drugs for successful chronic pain management. It is enabling personalised treatment through patient-specific simulations. By integrating physiological data with computational models, digital twins optimise drug absorption, patch application, and dosage adjustments in real-time, enhancing therapeutic outcomes while minimising side effects. Recent advancements highlight improvements in fentanyl patch optimisation, site-specific drug delivery, and thermally controlled systems. However, challenges such as ethical concerns, data security, and standardisation need to be addressed. Future research should focus on integrating AI and IoT to refine digital twin applications in precision medicine. It can be concluded from the findings of various studies that digital twin technology offers a promising future for precise and individualised transdermal drug delivery in chronic pain, paving the way for safer and more effective therapeutic interventions.
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Tachykinin Receptors and their Antagonists: Unraveling Their Role in Metabolic Disorders and Therapeutic Innovations
More LessAuthors: Waquar Ahsan, Sadique A. Javed, Asim Najmi and Khalid ZoghebiIntroductionMetabolic disorders are major global health concerns with increasing prevalence worldwide. Experimental evidence suggests the role of tachykinins and their receptors in metabolic regulation, neuroendocrine control, and inflammatory responses. This review aims to explore the implications of tachykinin receptors and their antagonists in the management of metabolic disorders.
MethodsA comprehensive literature search was performed across major scientific databases to identify and analyze preclinical and clinical studies on tachykinin receptors and their antagonists in the context of metabolic disorders. The key mechanisms of action of drugs, important therapeutic outcomes, and challenges associated with drug development were covered.
ResultsThe reported experimental and clinical studies suggest that the antagonists of NK1R, NK2R, and NK3R could influence glucose metabolism, lipid homeostasis, and appetite regulation. While NK1R antagonists, such as aprepitant, demonstrated anti-inflammatory and neuroprotective effects, NK3R antagonists, including fezolinetant, showed promise in modulating energy balance and thermoregulation.
DiscussionThese studies emphasized the emerging potential of tachykinin receptors and their antagonists in the management of metabolic dysfunctions. However, the challenges associated with its clinical translation, including receptor redundancy, limited biomarker-based patient stratification, and variations in receptor expression across species, are still relevant and need to be addressed to improve therapeutic outcomes.
ConclusionTachykinin receptor antagonists hold significant potential as therapeutic agents in the management of metabolic disorders. Further studies are warranted to overcome translational barriers, address safety issues, validate biomarkers, and refine receptor selectivity to achieve maximum therapeutic benefits.
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Unraveling the Pivotal Role of LncRNA DUXAP9 in Cancer: Current Progress and Future Perspectives
More LessAuthors: Jingjie Yang, Siqi Yang, Wenjin Peng, Haodong He, Haoran Liu, Jiahe Zhang, Guihua Liao and Chengfu YuanDouble homeobox A pseudogene 9 (DUXAP9), also known as long intergenic non-coding RNA 1296 (LINC01296) and lymph node metastasis-associated transcript 1 (LNMAT1), is an emerging lncRNA encoded by a pseudogene. It has been reported to be upregulated in various tumor types and functions as an oncogenic factor. The high expression of DUXAP9 is closely related to clinical pathological features and poor prognosis in 16 types of malignant tumors. DUXAP9 is transcriptionally activated by YY-1 and Twist1 and functions as a guide or scaffold for biomolecular complexes and chromatin modifiers, or as a "decoy" for miRNAs, mRNAs, and proteins, thereby regulating gene expression. Moreover, the PI3K/AKT, NF-κB, MAPK/ERK, and Wnt/β- catenin signaling pathways are variously activated or inhibited by DUXAP9, subsequently influencing the biological behaviors of tumor cells, including proliferation, apoptosis, cell cycle arrest, migration, invasion, epithelial-mesenchymal transition (EMT), and drug resistance. This review summarizes recent research on DUXAP9 in oncology, offering insights into its expression characteristics, biological functions, molecular mechanisms, and clinical significance for cancer diagnosis, treatment, and prognosis.
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Targeting the Toll-like Receptor Signaling Pathway in Lung Cancer: Therapeutic Opportunities and Challenges
More LessAuthors: Muhammad Usama, Badar Raza, Mingfei Wu and Shanming JiLung cancer, particularly non-small cell lung cancer, is a leading cause of global mortality, with many cases diagnosed at advanced stages. The Toll-Like Receptor (TLR) signaling pathway plays a crucial role in linking inflammation to lung cancer progression, with both pro-tumor and anti-tumor effects. This perspective delves into the complex functions of TLR proteins in lung cancers, elucidating their involvement in tumor growth, angiogenesis, and metastasis. In addition, we highlight the therapeutic potentials of TLR agonists and antagonists, emphasizing their interplay with immune checkpoint inhibitors like PD-1/PD-L1 blockers to overcome immunosuppressive barriers. Nevertheless, the paradoxical effects of TLR activation, balancing immune stimulation and suppression, demand precise targeting strategies. Collectively, our study synthesizes the current understanding of TLR signaling pathways in lung cancers, offering insights into their potential for advancing lung cancer therapies.
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Volumes & issues
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Volume 26 (2025)
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Volume 25 (2024)
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Volume 24 (2023)
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Volume 23 (2022)
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Volume 22 (2021)
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Volume 21 (2020)
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Volume 20 (2019)
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Volume 19 (2018)
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Volume 18 (2017)
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Volume 17 (2016)
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Volume 16 (2015)
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Volume 15 (2014)
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Volume 14 (2013)
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Volume 13 (2012)
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Volume 12 (2011)
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Volume 11 (2010)
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Volume 10 (2009)
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Volume 9 (2008)
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Volume 8 (2007)
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Volume 7 (2006)
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Volume 6 (2005)
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Volume 5 (2004)
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Volume 4 (2003)
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Volume 3 (2002)
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Volume 2 (2001)
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Volume 1 (2000)
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