Archives of Pharmacal Research最新文献

{"title":"Curcumin for inflammatory bowel disease therapy: advances in mechanisms, clinical applications, and drug delivery.","authors":"Zilong Zhang, Chao Ding, Haonan Xu, Fujiang Guo, Yiming Li, Dongdong Zhang, Rui Wang","doi":"10.1007/s12272-025-01569-7","DOIUrl":"https://doi.org/10.1007/s12272-025-01569-7","url":null,"abstract":"<p><p>Inflammatory bowel disease (IBD) is a chronic and recurrent gastrointestinal disorder, which is typically characterized by symptoms such as abdominal pain, diarrhea, and weight loss, significantly impairing patients' quality of life. The etiology of IBD is multifactorial, involving complex interactions among genetic predisposition, immune dysregulation, environmental influences, and gut microbiota imbalance. Curcumin (CUR), a natural polyphenolic compound derived from the traditional Chinese medicine Curcuma longa, attracted considerable interest in pharmacological research due to its potent anti-inflammatory, antioxidant, and immunomodulatory properties. In the context of IBD, CUR exerts therapeutic effects by modulating key inflammatory signaling pathways, maintaining the integrity of the intestinal mucosal barrier, and restoring microbial homeostasis. Clinical studies demonstrated that CUR can alleviate IBD symptoms, suppress inflammatory responses, and improve patients' quality of life. Nevertheless, its clinical application is limited by poor aqueous solubility and low oral bioavailability. To address these limitations, a variety of nanodelivery systems-including polymeric nanoparticles, lipid-based carriers, and nanofibers-have been developed to enhance the solubility, stability, and targeted delivery of CUR. This review provides a comprehensive overview of recent advances in the mechanistic insights, clinical applications, and drug delivery strategies of CUR in IBD therapy, to support future research and clinical translation.</p>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":" ","pages":""},"PeriodicalIF":7.5,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147479","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Germacrane and humulane sesquiterpenes from the roots and rhizomes of Valeriana officinalis var. latifolia and their anti-inflammatory and anti-influenza virus activities.","authors":"Jia-Jin Liu, Li-Zhong Wang, Yuan-Ting Duan, Rong-Tao Li, Dan Liu, Hong-Mei Li","doi":"10.1007/s12272-025-01571-z","DOIUrl":"https://doi.org/10.1007/s12272-025-01571-z","url":null,"abstract":"<p><p>Twenty-seven sesquiterpenes, including twenty-one new germacrane-type ones (1-5, 8-16, and 19-25) and a new humulane-type one (27), were isolated from the roots and rhizomes of Valeriana officinalis var. latifolia. The structures and absolute configurations of the new compounds were elucidated using extensive spectroscopic techniques (1D and 2D NMR, and HRESIMS) and quantum chemical calculations. Structurally, compound 20 was a new germacrane-type norsesquiterpene, while compound 27 was a new humulane-type norsesquiterpene. In addition, compound 27 significantly inhibited the production of nitric oxide with an IC₅₀ value of 3.65 ± 1.06 μM. It reduced the expression of cytokines such as IL-1 and IL-6, as well as inflammation-related proteins induced by LPS or influenza A virus in macrophages, thereby exhibiting significant anti-inflammatory activity. This effect may be related to blocking the formation of the inflammasome and the activation of the NF-κB signaling pathway. Furthermore, compound 10 showed anti-influenza virus activity with an EC₅₀ value of 27.28 ± 5.63 µM. The study may provide a scientific basis for the development and utilization of functional foods and medicines derived from V. officinalis var. latifolia.</p>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":" ","pages":""},"PeriodicalIF":7.5,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147489","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dual inhibitors of P-glycoprotein and breast cancer resistance protein for overcoming the blood-brain barrier: in silico discovery and preclinical evaluation.","authors":"Jiyeon Kang, Yukyeong Paik, Hwa Jeong Ryu, Jaeok Lee, Irin Shin, Ye Won Park, Jihye Kim, Yoon Jeong Lim, Hyerim Shin, Wankyu Kim, Hwa Jeong Lee","doi":"10.1007/s12272-025-01567-9","DOIUrl":"https://doi.org/10.1007/s12272-025-01567-9","url":null,"abstract":"<p><p>P-glycoprotein (P-gp) and breast cancer resistance protein (BCRP) are typical ABC efflux transporters that play important physiological and pharmacological roles. At the blood-brain barrier (BBB), P-gp and BCRP function cooperatively as the main efflux transporters, hindering the entry of drugs into the brain. Therefore, dual inhibition of P-gp and BCRP is needed to deliver drugs effectively to the brain. This study sought potential dual P-gp/BCRP inhibitors to determine their ability to enhance brain penetration of the anticancer drug mitoxantrone (MX) and thereby improve its therapeutic efficacy against brain cancer. Candidate compounds for dual P-gp/BCRP inhibitors were extracted using in silico algorithms. The dual P-gp/BCRP inhibitory activity of 75 extracted candidates was investigated through MX accumulation studies in breast cancer cell lines overexpressing P-gp (MCF-7/ADR) and BCRP (MCF-7/MX100). The 5 compounds selected as final candidates were CDK 4/6 inhibitor IV, BX795, foretinib, BI-D1870, and CGP60474. Each of these 5 candidates increased MX accumulation and reversed MX resistance in MCF-7/ADR and MCF-7/MX100 cells. Additionally, they increased MX permeability across the BBB in an in vitro model. In situ brain perfusion studies showed that CDK 4/6 inhibitor IV, BX795, and CGP60474 improved the brain delivery of MX in rats. Moreover, in a mouse brain tumor model, CDK 4/6 inhibitor IV and BX795 potentiated the anticancer effect of MX against brain cancer, leading to a considerable reduction in tumor burden. In conclusion, potential dual P-gp/BCRP inhibitors were discovered through in silico screening and verified through in vitro and in vivo studies. CDK 4/6 inhibitor IV was the most effective dual P-gp/BCRP inhibitor candidate for enhancing the brain penetration of an anticancer drug for the treatment of brain tumors.</p>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":" ","pages":""},"PeriodicalIF":7.5,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145136239","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Extracellular matrix protein 1 in cancer: multifaceted roles in tumor progression, prognosis, and therapeutic targeting.","authors":"Jue Wang, Qionglian Huang, Hanjuan Ning, Weiwei Liu, Xianghui Han","doi":"10.1007/s12272-025-01572-y","DOIUrl":"https://doi.org/10.1007/s12272-025-01572-y","url":null,"abstract":"<p><p>Extracellular matrix protein 1 (ECM1) is a multifunctional glycosylated protein associated with the cell membrane. Increasing evidence indicates that aberrant ECM1 expression in cancer cells promotes tumor growth and metastasis by regulating proliferation, invasion, migration, and drug resistance. Beyond its direct effects on cancer cells, ECM1 plays a pivotal role in shaping the tumor microenvironment by contributing to angiogenesis, inflammatory responses, and the activation of cancer-associated fibroblasts, which collectively drive malignant progression. Immunohistochemical studies have demonstrated that ECM1 is highly expressed in a wide range of invasive cancers compared with adjacent normal tissues, underscoring its potential as a diagnostic and prognostic biomarker. Moreover, elevated ECM1 expression is consistently associated with poor clinical outcomes across multiple malignancies. In this review, we comprehensively summarize research from the past decade on the role of ECM1 in cancer progression, evaluate its potential as a prognostic biomarker, and highlight recent advances in ECM1-targeted therapeutic strategies. Overall, this review provides new insights into the multifaceted roles of ECM1 in cancer biology and its promise as a molecular target for innovative cancer therapies.</p>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":" ","pages":""},"PeriodicalIF":7.5,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145136265","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Engineering a BMP2-risedronate complex with sustained release for osteoporosis therapy.","authors":"Sang-Ok Jeon, Shrawani Lamichhane, Dong-Ho Oh, Jo-Eun Seo, Vinit Raj, Sangkil Lee","doi":"10.1007/s12272-025-01568-8","DOIUrl":"https://doi.org/10.1007/s12272-025-01568-8","url":null,"abstract":"<p><p>Human bone morphogenetic protein 2 (BMP2) is a key inducer of osteogenesis; however, conventional delivery systems often result in burst release and adverse effects. To address this limitation, we fabricated an ionic complex of BMP2 with the clinically used osteogenesis inducer risedronate drug through an ion-pairing method. Fourier-transform infrared spectroscopy and ultra-resolution imaging confirmed the electrostatic interactions between BMP2 and risedronate. The resulting BMP2-risedronate complex exhibited a uniform particle size of 326 ± 149 nm, a polydispersity index of 0.2-0.3, and a zeta potential of - 38.08 ± 0.12 mV. The complex demonstrated a high complexation efficiency (˃ 95%). In vitro bioactivity studies using C2C12 myoblast cells demonstrated that BMP2, combined with risedronate, effectively induced osteoblastic differentiation. Furthermore, incorporation of the complex into 1.5% hyaluronic acid (HA) and 1% HA-19% poloxamer 407 (P407) hybrid hydrogel mitigated rapid release and retention, achieving a controlled release profile. In vivo studies confirmed that fabricated BMP2-risedronate complex loaded in hydrogels promotes sustained BMP2 release and, in combination with risedronate, enhances osteogenic efficacy. These findings suggest that the BMP2-risedronate ionic complex is a promising candidate for localized BMP2 delivery in osteogenesis therapy.</p>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":" ","pages":""},"PeriodicalIF":7.5,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145129822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Histone lactylation in gastrointestinal cancers: developing immunotherapeutic drugs targeting epigenetics.","authors":"Mingyao Huang","doi":"10.1007/s12272-025-01570-0","DOIUrl":"https://doi.org/10.1007/s12272-025-01570-0","url":null,"abstract":"<p><p>Gastrointestinal cancers (GICs) remain a major global health burden due to their aggressive nature, therapeutic resistance, and immunosuppressive tumor microenvironment (TME). Histone lactylation, a novel epigenetic modification driven by tumor-derived lactate, has emerged as a key mediator linking metabolic reprogramming to gene expression and immune regulation. In GICs, aberrant lactylation contributes to M2 macrophage polarization, increased PD-L1 expression, and diminished cytotoxic immune cell infiltration, all of which are associated with poor prognosis and resistance to immunotherapy. Targeting histone lactylation-related enzymes-such as p300, SIRT2, and LDHA-or interfering with lactate metabolism offers promising avenues to reshape the TME and enhance responses to immune checkpoint blockade. This review highlights the mechanistic underpinnings and immunological consequences of histone lactylation in GICs and discusses emerging therapeutic strategies that leverage this epigenetic axis to improve cancer immunotherapy outcomes.</p>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":" ","pages":""},"PeriodicalIF":7.5,"publicationDate":"2025-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145111827","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Human YKL-40 antibody alleviates atopic dermatitis-like skin inflammation by inhibiting exosome secretion via the JAK3/STAT6 pathway.","authors":"Jun Sang Yu, Tae Hun Kim, Sung Sik Park, Sang-Bae Han, Jaesuk Yun, Dong Ju Son, Joong-Kook Choi, In Sook Jeon, Jin Tae Hong","doi":"10.1007/s12272-025-01564-y","DOIUrl":"https://doi.org/10.1007/s12272-025-01564-y","url":null,"abstract":"<p><p>Atopic dermatitis (AD) is an inflammatory skin disease that produces a variety of inflammatory cytokines and chemokines. Chitinase-3-like protein 1 (CHI3L1, YKL-40) significantly contributes to AD-associated inflammatory response and is highly expressed in patients with AD. Therefore, this study elucidated the effects and potential mechanisms of human YKL-40 antibody on AD-affected skin. The anti-AD like inflammatory effects and inhibition of exosome release effectors of human YKL-40 antibody were evaluated. Since exosomes have been closely related to AD inflammation and cytokine production, we detected exosome release in in vitro reconstituted human skin (RHS) models and HaCaT cells. Cytokine expression was analyzed using enzyme-linked immunosorbent assay (ELISA) and reverse transcription-quantitative polymerase chain reaction (RT-qPCR). In addition, related signaling pathways were evaluated using Western blotting and immunofluorescence staining. Human YKL-40 antibody significantly inhibited epidermal hyperplasia commonly induced by AD in the RHS model. In addition, this antibody effectively reduced the secretion of AD-associated inflammatory cytokines. Furthermore, it inhibited the expression of CD63, a marker for exosomes, and the phosphorylation of JAK3/STAT6, which are primarily involved in signaling pathways for AD and exosome release. This study provides strong evidence supporting the potential therapeutic efficacy of human YKL-40 antibody in the treatment of AD. It offers a new therapeutic approach for patients with incurable inflammatory skin diseases.</p>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":" ","pages":""},"PeriodicalIF":7.5,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145022805","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"p62/SQSTM1 signaling nexus and orchestration of ERK and mTOR pathways are crucial for Bacoside A- induced autophagy-mediated apoptosis in chronic myelogenous leukemia.","authors":"Sweta Kundu, Suvodeep Saha, Suparna Ghosh, Sampriti Sarkar, Atanu Kotal, Avik Acharya Chowdhury","doi":"10.1007/s12272-025-01565-x","DOIUrl":"https://doi.org/10.1007/s12272-025-01565-x","url":null,"abstract":"<p><p>Bacoside A (BCA), a triterpenoid saponin isolated from Bacopa monnieri, exhibits diverse pharmacological properties, including neuroprotective, hepatoprotective, anti-stress, anti-inflammatory, and anti-ulcer effects. In the present study, BCA demonstrates pronounced anticancer activity against K562 chronic myelogenous leukemia (CML) cells by modulating autophagy-apoptosis dynamics. BCA induces dose- and time-dependent cytotoxicity in K562 cells while sparing normal human peripheral blood mononuclear cells (hPBMCs) and Vero cells, indicating therapeutic selectivity. Mechanistically, BCA elicits a biphasic cellular response characterized by autophagy induction at 24 h, followed by caspase-dependent apoptosis at 48 h. Autophagy activation was confirmed by the formation of Monodansylcadaverine-positive autophagic vacuoles, upregulation of Beclin-1 and LC3-II, and increased LC3 puncta in EGFP-LC3-transfected K562 cells. Notably, BCA treatment led to persistent accumulation of p62/SQSTM1 despite functional autophagic flux. Co-immunoprecipitation analysis revealed p62/SQSTM1-LC3-II interactions, while siRNA-mediated silencing of p62/SQSTM1 attenuated LC3-II accumulation, implicating p62/SQSTM1 as a positive modulator of autophagy. Moreover, p62/SQSTM1 facilitated apoptosis progression by interacting with and activating caspase-8, thereby bridging autophagy and apoptosis. Pharmacological inhibition of autophagy using 3-methyladenine abrogated both autophagic and apoptotic responses, establishing autophagy as a prerequisite for BCA-induced cell death. BCA promoted ERK1/2 activation and concomitant suppression of mTOR pathway via dephosphorylation of mTOR and 4E-BP1. Inhibition of ERK1/2 using PD98059 reversed mTOR dephosphorylation and autophagy induction, whereas mTOR overexpression restored ERK1/2 phosphorylation to basal levels. Collectively, these findings delineate BCA as a novel autophagy-inducing agent in CML, exerting cytotoxic effects via ERK1/2-mTOR signaling and p62/SQSTM1-mediated autophagy-apoptosis crosstalk.</p>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":" ","pages":""},"PeriodicalIF":7.5,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145022745","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advances in JNK inhibitor development: therapeutic prospects in neurodegenerative diseases and fibrosis.","authors":"Swapnil P Bhujbal, Jung-Mi Hah","doi":"10.1007/s12272-025-01566-w","DOIUrl":"https://doi.org/10.1007/s12272-025-01566-w","url":null,"abstract":"<p><p>c-Jun N-terminal kinases (JNKs), a subfamily of mitogen-activated protein kinases (MAPKs), are key mediators of cellular responses to environmental stress, inflammation, and apoptotic signals. The three isoforms-JNK1, JNK2, and JNK3 exhibit both overlapping and isoform-specific functions. While JNK1 and JNK2 are broadly expressed across tissues and regulate immune signaling, cell proliferation, and apoptosis, JNK3 expression is largely restricted to the brain, heart, and testis, where it plays a crucial role in neuronal function and survival. Subtle structural variations among the isoforms, particularly within the ATP-binding pocket and activation loop, provide a basis for the developing isoform-selective inhibitors to improve therapeutic precision. JNK3 has been increasingly recognized for its involvement in the pathogenesis of neurodegenerative disorders, including Alzheimer's and Parkinson's diseases, through mechanisms involving neuroinflammation, oxidative stress, and neuronal apoptosis. Given the limited efficacy of current therapies, which remain largely symptomatic and do not modify disease progression, covalent inhibitors of JNK3 represent a compelling alternative due to their potential for high selectivity and sustained target engagement. In parallel, JNK signaling contributes to fibrosis, with JNK1 serving as the predominant isoform driving profibrotic pathways such as fibroblast activation and extracellular matrix (ECM) deposition. Current antifibrotic agents provide only partial benefit and lack specificity for downstream effectors like JNK1. PROteolysis TArgeting Chimeras (PROTACs), which induce selective protein degradation via the ubiquitin-proteasome system, represent a promising modality to overcome these limitations. Selective degradation of JNK1 could provide a novel therapeutic avenue for fibrotic diseases. This review highlights therapeutic efforts to date and discusses how emerging approaches-particularly covalent JNK3 inhibitors for neurodegeneration and PROTACs for JNK1 in fibrosis-may advance future treatment paradigms.</p>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":" ","pages":""},"PeriodicalIF":7.5,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145013744","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Enhancer regulation in cancer: from epigenetics to m6A RNA modification","authors":"Arathy Vasukutty,&nbsp;Poshan Yugal Bhattarai,&nbsp;Hong Seok Choi","doi":"10.1007/s12272-025-01561-1","DOIUrl":"10.1007/s12272-025-01561-1","url":null,"abstract":"<div><p>Enhancers are crucial cis-regulatory DNA elements that regulate gene transcription by interacting with promoters, often over long genomic distances. Unlike promoters, their activity is independent of orientation or proximity to the gene. Active enhancers are transcribed into non-coding enhancer RNAs (eRNAs), which help stabilize enhancer-promoter loops, recruit transcription machinery, and shape the chromatin architecture. These eRNAs are regulated post-transcriptionally, through modifications such as the N6-methyladenosine (m⁶A) modification, which enhances their stability, facilitates interactions with nuclear reader proteins, and supports transcriptional condensate formation, thereby boosting enhancer activity. Super-enhancers, clusters of strong enhancers marked by high levels of modified H3 histone protein, acetylated at lysine 27, generate abundant eRNAs and are key drivers of gene expression in development and cancer. This review offers a comprehensive overview of the structure and function of enhancers and super-enhancers, highlights their regulatory roles, and examines the emerging contribution of m⁶A RNA modification in enhancer-mediated transcription during carcinogenesis. Additionally, we discuss experimental approaches for studying enhancer activity and explore potential therapeutic strategies targeting enhancer-associated pathways in cancer. By integrating recent advances in enhancer research, we aim to shed light on the intricate molecular choreography that orchestrates gene expression and its dysregulation in cancer.</p></div>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":"48 7-8","pages":"706 - 735"},"PeriodicalIF":7.5,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144881951","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}