Current molecular pharmacology最新文献

{"title":"Effect of Curcumin on the Head and Neck Squamous Cell Carcinoma Cell Line HN5.","authors":"Elaheh Dalir Abdolahinia,&nbsp;Shahin Ahmadian,&nbsp;Sepideh Bohlouli,&nbsp;Faezeh Jafarmadar Gharehbagh,&nbsp;Negar Ghorbani Jahandizi,&nbsp;Sepideh Zununi Vahed,&nbsp;Yalda Rahbar Saadat,&nbsp;Amirala Aghbali,&nbsp;Simin Sharifi,&nbsp;Solmaz Maleki Dizaj,&nbsp;Khalaf F Alsharif,&nbsp;Haroon Khan","doi":"10.2174/1874467215666220414143441","DOIUrl":"https://doi.org/10.2174/1874467215666220414143441","url":null,"abstract":"<p><strong>Background: </strong>Curcumin has been isolated from the rhizomes of Curcuma longa. Over the years, it has shown outstanding therapeutic potential in various human disorders, including cancers.</p><p><strong>Objective: </strong>The aim is to study curcumin's effects on the apoptosis signaling pathway in the head and neck squamous cell carcinoma (HNSCC) cell line HN5.</p><p><strong>Methods: </strong>The cytotoxicity of curcumin on HN5 cells were assessed. In addition, HN5 cells were also treated with curcumin to evaluate its effect on the caspase-8, -9, Bcl-2, Bax, and Stat3 gene expressions.</p><p><strong>Results: </strong>The results exhibited that cell viability reduced following curcumin treatment in a concentration- dependent manner. Curcumin treatment caused decreased expression of Bcl2, with simultaneous upregulation of the Bax/Bcl2 ratio. Curcumin increased caspase-9 expression, did not affect caspase-8, and decreased Stat3 expression. The induction of the mitochondria-dependent apoptosis pathway of curcumin happened by modulating the expression of Bcl2 and Bax genes, resulting in the caspase-9 activation. Furthermore, curcumin decreased the expression of the Stat3 in HN-5 cells.</p><p><strong>Conclusions: </strong>In conclusion, curcumin showed marked anticancer effects in the HN-5 cell line by modulating Stat-3; Bax/Bcl-2 expression in vitro.</p>","PeriodicalId":10865,"journal":{"name":"Current molecular pharmacology","volume":"16 3","pages":"374-380"},"PeriodicalIF":2.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9493600","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Research Progress and Future Development Potential of Oridonin in Pharmacological Activities.","authors":"Shiying Ye,&nbsp;Shaowei Sun,&nbsp;Jiye Cai,&nbsp;Jinhuan Jiang","doi":"10.2174/1874467216666221130163634","DOIUrl":"https://doi.org/10.2174/1874467216666221130163634","url":null,"abstract":"<p><p>In recent years, attention has increasingly focused on herbal medicines and their bioactive components attributed to their multi-target pharmacological activity and low side effects. Oridonin is a natural diterpenoid extracted from the traditional Chinese herb and is one of the main active components of Rabdosia rubescens. Modern pharmacological studies have shown that oridonin has anti-tumor, anti-bacterial, anti-inflammatory, anti-oxidant, cardiovascular protective, immunomodulatory, and other effects. Based on the published literature in recent years, we outline the pharmacological activities of oridonin, aiming to provide a theoretical basis for the design and development of new oridonin-based drugs, as well as to facilitate the process of oridonin for clinical use.</p>","PeriodicalId":10865,"journal":{"name":"Current molecular pharmacology","volume":"16 7","pages":"691-706"},"PeriodicalIF":2.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9842705","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Influence of SGLT2 Inhibitors in Remodeling, Substrate and Ion Metabolism of Myocardium to Prevent Cardiovascular Risks: Recent Work and Advancement.","authors":"Nishant Johri,&nbsp;Prithpal S Matreja,&nbsp;Davis John,&nbsp;Shubham Dutta,&nbsp;Ashok Kumar Parida,&nbsp;Susanta Nath Sarma","doi":"10.2174/1874467216666221017123333","DOIUrl":"https://doi.org/10.2174/1874467216666221017123333","url":null,"abstract":"<p><p>Sodium-glucose cotransporter 2 (SGLT2) inhibitors are a new class of drugs that lower blood glucose levels while decreasing blood pressure, volume loss, and weight loss. SGLT2 inhibitors were studied to determine their effectiveness in treating cardiovascular disease and their side effects. Study outcomes related to cardiovascular and metabolic outcomes were examined in patients on SGLT2 inhibitors by searching PubMed, Embase, Cochrane, and SCOPUS. Articles related to clinical trials, reviews, and meta-analyses were considered. A review of SGLT2 inhibitors' mechanisms of action in preventing cardiovascular (CVS) disease progression was described. We then reviewed the possible effects of SGLT2 inhibitors on CVS dysfunction development, composition, and stability. In the following, we discussed the impact of SGLT2 inhibitors on CVD events, such as ischemic strokes and myocardial infarctions, and their role in treating congestive heart failure and cardiovascular mortality.</p>","PeriodicalId":10865,"journal":{"name":"Current molecular pharmacology","volume":"16 5","pages":"580-591"},"PeriodicalIF":2.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9859458","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of SIRT-1 as a Target for Treatment and Prevention of Diabetic Nephropathy: A Review.","authors":"Anita Kumari,&nbsp;Nalini Sodum,&nbsp;V Ravichandiran,&nbsp;Nitesh Kumar","doi":"10.2174/1874467216666230109140134","DOIUrl":"https://doi.org/10.2174/1874467216666230109140134","url":null,"abstract":"<p><p>Type-2 diabetes mellitus is a prime factor for the development of Diabetic Nephropathy (DN) that affects the vital organ namely the kidneys, and further alters the functions of the nephron system. DN is nowadays becoming a challenge for scientists towards the world because of its high pervasiveness and complexity of medication. Various risk factors are involved in the initiation of pathogenic DN, which are associated with different pathways against drug activity. Due to this DN becomes an unpredictable query to the researchers. SIRT1 is a silent information regulator factor 2 related enzyme 1 (SIRT1) is nicotinamide adenine dinucleotide (NAD+) dependent deacetylase that functions as an intracellular regulator of transcriptional activity. An activated version of SIRT-1 improves the metabolic diseased conditions associated with other molecular pathways. SIRT1 attenuates diabetic nephropathy in in vitro and in vivo experimental models of diabetes containing Podocytes, Mesangial cells, and Renal proximal tubular cells. SIRT1 shows nephroprotective effects in DN in part through deacetylation of transcription factors i.e., imply in the disease like p53, PTP1B, FOXO, RelA, NF- kβ, STAT-3, and PGC-1α/ PPARγ. It has been shown that some natural products like resveratrol and synthetic compounds are activating the SIRT1, this further involved the cascade pathways to prevent the DN. This review will help regarding the effectiveness of SIRT1as target in the prevention and treatment of DN.</p>","PeriodicalId":10865,"journal":{"name":"Current molecular pharmacology","volume":"16 8","pages":"811-831"},"PeriodicalIF":2.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9563869","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FASN Inhibitors Enhance Bestatin-Related Tumor Cell Apoptosis Through Upregulating PEPT1.","authors":"Jun Ni,&nbsp;Yue Shang,&nbsp;Wen-Die Wang,&nbsp;Chen Wang,&nbsp;Ai-Min Wang,&nbsp;Gao-Jie Li,&nbsp;Shu-Zhen Chen","doi":"10.2174/1874467216666221121121549","DOIUrl":"https://doi.org/10.2174/1874467216666221121121549","url":null,"abstract":"<p><strong>Background: </strong>Fatty acid synthase (FASN) is generally over-expressed in human tumor tissues and catalyzes de novo synthesis of fatty acids on which tumor cells depend. Bestatin, an inhibitor of aminopeptidase/CD13, is one of the dipeptide substrates for the human oligopeptide transporter 1 (PEPT1).</p><p><strong>Objectives: </strong>In the current study, we aimed to uncover the role of FASN inhibitors in bestatininduced tumor cell apoptosis and the underlying mechanism, extending our understanding of the correlations between FASN and PEPT1 in cancer and providing a new strategy for tumor targeted treatment.</p><p><strong>Methods: </strong>Cerulenin, orlistat and siRNAs were applied to inhibit FASN. The cell viability and apoptosis were assessed with MTT (thiazolyl blue tetrazolium bromide) assays and annexin VFITC/ PI staining with flow cytometry analysis. Western blot and qRT-PCR analysis were used to detect the protein levels and mRNA levels of the indicated genes in tumor cells, respectively. Protein degradation or stability was examined with cycloheximide chase assays. CD13 activity was detected by gelatin zymography. The HT1080 and C26 xenografts models were conducted to assess the efficacy <i>in vivo</i>.</p><p><strong>Results: </strong>In the current study, we found that inhibiting FASN by cerulenin and orlistat both augmented the effects of bestatin in decreasing tumor cell viability. Cerulenin increased the apoptosis rates and enhanced the cleavage of PARP caused by bestatin. Furthermore, cerulenin, orlistat and siFASNs markedly elevated PEPT1 protein levels. Indeed, cerulenin induced the upregulation of PEPT1 mRNA expression rather than affecting the protein level after the cells were treated with CHX. And Gly-Sar, a typical competitive substrate of PEPT1, could attenuate the augment of bestatin-induced cell killing by cerulenin. Moreover, synergistic restrain of tumor growth accompanied by a reduction of Ki-67 and increment of TUNEL was significantly achieved in the xenograft models. Interestingly, no clear correlation was observed between the CD13 with FASN and/or PEPT1 in tumor cells.</p><p><strong>Conclusion: </strong>FASN inhibitors facilitate tumor cells susceptible to bestatin-induced apoptosis involving the up-regulation of PEPT1 at the mRNA translation level and the transport of bestatin by PEPT1, emerging as a promising strategy for tumor targeted therapy.</p>","PeriodicalId":10865,"journal":{"name":"Current molecular pharmacology","volume":"16 7","pages":"771-786"},"PeriodicalIF":2.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9859464","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endoplasmic Reticulum Stress and Renin-Angiotensin System Crosstalk in Endothelial Dysfunction.","authors":"Himanshu Sankrityayan,&nbsp;Pooja Dhileepkumar Rao,&nbsp;Vishwadeep Shelke,&nbsp;Yogesh A Kulkarni,&nbsp;Shrikant R Mulay,&nbsp;Anil Bhanudas Gaikwad","doi":"10.2174/1874467215666220301113833","DOIUrl":"https://doi.org/10.2174/1874467215666220301113833","url":null,"abstract":"<p><strong>Background: </strong>Vascular endothelial dysfunction (VED) significantly results in catastrophic cardiovascular diseases with multiple aetiologies. Variations in vasoactive peptides, including angiotensin II and endothelin 1, and metabolic perturbations like hyperglycaemia, altered insulin signalling, and homocysteine levels result in pathogenic signalling cascades, which ultimately lead to VED. Endoplasmic reticulum (ER) stress reduces nitric oxide availability, causes aberrant angiogenesis, and enhances oxidative stress pathways, consequently promoting endothelial dysfunction. Moreover, the renin-angiotensin system (RAS) has widely been acknowledged to impact angiogenesis, endothelial repair and inflammation. Interestingly, experimental studies at the preclinical level indicate a possible pathological link between the two pathways in the development of VED. Furthermore, pharmacological modulation of ER stress ameliorates angiotensin-II mediated VED as well as RAS intervention either through inhibition of the pressor arm or enhancement of the depressor arm of RAS, mitigating ER stress-induced endothelial dysfunction and thus emphasizing a vital crosstalk.</p><p><strong>Conclusion: </strong>Deciphering the pathway overlap between RAS and ER stress may open potential therapeutic avenues to combat endothelial dysfunction and associated diseases. Several studies suggest that alteration in a component of RAS may induce ER stress or induction of ER stress may modulate the RAS components. In this review, we intend to elaborate on the crosstalk of ER stress and RAS in the pathophysiology of VED.</p>","PeriodicalId":10865,"journal":{"name":"Current molecular pharmacology","volume":"16 2","pages":"139-146"},"PeriodicalIF":2.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9259423","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of the Relationship between Aromatase/Sirtuin1 Interaction and miRNA Expression in Human Neuroblastoma Cells.","authors":"Yasemin Kartal,&nbsp;Unal Metin Tokat,&nbsp;Pelin Kelicen-Ugur,&nbsp;Serkan Yılmaz,&nbsp;Sevilay Karahan,&nbsp;Murat Timur Budak","doi":"10.2174/1874467215666220510112118","DOIUrl":"https://doi.org/10.2174/1874467215666220510112118","url":null,"abstract":"<p><strong>Background: </strong>Changes in activation/inhibition of Sirtuin-1 (SIRT1) and aromatase play an important role in a plethora of diseases. MicroRNAs (miRNAs) modulate multiple molecular pathways and affect a substantial number of physiological and pathological processes.</p><p><strong>Objective: </strong>The aim of this study was to investigate any possible interaction between aromatase and SIRT1 in SH-SY5Y cells and to see how there is a connection between this interaction and miRNA expression, if there is an interaction.</p><p><strong>Methods: </strong>In this study, cells were incubated in serum-deprived media for 6, 12, and 24 h. Aromatase and SIRT1 expressions were evaluated by Western blot. The IC50 concentration of SIRT1 activator (SRT1720), SIRT1 inhibitor (EX527), and aromatase inhibitors (letrozole and fadrozole) was determined by the XTT method. Then, CYP19A1 and SIRT1 levels were evaluated in the presence of SIRT1 siRNA or IC50 values for each activator/inhibitor. Finally, CYP19A1, SIRT1 expression and miRNA target gene were assessed with bioinformatic approaches.</p><p><strong>Results: </strong>Aromatase and SIRT1 protein levels were significantly elevated in the cells incubated at 24 h in serum-deprived media (p ≤ 0.05). SIRT1 also positively regulated CYP19A1 in SH-SY5Y cells in media with/without FBS. Serum deprivation depending on time course caused changes in the oxidant/ antioxidant system. While oxidative stress index tended to decrease in the absence of FBS at 24 h compared to the control, it showed a significant decrease at 48 h in a serum-deprived manner (p ≤ 0.001). As a result of bioinformatics analysis, we determined 3 miRNAs that could potentially regulate SIRT1 and CYP19A1. hsa-miR-27a-3p and hsa-miR-181a-5p correlated in terms of their expressions at 24 h compared to 12 h, and there was a significant decrease in the expression of these miRNAs. On the contrary, the expression of hsa-miR-30c-5p significantly increased at 24 h compared to 12 h.</p><p><strong>Conclusion: </strong>Considering the results, a direct link between aromatase and SIRT1 was observed in human neuroblastoma cells. The identification of key miRNAs, hsa-miR-27a-3p, hsa-miR-30c-5p, and hsa-miR-181a-5p targeting both aromatase and SIRT1, provides an approach with novel insights on neurology-associated diseases.</p>","PeriodicalId":10865,"journal":{"name":"Current molecular pharmacology","volume":"16 6","pages":"609-628"},"PeriodicalIF":2.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9487116","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Treatment of Parkinson's Disease with Sodium Oxybate.","authors":"Mortimer Mamelak","doi":"10.2174/1874467216666221103121135","DOIUrl":"10.2174/1874467216666221103121135","url":null,"abstract":"<p><p>Sodiun Oxybate (SO) has a number of attributes that may mitigate the metabolic stress on the substantia nigra pars compacta (SNpc) dopaminergic (DA) neurons in Parkinson's disease (PD). These neurons function at the borderline of energy sufficiency. SO is metabolized to succinate and supplies energy to the cell by generating ATP. SO is a GABAB agonist and, as such, also arrests the high energy requiring calcium pace-making activity of these neurons. In addition, blocking calcium entry impedes the synaptic release and subsequent neurotransmission of aggregated synuclein species. As DA neurons degenerate, a homeostatic failure exposes these neurons to glutamate excitotoxicity, which in turn accelerates the damage. SO inhibits the neuronal release of glutamate and blocks its agonistic actions. Most important, SO generates NADPH, the cell's major antioxidant cofactor. Excessive free radical production within DA neurons and even more so within activated microglia are early and key features of the degenerative process that are present long before the onset of motor symptoms. NADPH maintains cell glutathione levels and alleviates oxidative stress and its toxic consequences. SO, a histone deacetylase inhibitor also suppresses the expression of microglial NADPH oxidase, the major source of free radicals in Parkinson brain. The acute clinical use of SO at night has been shown to reduce daytime sleepiness and fatigue in patients with PD. With long-term use, its capacity to supply energy to DA neurons, impede synuclein transmission, block excitotoxicity and maintain an anti-oxidative redox environment throughout the night may delay the onset of PD and slow its progress.</p>","PeriodicalId":10865,"journal":{"name":"Current molecular pharmacology","volume":"16 5","pages":"564-579"},"PeriodicalIF":2.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9490292","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ethoxidol as a Broad-spectrum Adaptogen.","authors":"Zhigacheva Irina V,&nbsp;Krikunova Natalya I,&nbsp;Binyukov Vladimir,&nbsp;Mil Elena M,&nbsp;Rusina Irina F,&nbsp;Goloshchapov Alexander","doi":"10.2174/1874467215666220308115514","DOIUrl":"https://doi.org/10.2174/1874467215666220308115514","url":null,"abstract":"<p><strong>Background: </strong>Stress factors lead to a shift in the antioxidant-prooxidant relationship, allowing an increase in the generation of reactive oxygen species (ROS) by mitochondria, which results in the development of oxidative stress. Consequently, it is possible to put forward an assumption that drugs which reduce the excessive generation of ROS by these organelles should increase the body's resistance to stress factors. Antioxidants can be used as such drugs. In this regard, the aim of this work was to study the bioenergetics characteristic of mitochondria under stress conditions and under the action of 2-ethyl-6-methyl-3-hydroxypyridinium hydroxybutanedioate (ethoxidol).</p><p><strong>Methods: </strong>The antiradical activity of the drug was evaluated by the chemiluminescent method (CL). The functional state of the mitochondria was studied with reference to the level of lipid peroxidation by the spectrofluorimetry and in terms of fatty acid composition of mitochondrial membranes using the chromatography technique. The study of mitochondrial morphology was performed employing the method of atomic force microscopy.</p><p><strong>Results: </strong>The injection in mice of ethoxidol at a dose of 10^-5 mol/kg for 7 days led to the prevention of the stress-induced increase in the intensity of LPO in the membranes of the mitochondria, and swelling of these organelles; it also prevented a decrease in the content of unsaturated fatty acids, containing 18 and 20 carbon atoms. At the same time, ethoxidol increased the life expectancy of mice by 3.0-4.2 times in conditions of various types of hypoxia.</p><p><strong>Conclusion: </strong>The adaptogenic properties of ethoxidol can be attributed to its antiradical and antioxidant properties.</p>","PeriodicalId":10865,"journal":{"name":"Current molecular pharmacology","volume":"16 1","pages":"109-115"},"PeriodicalIF":2.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9493595","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MiR-129-2-3p Inhibits Esophageal Carcinoma Cell Proliferation, Migration, and Invasion <i>via</i> Targeting DNMT3B.","authors":"Xuyang Peng,&nbsp;Xuhui Wu,&nbsp;Gongzhi Wu,&nbsp;Chongxiong Peng,&nbsp;Bin Huang,&nbsp;Mingjiang Huang,&nbsp;Jianyang Ding,&nbsp;Chaofan Mao,&nbsp;Huaizhong Zhang","doi":"10.2174/1874467215666220308122716","DOIUrl":"https://doi.org/10.2174/1874467215666220308122716","url":null,"abstract":"<p><strong>Purpose: </strong>The study aims to explore the regulatory mechanism of miR-129-2-3p underlying esophageal carcinoma (EC) cell progression and generate new ideas for targeted treatment of EC.</p><p><strong>Methods: </strong>Mature miRNA expression data and total RNA sequencing data of EC in the TCGAESCA dataset were utilized to explore differentially expressed miRNAs (DEmiRNAs). StarBase database was then utilized to predict targets of miRNA. MiR-129-2-3p and DNMT3B expression in EC cell lines was assayed through qRT-PCR and Western blot. CCK-8, scratch healing, and transwell assays were conducted to assess the impact of miR-129-2-3p on EC cell phenotypes. In addition, a dual-luciferase assay was completed to identify the binding relationship between DNMT3B and miR-129-2-3p.</p><p><strong>Results: </strong>MiR-129-2-3p was noticeably less expressed in EC cell lines, while DNMT3B was highly expressed. MiR-129-2-3p could bind to DNMT3B. Furthermore, in vitro functional experiments uncovered that overexpressed miR-129-2-3p repressed EC cell progression while further overexpressing DNMT3B would restore the above inhibitory effect.</p><p><strong>Conclusion: </strong>MiR-129-2-3p is a cancer repressor in EC cells, and it could target DNMT3B, thus hampering the progression of EC cells.</p>","PeriodicalId":10865,"journal":{"name":"Current molecular pharmacology","volume":"16 1","pages":"116-123"},"PeriodicalIF":2.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9493596","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}