Current cancer drug targets最新文献

{"title":"Solid CaCO₃ Formation in Glioblastoma Multiforme and its Treatment with Ultra-Nanoparticulated NPt-Bionanocatalysts.","authors":"Tessy Lopez-Goerne, Alfonso Arellano, Francisco J Padilla-Godinez, Carlos Magana, Antonela Gonzalez-Bondani, Rafael Valiente","doi":"10.2174/0115680096289012240311023133","DOIUrl":"10.2174/0115680096289012240311023133","url":null,"abstract":"<p><strong>Background: </strong>Glioblastoma multiforme (GBM), the most prevalent form of central nervous system (CNS) cancer, stands as a highly aggressive glioma deemed virtually incurable according to the World Health Organization (WHO) standards, with survival rates typically falling between 6 to 18 months. Despite concerted efforts, advancements in survival rates have been elusive. Recent cutting-edge research has unveiled bionanocatalysts with 1% Pt, demonstrating unparalleled selectivity in cleaving C-C, C-N, and C-O bonds within DNA in malignant cells. The application of these nanoparticles has yielded promising outcomes.</p><p><strong>Objective: </strong>The objective of this study is to employ bionanocatalysts for the treatment of Glioblastoma Multiforme (GBM) in a patient, followed by the evaluation of obtained tissues through electronic microscopy.</p><p><strong>Methods: </strong>Bionanocatalysts were synthesized using established protocols. These catalysts were then surgically implanted into the GBM tissue through stereotaxic procedures. Subsequently, tissue samples were extracted from the patient and meticulously examined using Scanning Electron Microscopy (SEM).</p><p><strong>Results and discussion: </strong>Detailed examination of biopsies via SEM unveiled a complex network of small capillaries branching from a central vessel, accompanied by a significant presence of solid carbonate formations. Remarkably, the patient subjected to this innovative approach exhibited a three-year extension in survival, highlighting the potential efficacy of bionanocatalysts in combating GBM and its metastases.</p><p><strong>Conclusion: </strong>Bionanocatalysts demonstrate promise as a viable treatment option for severe cases of GBM. Additionally, the identification of solid calcium carbonate formations may serve as a diagnostic marker not only for GBM but also for other CNS pathologies.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":"270-280"},"PeriodicalIF":2.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140335084","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comprehensive Pan-cancer Analysis of CMPK2 as Biomarker and Prognostic Indicator for Immunotherapy.","authors":"Jingyuan Luo, Qianyue Zhang, Shutong Wang, Luojie Zheng, Jie Liu, Yuchen Zhang, Yingchen Wang, Ranran Wang, Zhigang Xiao, Zheng Li","doi":"10.2174/0115680096281451240306062101","DOIUrl":"10.2174/0115680096281451240306062101","url":null,"abstract":"<p><strong>Background: </strong>UMP-CMP kinase 2 (CMPK2) is involved in mitochondrial DNA synthesis, which can be oxidized and released into the cytoplasm in innate immunity. It initiates the assembly of NLRP3 inflammasomes and mediates various pathological processes such as human immunodeficiency virus infection and systemic lupus erythematosus. However, the role of CMPK2 in tumor progression and tumor immunity remains unclear.</p><p><strong>Methods: </strong>We identified CMPK2 expression patterns in the Genotype Tissue-Expression (GTEx), The Cancer Genome Atlas (TCGA), and the Cancer Cell Line Encyclopedia (CCLE) databases. Validation was performed using immunohistochemical staining data from the Human Protein Atlas (HPA) database and qPCR experiments. Receiver operating characteristic curve analysis and Kaplan-Meier survival analysis were conducted to assess the clinical relevance of CMPK2 expression. The Estimation of Stromal and Immune Cells in Malignant Tumor Tissues Using Expression Data (ESTIMATE) algorithm and the Tumor IMmune Estimation Resource (TIMER) database were used to evaluate the correlation between CMPK2 and immune infiltration in tumors. The Tumor Immune Syngeneic Mouse (TISMO) database and other public datasets were utilized to assess the impact of CMPK2 on immune therapy response. MEXPRESS and MethSurv databases were employed to investigate the effects of methylation on CMPK2 expression.</p><p><strong>Results: </strong>CMPK2 expression was elevated in 23 cancers and decreased in two cancers. Furthermore, CMPK2 expression had a high diagnostic value for 16 cancers. Elevated CMPK2 expression was associated with lower overall survival (OS), disease-specific survival (DSS), and progression- free interval (PFI) in four cancers. Immune microenvironment-related analysis revealed strong associations between CMPK2 expression and immune cell infiltration, as well as immune checkpoint expression across various tumors. Notably, in four mouse immunotherapy cohorts, CMPK2 expression in treated mouse tumors was higher post-treatment. In five clinical immunotherapy cohorts, patients with high CMPK2 expression show better responses to immunotherapy. Moreover, the methylation level of CMPK2 gene was closely correlated to its expression and tumor prognosis. Among these cancers, the clinical and immunological indications of skin cutaneous melanoma (SKCM) are particularly closely related to CMPK2 expression.</p><p><strong>Conclusion: </strong>Our analysis preliminarily describes the complex function of CMPK2 in cancer progression and immune microenvironment, highlighting its potential as a diagnostic and therapeutic target for immunotherapy.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":"209-229"},"PeriodicalIF":2.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140130957","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prognostic Significance and Functional Mechanism of UTS2 in Glioblastoma Multiforme.","authors":"Yanfei Wang, Langping Shen, Mingzhong Sun","doi":"10.2174/0115680096275291231226081320","DOIUrl":"10.2174/0115680096275291231226081320","url":null,"abstract":"<p><strong>Aim: </strong>We aimed to explore the role of urotensin 2 (UTS2) in glioblastoma (GBM).</p><p><strong>Background: </strong>GBM is the most malignant primary brain cancer with a poor prognosis. Previous studies have suggested that GBM vessels undergo dynamic remodeling modulated by tumor vasodilation and vasoconstriction instead of tumor angiogenesis.</p><p><strong>Objective: </strong>Here, we have first investigated the expression and function of UTS2, a potent vasoconstrictor, in GBM.</p><p><strong>Methods: </strong>The mRNA expression profiles and clinical information of GBM patients were obtained from the TCGA database. The clinical relevance of UTS2 was explored by the Mann-Whitney U test and Cox hazard regression survival test. We further explored the role of UTS2 in GBM cell proliferation, migration, and tumor immune microenvironment. Moreover, we established the in vivo mice model to validate its oncogenic effects on GBM progression.</p><p><strong>Results: </strong>Although we did not find significant correlations between UTS2 expression and patients' clinical characteristics, UTS2 was identified as a valid independent prognostic indicator according to multivariate survival analysis. Knockdown of UTS2 resulted in decreased GBM cell proliferation and migration. In addition, functional enrichment analysis implied UTS2 to be involved in the regulation of the immune microenvironment. <i>In vivo</i> studies showed that UTS2 knockdown suppressed GBM xenograft growth, highlighting the tumor-promoting effects of UTS2 on GBM.</p><p><strong>Conclusion: </strong>Our study identified that UTS2 could predict the prognosis of GBM patients and provided evidence regarding its oncogenic effects both <i>in vitro</i> and <i>in vivo</i>.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":"636-647"},"PeriodicalIF":2.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139542003","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Understanding Tankyrase Inhibitors and Their Role in the Management of Different Cancer.","authors":"Sinjini Das, Gowramma Byran, Kaushik Biswas, Kalirajan Rajagopal","doi":"10.2174/0115680096329753241015114119","DOIUrl":"https://doi.org/10.2174/0115680096329753241015114119","url":null,"abstract":"<p><p>Cancer manifests as uncontrolled cell proliferation. Tankyrase, a poly(ADP-ribose) polymerase member, is vital in Wnt signal transmission, making it a promising cancer therapy target. The Wnt/β-catenin pathway regulates critical biological processes like genomic stability, gene expression, energy utilization, and apoptosis. Its dysregulation contributes to cancer development. Targeting tankyrase within this pathway holds the potential for inhibiting aberrant cell growth and promoting programmed cell death, offering a promising avenue for cancer treatment. ADP-ribosylation, a reversible process, modifies proteins post-synthesis, regulating diverse cellular signaling pathways. Transferase enzymes like mono and poly(ADP- ribosyl) transferases transfer ADP-ribose from NAD+ to specific amino acid side chains or ADP-ribose units on target proteins. Blocking tankyrase has emerged as a promising strategy in cancer treatment. This article reviews recent advancements in developing novel tankyrase inhibitors. It delves into structure-activity relationships, molecular docking, polypharmacology profiles, and binding mechanisms at the active site. Insights into lead structure development aid in designing potent anti-cancer medications, shedding light on promising avenues in cancer therapy.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142925956","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GAPVD1 Promotes the Proliferation of Triple-negative Breast Cancer Cells by Regulating the ERK/MAPK Signaling Pathway.","authors":"Lu Wang, Lifen Zhang, Pei Luo, Zeyu Xia, Shan Shao, Qian Ning, Shanzhi Gu, Xinhan Zhao, Minna Luo","doi":"10.2174/0115680096303983240616191051","DOIUrl":"10.2174/0115680096303983240616191051","url":null,"abstract":"<p><strong>Background: </strong>Triple-Negative Breast Cancer (TNBC) accounts for 15-20% of all breast cancers and approximately 50% of breast cancer deaths. Chemotherapy remains the mainstay of systemic treatment due to the lack of effective therapy targets. Thus, more studies are urgently needed to identify new therapeutic targets in TNBC patients.</p><p><strong>Methods: </strong>GAPVD1 expression and prognosis value in breast cancer samples were explored in The Cancer Genome Atlas database (TCGA). GAPVD1 knockdown and overexpression TNBC cell lines were constructed. CCK-8 and colony formation assays were performed to detect cell viability. Flow cytometry analysis was performed to detect cell cycle variation. Western blotting was conducted to determine the levels of target genes. Finally, an enrichment analysis of Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were performed.</p><p><strong>Results: </strong>GAPVD1 is overexpressed in breast cancer tissues and predicts poor prognosis. <i>In vitro</i> experiments demonstrated that GAPVD1 is correlated with cell proliferation and the cell cycle of TNBC cells. Mechanistically, alteration in GAPVD1 expression was found to be associated with cell cycle-related proteins PCNA, Cyclin A, and the activity of the ERK/MAPK signaling pathway. Consistent with these findings, enrichment analysis of GAPVD1-involving partners and signaling pathways revealed that the cellular biosynthetic process, macromolecule biosynthetic process, and cell cycle signaling are related to GAPVD1. <i>In vivo</i> experiment demonstrated that GAPVD1 inhibition impedes tumor growth and expression of cell cycle-related proteins.</p><p><strong>Conclusion: </strong>Taken together, our results indicate that GAPVD1 may participate in TNBC cell growth by regulating the cell cycle and ERK/MAPK signaling pathway.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":"509-519"},"PeriodicalIF":2.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141632922","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Decoding the Expressions, Immune Relevance, and Prognostic Values of Ferroptosis Gene TMEM189: A Pan-cancer Analysis.","authors":"Guanzhong Qiu, Chaoli Song, Meiqing Lou, Jing Lin","doi":"10.2174/0115680096308701240605114342","DOIUrl":"10.2174/0115680096308701240605114342","url":null,"abstract":"<p><strong>Background: </strong>TMEM189 is a recently discovered transmembrane protein involved in ether glycerophospholipid synthesis and ferroptosis regulation. However, its role in tumors is not well understood.</p><p><strong>Objective: </strong>This study aimed to elucidate the oncogenic effects and prognostic values of TMEM189 in tumors.</p><p><strong>Methods: </strong>We performed a pan-cancer analysis of TMEM189 using various databases, bioinformatics and statistical tools, and tissue microarray analysis.</p><p><strong>Results: </strong>TMEM189 was upregulated in tumors compared to normal tissues. High TMEM189 expression was found to be linked to reduced promoter methylation. Moreover, TMEM189 exhibited a negative correlation with immunogenic markers, immune cell infiltration, and expression of Immune Checkpoint Genes (ICGs) in most cancers, implicating its immunosuppressive role in tumor microenvironments (TME). The genes that interact and are similar to TMEM189 were involved in hotspot signaling pathways in pan-cancer. TMEM189 overexpression was found to be usually associated with poor prognosis, especially an independent prognostic risk factor for BLCA, BRCA, LUAD, MESO, LIHC, and SKCM.</p><p><strong>Conclusion: </strong>TMEM189 is overexpressed and exerts immunosuppressive effects in many tumors with a significant association with poor prognosis, suggesting its potential as a therapeutic target in cancer treatment.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":"520-537"},"PeriodicalIF":2.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141455802","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gamma-tocotrienol Inhibits Proliferation and Growth of HSD17B4 Overexpressing HepG2 Liver Cancer Cells.","authors":"Xiaoming Wang, Xijia Liang, Nan Zhang, Yaqi Wang, Meng Hu, Yun Shi, Min Yao, Lianguo Hou, Lingling Jiang","doi":"10.2174/0115680096319171240623091614","DOIUrl":"10.2174/0115680096319171240623091614","url":null,"abstract":"<p><strong>Introduction: </strong>Hydroxysteroid 17-beta dehydrogenase 4 (HSD17B4) is involved in the progression of hepatocellular carcinoma (HCC).</p><p><strong>Aims: </strong>This study aimed to investigate the inhibitory effect of gamma-tocotrienol (γ-T3) on the proliferation and growth of HSD17B4-overexpressing HepG2 cells.</p><p><strong>Methods: </strong>HepG2 cells were transfected with empty or HSD17B4-overexpressing plasmids, followed by vitamin E (VE) or γ-T3 treatment. MTS assay, Western blotting, qRT-PCR, and flow cytometry were employed to assess cell proliferation, protein expression, mRNA levels, and apoptosis. HSD17B4 interaction with γ-T3 was assessed by quantifying γ-T3 in the collected precipitate of HSD17B4 using anti-flag magnetic beads. Tumor xenografts were established in NSG mice, and tumor growth was monitored.</p><p><strong>Results: </strong>HSD17B4 overexpression significantly promoted HepG2 cell proliferation, which was effectively counteracted by VE or γ-T3 treatment in a dose-dependent manner. VE and γ-T3 did not exert their effects through direct regulation of HSD17B4 expression. Instead, γ-T3 was found to interact with HSD17B4, inhibiting its activity in catalyzing the conversion of estradiol (E2) into estrone. Moreover, γ-T3 treatment led to a reduction in cyclin D1 expression and suppressed key proliferation signaling pathways, such as ERK, MEK, AKT, and STAT3. Additionally, γ-T3 promoted apoptosis in HSD17B4-overexpressing HepG2 cells. In an in vivo model, γ-T3 effectively reduced the growth of HepG2 xenograft tumors.</p><p><strong>Conclusion: </strong>In conclusion, our study demonstrates that γ-T3 exhibits potent anti-proliferative and anti-tumor effects against HepG2 cells overexpressing HSD17B4. These findings highlight the therapeutic potential of γ-T3 in HCC treatment and suggest its role in targeting HSD17B4-associated pathways to inhibit tumor growth and enhance apoptosis.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":"170-182"},"PeriodicalIF":2.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141455803","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An Overview of the Dichotomous Role of Microbiota in Cancer Progression and Management.","authors":"Pooja Jain, Sradhanjali Mohapatra, Uzma Farooq, Nazia Hassan, Mohd Aamir Mirza, Zeenat Iqbal","doi":"10.2174/0115680096282503240124104029","DOIUrl":"10.2174/0115680096282503240124104029","url":null,"abstract":"<p><p>It is a well-known fact that cancer is considered the second leading cause of mortality across the globe. Although the human oral cavity and intestine are the natural habitat of thousands of microbes, dysbiosis results in malignancies, such as oral squamous cell carcinoma and colorectal cancer. Amongst the intestinal microbes, <i>H. pylori</i> is a deadly carcinogen. Also, causative pathogens for the development of pancreatic and colorectal cancer are found in the oral cavity, such as <i>Fusobacterium nucleatum</i> and <i>Porphyromonas gingivalis</i>. Many periodontopathic micro- organisms, like <i>Streptococcus</i> sp., Peptostreptococcus sp., Prevotella sp., Fusobacterium sp., Porphyromonas gingivalis, and Capnocytophaga gingivalis, strongly have an impact on the development of oral cancers. Three basic mechanisms are involved in pathogen-mediated cancer development, like chronic inflammation-mediated angiogenesis, inhibition of cellular apoptosis, and release of carcinogenic by-products. Microbiota has a dichotomous role to play in cancer, i.e., microbiota can be used for cancer management too. Shreds of evidence are there to support the fact that microbiota enhances the chemotherapeutic drug efficacy. This review presents the possible mechanism of the oncogenic effect of microbiota with emphasis on the oral microbiome and also attempts to explain the intricate role of microbiota in cancer management.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":"38-48"},"PeriodicalIF":2.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139971252","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LncRNA DERCNC in Hepatocellular Carcinoma with Cirrhosis Aggravates Tumor Proliferation by Targeting SOX9.","authors":"Yun-Bing Wang, Haitham Salameen, Yi-Yu Hu, Shi-Ji Zhou, Jun-Hua Gong","doi":"10.2174/0115680096310229240626102449","DOIUrl":"10.2174/0115680096310229240626102449","url":null,"abstract":"<p><strong>Purpose: </strong>This study aims to understand the role of cirrhosis in promoting hepatocellular carcinoma (HCC) progression by analyzing the differential expression of long noncoding RNAs (lncRNAs) between cirrhotic hepatocellular carcinoma (CHCC) and noncirrhotic hepatocellular carcinoma (NCHCC).</p><p><strong>Methods: </strong>A transcriptional profile array was used to identify differentially expressed lncRNAs. Subsequently, a specific lncRNA was selected to evaluate the clinical significance, potential functions, regulatory targets, and pathways through both <i>in vitro</i> and <i>in vivo</i> experiments.</p><p><strong>Results: </strong>The study identified a lncRNA, which we termed DERCNC, an acronym for Differentially Expressed RNA between Cirrhotic and Non-Cirrhotic HCC. DERCNC was significantly more highly expressed in CHCC than in NCHCC. Clinically, elevated levels of DERCNC expression were positively correlated with both the cirrhotic state and tumor stage and inversely correlated with tumor differentiation. Furthermore, high expression of DERCNC was associated with a poor prognosis for patients. Conditioned medium from the hepatic stellate cell (LX2) was found to enhance DERCNC expression, SOX9 expression, and tumor proliferation. Overexpression of DERCNC similarly promoted tumor proliferation and increased SOX9 levels. Conversely, DERCNC silencing resulted in the opposite effects. Moreover, the pro-proliferative function of DERCNC was reversible through the modulation of SOX9 expression. Further mechanistic studies revealed that DERCNC upregulated SOX9 by increasing the enrichment of H3K27ac modifications near the SOX9 promoter.</p><p><strong>Conclusion: </strong>In conclusion, DERCNC expression in CHCC has significant clinical implications and can aggravate tumor proliferation by targeting SOX9. This represents a novel mechanism by which cirrhosis promotes tumor progression.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":"665-679"},"PeriodicalIF":2.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141747584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to: Low Expression MCEMP1 Promotes Lung Adenocarcinoma Progression and its Clinical Value.","authors":"Liqun Ling, Tianqi Hu, Chenkang Zhou, Shuhui Chen, Lunan Chou, Yuxin Chen, Zhaoting Hu, Kate Huang, Jie Chen, Yumin Wang, Junjun Wang","doi":"10.2174/1568009625999250210092856","DOIUrl":"https://doi.org/10.2174/1568009625999250210092856","url":null,"abstract":"<p><p>An error was noted on the page number 281, paragraph 1, of the article entitled \"Low Expression MCEMP1 Promotes Lung Adenocarcinoma Progression and its Clinical Value\" published in Current Cancer Drug Targets, 2025, 25(3), 281-293 [1], A phrase \"continued=\" yes\"\" was erroneously added which has now been removed. Details of the error and a correction are provided here. ORIGINAL: 1. INTRODUCTION It is worth noting that according to the 2020 Global Cancer Report statistics, LUAD has an incidence rate of 11.4%, ranking second after breast cancer (11.7%), but the mortality rate of LUAD is still the first, accounting for 18.0% of the total cancer deaths [1]. LUAD is the most common in non-small cell lung cancer (NSCLC), and LUAD is the main pathological subtype of NCSLC [2]. Because most patients with LUAD lack clear symptoms and signs in the early stage of the lesion, most of the lesions are in the middle and late stage, and most patients eventually die due to tumor recurrence, metastasis, and drug resistance, the long-term prognosis of patients with LUAD is still poor [3-6]. continued=\" yes\" Therefore, it has become one of the pathogen-esis and evolution mechanisms of LUAD and the more specific molecular targets, diagnosis and prognosis of LUAD at home and abroad. CORRECTED: 1. INTRODUCTION It is worth noting that according to the 2020 Global Cancer Report statistics, LUAD has an incidence rate of 11.4%, ranking second after breast cancer (11.7%), but the mortality rate of LUAD is still the first, accounting for 18.0% of the total cancer deaths [1]. LUAD is the most common in non-small cell lung cancer (NSCLC), and LUAD is the main pathological subtype of NCSLC [2]. Because most patients with LUAD lack clear symptoms and signs in the early stage of the lesion, most of the lesions are in the middle and late stage, and most patients eventually die due to tumor recurrence, metastasis, and drug resistance, the long-term prognosis of patients with LUAD is still poor [3-6]. Therefore, it has become one of the pathogenesis and evolution mechanisms of LUAD and the more specific molecular targets, diagnosis and prognosis of LUAD at home and abroad. We regret the error and apologize to readers. The original article can be found online at: https://www.eurekaselect.com/article/140008.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":"25 6","pages":"680"},"PeriodicalIF":2.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149982","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}