Molecular Carcinogenesis最新文献_第5页

ENC1 Promotes the Malignant Progression and Metastasis by Suppressing TRIM21 Mediated Vimentin Degradation in Wilms Tumor. ENC1通过抑制TRIM21介导的维entin降解促进Wilms肿瘤的恶性进展和转移。

IF 3 2区医学

Molecular Carcinogenesis Pub Date : 2025-04-13 DOI: 10.1002/mc.23918

Zhiyi Lu, Hongjie Gao, Fan Huang, Zuohui Zhao, Jiawei Chen, Fengyin Sun

{"title":"ENC1 Promotes the Malignant Progression and Metastasis by Suppressing TRIM21 Mediated Vimentin Degradation in Wilms Tumor.","authors":"Zhiyi Lu, Hongjie Gao, Fan Huang, Zuohui Zhao, Jiawei Chen, Fengyin Sun","doi":"10.1002/mc.23918","DOIUrl":"https://doi.org/10.1002/mc.23918","url":null,"abstract":"Ectodermal neural cortex 1 (ENC1) is significantly upregulated in various cancers and shows a positive correlation with poor prognosis and advanced clinical stages, such as colorectal cancer, endometrial cancer and breast cancer. However, the role of ENC1 in Wilms tumor (WT) has not been previously reported. In this study, we conducted several in vitro functional experiments and established xenograft models to confirm the oncogenic potential of ENC1. The binding proteins of ENC1 were identified through co-immunoprecipitation and mass spectrometry to screen the mechanism of malignant progression. Further analysis elucidated the mechanism by which ENC1 promotes tumorigenesis. The results demonstrated that ENC1 was significantly overexpressed in tumor and recurrence samples, with elevated ENC1 expression showing a significant negative correlation with both overall survival and recurrence-free survival of patients. Functionally, the role of ENC1 in tumor oncogenicity was elucidated through the assessment of tumor cell proliferation, migration, and invasion capabilities. Mechanistically, through immunoprecipitation and mass spectrometry, we identified Vimentin as an interacting protein of ENC1. ENC1 competed with the E3 ubiquitin ligase TRIM21 for Vimentin binding, thereby reducing the ubiquitination level of Vimentin and enhancing its protein stability. In conclusion, this study demonstrates that ENC1 functions as a novel oncogenic target for Wilms tumor by disrupting TRIM21-mediated ubiquitination of Vimentin, which presents novel insights for the treatment of Wilms tumor and the development of prognostic markers.","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143990591","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Potential Value of AURKA and CDK6 Amplification for the Response of Patients With Gastric Cancer to Neoadjuvant Chemotherapy. AURKA和CDK6扩增对胃癌患者新辅助化疗反应的潜在价值

IF 3 2区医学

Molecular Carcinogenesis Pub Date : 2025-04-13 DOI: 10.1002/mc.23921

Yuen Tan, Yao Xing, Shuai Yuan, Fan Sun, Xiaohui Lin, Simeng Bao, Dongyue Jiang, Jianjun Zhang, Shu-Lan Sun

{"title":"Potential Value of AURKA and CDK6 Amplification for the Response of Patients With Gastric Cancer to Neoadjuvant Chemotherapy.","authors":"Yuen Tan, Yao Xing, Shuai Yuan, Fan Sun, Xiaohui Lin, Simeng Bao, Dongyue Jiang, Jianjun Zhang, Shu-Lan Sun","doi":"10.1002/mc.23921","DOIUrl":"https://doi.org/10.1002/mc.23921","url":null,"abstract":"Many patients respond poorly to neoadjuvant chemotherapy (NACT), negatively affecting the surgical success rate. Identifying effective biomarkers and understanding the potential resistance mechanisms are urgently needed. Data of 18 patients with advanced stomach cancer who were treated with NACT categorized according to tumor regression grade into major histological response (MJHR) and nonhistological response (NHR) groups were retrospectively analyzed. Genomic signatures associated with the response to NACT were identified using whole-exome and RNA sequencing. Extraction of molecular signatures revealed increased deficient mismatch repair signature and tumor mutation levels in the NHR group. Compared to the MJHR group, the NHR group was also characterized by a greater number of copy number alterations (p = 0.08), which was further confirmed by RNA sequencing, and upregulation of aurora kinase A (AURKA) (p = 0.05) and cyclin-dependent kinase 6 (CDK6) (p = 0.049). Western blot analysis and immunohistochemical analyses further confirmed high CDK6 (p < 0.01/p < 0.0001) and AURKA (p < 0.01/p < 0.001) expression levels in the NHR group. Finally, palbociclib, an inhibitor of CDK4/6, effectively inhibited the proliferation (p < 0.05) and induced apoptosis of oxaliplatin-resistant gastric cancer cells (p < 0.01) in vitro. These findings support the potential value of AURKA and CDK6 amplification, as well as their effects on the tumor microenvironment, in predicting poor outcomes of NACT in patients with locally advanced gastric cancer. Thus, CDK4/6 inhibitors could be used to treat NACT-resistant patients with gastric cancer.","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144029148","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Four-gene Prognostic Signature and Risk of Brain Metastasis of Lung Adenocarcinoma. 肺腺癌脑转移的四基因预后特征及风险分析。

IF 3 2区医学

Molecular Carcinogenesis Pub Date : 2025-04-13 DOI: 10.1002/mc.23922

Zheng Gong, Fengyuan Yu, Chen Li, Bingying Zhao, Miaowei Wen, Shanshan Zhang, Zhezhe Xu, Ailu Wu, Rukun Zang, Yuan Li, Hongwei Li, Yipeng Song

{"title":"Four-gene Prognostic Signature and Risk of Brain Metastasis of Lung Adenocarcinoma.","authors":"Zheng Gong, Fengyuan Yu, Chen Li, Bingying Zhao, Miaowei Wen, Shanshan Zhang, Zhezhe Xu, Ailu Wu, Rukun Zang, Yuan Li, Hongwei Li, Yipeng Song","doi":"10.1002/mc.23922","DOIUrl":"https://doi.org/10.1002/mc.23922","url":null,"abstract":"Brain metastasis has a high incidence and poor prognosis in lung adenocarcinoma (LUAD). We sought to identify genes associated with LUAD brain metastasis and with the prognosis of patients with LUAD. Differential gene expression analysis was performed on LUAD patients with and without distant metastasis from the Cancer Genome Atlas (TCGA) database and LUAD patients with and without brain metastasis from the GEO GSE14108 and GSE10072 data sets. Subsequently, a LASSO model was constructed using the genes differentially expressed in both analyses to screen for prognostic genes. A risk model based on 11 genes was established by screening prognostic genes. Subsequently, a prognostic prediction model was developed based on the risk model. Expression and survival analysis of the identified genes in metastatic LUAD was assessed. As a result, differential gene expression analysis indicated that compared to primary lung cancer, the expression of CMAS, NEK2, and SHCBP1 was significantly upregulated in metastatic lung cancer, whereas the expression of IL2 was significantly downregulated. Additionally, these genes exhibited strong correlations with the overall survival of LUAD patients. Finally, compared with LUAD patients without brain metastasis, immunohistochemistry analysis verified CMAS, NEK2, and SHCBP1 exhibited increased expression in LUAD with brain metastasis.","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144037099","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Correction to "Cucurbitacin B Induces Inhibitory Effects via CIP2A/PP2A/Akt Pathway in Glioblastoma Multiforme". 更正“葫芦素B通过CIP2A/PP2A/Akt通路诱导多形性胶质母细胞瘤的抑制作用”。

IF 3 2区医学

Molecular Carcinogenesis Pub Date : 2025-04-07 DOI: 10.1002/mc.23917

引用次数: 0

Diagnostic Utility of microRNA146a and microRNA19a in Gallbladder Cancer: A Pilot Study. 胆囊癌中 microRNA146a 和 microRNA19a 的诊断效用：一项试点研究

IF 3 2区医学

Molecular Carcinogenesis Pub Date : 2025-04-06 DOI: 10.1002/mc.23916

Rahul Saxena, Sarath Krishnan Mp, Amit Gupta, Sweety Gupta, Anissa A Mirza, Nitin Chaudhary, Bela Goyal

{"title":"Diagnostic Utility of microRNA146a and microRNA19a in Gallbladder Cancer: A Pilot Study.","authors":"Rahul Saxena, Sarath Krishnan Mp, Amit Gupta, Sweety Gupta, Anissa A Mirza, Nitin Chaudhary, Bela Goyal","doi":"10.1002/mc.23916","DOIUrl":"https://doi.org/10.1002/mc.23916","url":null,"abstract":"Gallbladder cancer (GBC) is a rare but aggressive malignancy, often diagnosed at advanced stages due to its asymptomatic progression and lack of reliable biomarkers. Chronic inflammation plays a crucial role in its pathogenesis, with inflammatory pathways contributing to tumor development. This study evaluates the diagnostic potential of microRNA19a and microRNA146a, key regulators of inflammatory and oncogenic pathways, in distinguishing GBC from cholelithiasis and healthy controls. An observational analytical study was conducted on 60 participants, divided into three groups: GBC (n = 20), cholelithiasis (n = 20), and non-dysplastic/healthy controls (n = 20). microRNA expression levels in tissue and plasma samples were quantified using RT-PCR and qPCR, with ΔCq values normalized to U6 RNA. Receiver Operating Characteristic (ROC) analysis assessed diagnostic performance, and correlations between tissue and plasma expression levels were examined. Most GBC cases (65%) were diagnosed at Stage IV, with 75% showing liver infiltration. microRNA19a and microRNA146a expression levels were significantly elevated in GBC tissues compared to the other groups (p < 0.0001). Plasma microRNA146a demonstrated high diagnostic accuracy, with an AUC of 0.953, sensitivity of 80%, and specificity of 95%, outperforming microRNA19a (AUC 0.388, sensitivity 20%, specificity 95%). Strong positive correlations between tissue and plasma expression were observed for microRNA146a (r = 0.693, p = 0.0007) and microRNA19a (r = 0.564, p = 0.010), supporting their potential as circulating biomarkers. microRNA146a exhibits good diagnostic utility in differentiating GBC, particularly in advanced disease stages, while microRNA19a reflects inflammation-driven carcinogenesis. Plasma-based microRNA detection offers a promising noninvasive diagnostic approach for early and accurate GBC detection. Further large-scale studies are warranted to validate these biomarkers and explore their therapeutic implications.","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-04-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143795705","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

VPS45 Contributes to the Progression of Hepatocellular Carcinoma by Triggering the Wnt/β-Catenin Signaling Pathway. VPS45通过触发Wnt/β-Catenin信号通路参与肝细胞癌的进展

IF 3 2区医学

Molecular Carcinogenesis Pub Date : 2025-04-01 Epub Date: 2025-01-21 DOI: 10.1002/mc.23884

Renhou Zhi, Qi Li, Huiqin Zhang, Fan Fan

{"title":"VPS45 Contributes to the Progression of Hepatocellular Carcinoma by Triggering the Wnt/β-Catenin Signaling Pathway.","authors":"Renhou Zhi, Qi Li, Huiqin Zhang, Fan Fan","doi":"10.1002/mc.23884","DOIUrl":"10.1002/mc.23884","url":null,"abstract":"Vacuolar protein sorting 45 (VPS45) has recently been implicated in the development of ovarian cancer and non-small cell lung cancer. However, its role in the onset and progression of hepatocellular carcinoma (HCC) remains unclear. This study aims to elucidate the function of VPS45 in HCC. Bioassays were conducted to assess the prognostic significance of VPS45 in HCC. Techniques such as western blotting and real-time quantitative polymerase chain reaction (qRT-PCR) were used to confirm the expression levels of VPS45 in HCC tissues and cell lines, as well as to evaluate the expression of downstream effectors in its potential tumorigenic pathways. The impact of VPS45 on HCC cell invasion, proliferation, and migration was assessed using the Cell Counting Kit-8 (CCK-8), wound healing, and transwell assays. Furthermore, the effect of VPS45 on HCC tumorigenesis in vivo was evaluated through subcutaneous tumor formation assays in BALB/c nude mice. VPS45 is markedly overexpressed in both HCC tissues and cell lines. Its expression escalates with advancing tumor grade and clinical stage, and high VPS45 levels are indicative of poor prognosis. In vitro experiments revealed that VPS45 overexpression significantly boosts HCC cell proliferation, migration, and invasion. Conversely, VPS45 knockdown hindered HCC progression in vivo. Investigation into pathway protein expression suggests that VPS45 facilitates HCC progression through its involvement in the Wnt/β-catenin signaling pathway. The overexpression of VPS45 contributes to the development of malignant phenotypes in HCC cells, resulting in a poor prognosis. Targeting VPS45 may offer a viable therapeutic strategy for managing HCC.","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":"744-755"},"PeriodicalIF":3.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11890426/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143008768","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

RNF7-Mediated ROS Targets Malignant Phenotype and Radiotherapy Sensitivity in Glioma With Different IDH1 Genotypes. rnf7介导的ROS靶向不同IDH1基因型胶质瘤的恶性表型和放疗敏感性

IF 3 2区医学

Molecular Carcinogenesis Pub Date : 2025-04-01 Epub Date: 2025-01-09 DOI: 10.1002/mc.23876

Yiran Tao, Zimin Shi, Xianyin Liang, Yuqian Zheng, Lirui Dai, Xiang Li, Zian Li, Wulong Liang, Gaojie Bai, Hao Li, Yuan Lyu, Junqi Li, Tao Zhang, Weihua Hu, Shaolong Zhou, Qiao Shan, Xudong Fu, Xinjun Wang

{"title":"RNF7-Mediated ROS Targets Malignant Phenotype and Radiotherapy Sensitivity in Glioma With Different IDH1 Genotypes.","authors":"Yiran Tao, Zimin Shi, Xianyin Liang, Yuqian Zheng, Lirui Dai, Xiang Li, Zian Li, Wulong Liang, Gaojie Bai, Hao Li, Yuan Lyu, Junqi Li, Tao Zhang, Weihua Hu, Shaolong Zhou, Qiao Shan, Xudong Fu, Xinjun Wang","doi":"10.1002/mc.23876","DOIUrl":"10.1002/mc.23876","url":null,"abstract":"RNF7 (Ring Finger Protein 7) is a key component of CRLs (Cullin-RING-type E3 ubiquitin ligases) and has been found to possess intrinsic anti-ROS capabilities. Aberrant expression of RNF7 has been observed in various tumor types and is known to significantly influence tumor initiation and progression. However, the specific role of RNF7 in glioblastoma remains unclear. IDH (isocitrate dehydrogenase) mutations, which induce metabolic reprogramming and result in notable heterogeneity among glioma with different IDH genotypes. Through analysis of public glioma databases, we identified a high expression of RNF7 in glioma and its correlation with patient prognosis. Moreover, we observed variations in RNF7 expression and its association with patient outcomes under different treatment modalities among different IDH genotypes. In this study, we demonstrated the critical role of RNF7 in the malignant phenotype of IDH1-mutant glioma and its contribution to radiation resistance. Subsequent functional enrichment analysis of RNF7 in glioma, coupled with validation through cellular experiments, confirmed its significant involvement in maintaining redox balance. Our findings suggest that RNF7 exerts a buffering effect against radiation-induced oxidative stress and counterbalances the redox stress induced by IDH1 mutation through its anti-ROS activity. Additionally, our follow-up investigations revealed that the upregulation of RNF7 after radiation exposure and in IDH1-mutant glioma cells is induced by ROS. Collectively, our study underscores the potential of RNF7 as a molecular biomarker in glioma. Elevated RNF7 expression often indicates a heightened metabolic resilience in glioma, leading to resistance against radiotherapy.","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":"652-667"},"PeriodicalIF":3.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11890431/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142952059","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

FKBP Prolyl Isomerase 11: A Novel Oncogene Interacting With SRSF1 in Esophageal Squamous Cell Carcinoma. FKBP脯氨酸异构酶11：食管癌中与SRSF1相互作用的新癌基因

IF 3 2区医学

Molecular Carcinogenesis Pub Date : 2025-04-01 Epub Date: 2025-01-08 DOI: 10.1002/mc.23877

Zheng Ding, Zhichao Hou, Tangjuan Zhang, Peng Wang, Xue Pan, Xiangnan Li, Song Zhao

{"title":"FKBP Prolyl Isomerase 11: A Novel Oncogene Interacting With SRSF1 in Esophageal Squamous Cell Carcinoma.","authors":"Zheng Ding, Zhichao Hou, Tangjuan Zhang, Peng Wang, Xue Pan, Xiangnan Li, Song Zhao","doi":"10.1002/mc.23877","DOIUrl":"10.1002/mc.23877","url":null,"abstract":"Esophageal squamous cell carcinoma (ESCC) is one of the main subtypes of esophageal carcinoma with high morbidity. This study aimed to explore the role of FKBP prolyl isomerase 11 (FKBP11) in ESCC and investigate the underlying mechanism. FKBP11 levels in ESCC tumor tissues and cell lines were measured. Cell function assays were conducted to evaluate the role of FKBP11 in ESCC cells. The xenograft mouse model was established to validate the effect of FKBP11 on ESCC tumorigenesis in vivo. The co-immunoprecipitation assay was performed to determine the FKBP11-interacting proteins. Obvious upregulations in FKBP11 expression were found in ESCC tumor tissues and cell lines. In vitro, FKBP11 knockdown weakened cell proliferation, migration, and invasion capacities and reinforced cell apoptosis in ESCC cells. In vivo, FKBP11 knockdown slowed ESCC tumorigenesis. The following mechanism investigation determined serine and arginine-rich splicing factor 1 (SRSF1) as the FKBP11-interacting protein in ESCC cells. FKBP11 directly bound to SRSF1 and FKBP11 knockdown decreased SRSF1 mRNA level. SRSF1 overexpression abrogated the inhibitory effect of FKBP11 knockdown on the proliferation and migration of ESCC cells. KBP11 functions as an oncogene in ESCC by targeting SRSF1.","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":"638-651"},"PeriodicalIF":3.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142952056","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

LncRNA FGD5-AS1 Facilitates Hepatocellular Carcinoma Cell Stemness by Enhancing PKD1 mRNA Stability Through Binding With MSI2. LncRNA FGD5-AS1通过与MSI2结合增强PKD1 mRNA稳定性，促进肝癌细胞的干细胞性

IF 3 2区医学

Molecular Carcinogenesis Pub Date : 2025-04-01 Epub Date: 2025-01-13 DOI: 10.1002/mc.23873

Chenkun He, Rongrong Liu, Tianli Zhou

{"title":"LncRNA FGD5-AS1 Facilitates Hepatocellular Carcinoma Cell Stemness by Enhancing PKD1 mRNA Stability Through Binding With MSI2.","authors":"Chenkun He, Rongrong Liu, Tianli Zhou","doi":"10.1002/mc.23873","DOIUrl":"10.1002/mc.23873","url":null,"abstract":"Hepatocellular carcinoma (HCC) is a major global health concern that accounts for more than 80% of all primary hepatic carcinomas. The long noncoding RNA FGD5 antisense RNA 1 (FGD5-AS1) has been linked to HCC cell stemness and proliferation. However, the exact function of FGD5-AS1 in HCC remains unclear. Cell viability and proliferation were examined using the CCK8 and colony formation assays, respectively. Cell stemness was examined using a sphere formation assay. To investigate the relation between Musashi 2 (MSI2) and FGD5-AS1 (or protein kinase D1 [PKD1]), RNA immunoprecipitation and RNA pull-down assays were used. Furthermore, a xenograft mouse model was established to evaluate the function of FGD5-AS1 in vivo. FGD5-AS1, MSI2, and PKD1 were upregulated in the HCC tissues. FGD5-AS1 knockdown significantly inhibited the viability, proliferation, and stemness of HCC cells and decreased the expression of MSI2, PKD1, octamer-binding transcription factor 4, SOX2, NANOG, and Prominin-1 in HCC cells. Mechanistically, FGD5-AS1 increased PKD1 mRNA stability by upregulating MSI2 expression. Both MSI2 and PKD1 ameliorated sh-FGD5-AS1's inhibition of HCC cell viability, proliferation, and stemness. Furthermore, FGD5-AS1 silencing inhibited HCC tumor growth and stemness in vivo. FGD5-AS1 promotes the stemness of HCC cells by activating the MSI2/PKD1 axis. Our study provides a new theoretical foundation for the development of novel HCC treatments.","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":"680-690"},"PeriodicalIF":3.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142971483","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

β-Elemene Inhibits Adrenocortical Carcinoma Cell Proliferation and Migration, and Induces Apoptosis by Up-Regulating miR-486-3p/Targeting NPTX1 Axis. β-榄香烯通过上调miR-486-3p/靶向NPTX1轴抑制肾上腺皮质癌细胞增殖和迁移，诱导细胞凋亡。

IF 3 2区医学

Molecular Carcinogenesis Pub Date : 2025-04-01 Epub Date: 2025-01-13 DOI: 10.1002/mc.23879

Yan Lin, Tailin Guo, Lishuang Che, Jieqiong Dong, Ting Yu, Chaiming Zeng, Ziyu Wu

{"title":"β-Elemene Inhibits Adrenocortical Carcinoma Cell Proliferation and Migration, and Induces Apoptosis by Up-Regulating miR-486-3p/Targeting NPTX1 Axis.","authors":"Yan Lin, Tailin Guo, Lishuang Che, Jieqiong Dong, Ting Yu, Chaiming Zeng, Ziyu Wu","doi":"10.1002/mc.23879","DOIUrl":"10.1002/mc.23879","url":null,"abstract":"β-elemene has a variety of anti-inflammatory, antioxidant, and antitumor effects. Currently, the influence of β-elemene on adrenocortical carcinoma (ACC) malignant progression and action mechanism remains unclear. This research aims to explore the influence and action mechanism of β-elemene on ACC progression. The impacts of β-elemene on ACC cell viability, proliferation, migration, and apoptosis were investigated through CCK-8 assay, clone formation assay, Transwell experiment, Wound healing assay, and flow cytometry. The miR-486-3p expression was analyzed utilizing RT-qPCR. According to different databases, neuronal pentraxin 1 (NPTX1) is the predicted downstream target gene of miR-486-3p. Western blot and RT-qPCR were utilized to examine NPTX1 expression. Silencing miR-486-3p or Overexpression NPTX1 in ACC cells further explored whether β-elemene affects ACC cells by regulating miR-486-3p/NPTX1. Finally, a subcutaneous graft tumor model was constructed to investigate how β-elemene may impact tumor growth in vivo. β-elemene decreased the cell viability, hindered cell proliferation and migration capacity, and induced apoptosis of ACC cells. miR-486-3p level in ACC cells was notably reduced in comparison to normal cells, but treatment with β-elemene markedly increased miR-486-3p expression. Additionally, ACC cells showed high level of NPTX1, while miR-486-3p targeted negative regulation of NPTX1. Overexpression miR-486-3p hindered the malignant progression of ACC cells, whereas overexpression NPTX1 reversed the impact of overexpression miR-486-3p. Silencing miR-486-3p or overexpression NPTX1 both attenuated the suppressive influence of β-elemene on the malignant behavior of ACC cells. Additionally, tumor growth was suppressed and apoptosis was induced in tumor cells in vivo by β-elemene. In conclusion, β-elemene reduces ACC cell viability, hinders proliferation and migration, and induces apoptosis through the miR-486-3p/NPTX1 axis.","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":"691-702"},"PeriodicalIF":3.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142971634","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0