Carcinogenesis最新文献_第7页

LncRNA UCA1 promotes vasculogenic mimicry by targeting miR-1-3p in gastric cancer. LncRNA UCA1通过靶向miR-1-3p促进胃癌血管生成模拟。

IF 3.3 3区医学

Carcinogenesis Pub Date : 2024-09-11 DOI: 10.1093/carcin/bgae031

Yida Lu, Bo Yang, Aolin Shen, Kexun Yu, MengDi Ma, Yongxiang Li, Huizhen Wang

{"title":"LncRNA UCA1 promotes vasculogenic mimicry by targeting miR-1-3p in gastric cancer.","authors":"Yida Lu, Bo Yang, Aolin Shen, Kexun Yu, MengDi Ma, Yongxiang Li, Huizhen Wang","doi":"10.1093/carcin/bgae031","DOIUrl":"10.1093/carcin/bgae031","url":null,"abstract":"Long noncoding RNA urothelial carcinoma-associated 1 (UCA1) has been implicated in several tumors. UCA1 promotes cell proliferation, migration, and invasion of gastric cancer (GC) cells, but the molecular mechanism has not been fully elucidated. This study revealed the oncogenic effects of UCA1 on cell growth and invasion. Furthermore, UCA1 expression was significantly correlated with the overall survival of GC patients, and the clinicopathological indicators, including tumor size, depth of invasion, lymph node metastasis, and TNM stage. Additionally, miR-1-3p was identified as a downstream target of UCA1, which was negatively regulated by UCA1. MiR-1-3p inhibited cell proliferation and vasculogenic mimicry (VM), and induced cell apoptosis by upregulating BAX, BAD, and tumor suppressor TP53 expression levels. Moreover, miR-1-3p almost completely reversed the oncogenic effect caused by UCA1, including cell growth, migration, and VM formation. This study also confirmed that UCA1 promoted tumor growth in vivo. In this study, we also revealed the correlation between UCA1 and VM formation, which is potentially crucial for tumor metastasis. Meanwhile, its downstream target miR-1-3p inhibited VM formation in GC cells. In summary, these findings indicate that the UCA1/miR-1-3p axis is a potential target for GC treatment.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":"658-672"},"PeriodicalIF":3.3,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140915905","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}

引用次数: 0

Correction to: Epigenetic silencing of O6 -methylguanine DNA methyltransferase gene in NiS-transformed cells. 更正：NiS 转化细胞中 O6 -methylguanine DNA 甲基转移酶基因的表观遗传沉默。

IF 3.3 3区医学

Carcinogenesis Pub Date : 2024-09-11 DOI: 10.1093/carcin/bgae050

引用次数: 0

Transposable elements alter gene expression and may impact response to cisplatin therapy in ovarian cancer. 可转座元件会改变基因表达，并可能影响卵巢癌患者对顺铂疗法的反应。

IF 3.3 3区医学

Carcinogenesis Pub Date : 2024-09-11 DOI: 10.1093/carcin/bgae029

Daniela Moreira Mombach, Rafael Luiz Vieira Mercuri, Tiago Minuzzi Freire da Fontoura Gomes, Pedro A F Galante, Elgion Lucio Silva Loreto

{"title":"Transposable elements alter gene expression and may impact response to cisplatin therapy in ovarian cancer.","authors":"Daniela Moreira Mombach, Rafael Luiz Vieira Mercuri, Tiago Minuzzi Freire da Fontoura Gomes, Pedro A F Galante, Elgion Lucio Silva Loreto","doi":"10.1093/carcin/bgae029","DOIUrl":"10.1093/carcin/bgae029","url":null,"abstract":"Cisplatin is widely employed for cancer treatment; therefore, understanding resistance to this drug is critical for therapeutic practice. While studies have delved into differential gene expression in the context of cisplatin resistance, findings remain somewhat scant. We performed a comprehensive investigation of transposable elements (TEs) expression and their impact in host genes in two cisplatin-treated ovarian cancer cell lines. RNA-seq, ATAC-seq, and in-depth bioinformatics analysis were used to compare cisplatin-sensitive and -resistant ovarian cancer cell lines. Our results reveal that cisplatin therapy alters not only the expression of protein-coding genes, but also key TEs, including LINE1, Alu, and endogenous retroviruses, in both cisplatin-sensitive and -resistant cell lines. By co-expressing with downstream genes or by creating chimeric transcripts with host genes at their insertion sites, these TEs seem to control the expression of protein-coding genes, including tumor-related genes. Our model uncovers TEs influencing the expression of cancer genes and cancer pathways. Collectively, our findings indicate that TE alterations associated with cisplatin treatment occur in critical cancer genes and cellular pathways synergically. This research highlights the importance of considering the entire spectrum of transcribed elements in the genome, especially TE expression, for a complete understanding of complex models like cancer response to treatment.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":"685-695"},"PeriodicalIF":3.3,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140897355","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}

引用次数: 0

Exosomal circPVT1 promotes angiogenesis in laryngeal cancer by activating the Rap1b-VEGFR2 signaling pathway. 外泌体 circPVT1 通过激活 Rap1b-VEGFR2 信号通路促进喉癌的血管生成。

IF 3.3 3区医学

Carcinogenesis Pub Date : 2024-09-11 DOI: 10.1093/carcin/bgae030

Kexing Lyu, Bingjie Tang, Bixue Huang, Zhenglin Xu, Tesi Liu, Ruihua Fang, Yun Li, Yi Chen, Lin Chen, Minjuan Zhang, Lifan Chen, Wenbin Lei

{"title":"Exosomal circPVT1 promotes angiogenesis in laryngeal cancer by activating the Rap1b-VEGFR2 signaling pathway.","authors":"Kexing Lyu, Bingjie Tang, Bixue Huang, Zhenglin Xu, Tesi Liu, Ruihua Fang, Yun Li, Yi Chen, Lin Chen, Minjuan Zhang, Lifan Chen, Wenbin Lei","doi":"10.1093/carcin/bgae030","DOIUrl":"10.1093/carcin/bgae030","url":null,"abstract":"Laryngeal cancer (LC) is the second most common head and neck cancer and has a decreasing 5-year survival rate worldwide. Circular RNAs (circRNAs) regulate cancer development in diverse ways based on their distinct biogenesis mechanisms and expansive regulatory roles. However, currently, there is little research on how exosomal circRNAs are involved in the development of LC. Here, we demonstrated that circPVT1, a circRNA derived from the well-studied long noncoding RNA PVT1, is correlated with disease progression in LC and promotes angiogenesis both in vivo and in vitro. Mechanistically, circPVT1 is loaded into LC cell-secreted exosomes and taken up by vascular epithelium cells. By sponging miR-30c-5p, exosomal circPVT1 promotes Rap1b expression, which dramatically enhances vascular endothelial growth factor receptor 2 and the phosphatidylinositol 3-kinase (PI3K)/AKT pathway activation, ultimately resulting in the induction of angiogenesis. Furthermore, our xenograft models demonstrated that the combination of short hairpin RNA-circPVT1 and cetuximab showed high efficacy in inhibiting tumor growth and angiogenesis. Collectively, these findings uncover a novel mechanism of exosomal circRNA-mediated angiogenesis modulation and provide a preclinical rationale for testing this analogous combination in patients with LC.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":"642-657"},"PeriodicalIF":3.3,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141186436","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}

引用次数: 0

Enhancing carboplatin sensitivity in ovarian cancer cells by blocking the mercapturic acid pathway transporter. 通过阻断巯基酸途径转运体提高卵巢癌细胞对卡铂的敏感性

IF 3.3 3区医学

Carcinogenesis Pub Date : 2024-09-11 DOI: 10.1093/carcin/bgae047

B Madhu Krishna, Sravani K Ramisetty, Pankaj Garg, Atish Mohanty, Edward Wang, David Horne, Sanjay Awasthi, Prakash Kulkarni, Ravi Salgia, Sharad S Singhal

{"title":"Enhancing carboplatin sensitivity in ovarian cancer cells by blocking the mercapturic acid pathway transporter.","authors":"B Madhu Krishna, Sravani K Ramisetty, Pankaj Garg, Atish Mohanty, Edward Wang, David Horne, Sanjay Awasthi, Prakash Kulkarni, Ravi Salgia, Sharad S Singhal","doi":"10.1093/carcin/bgae047","DOIUrl":"10.1093/carcin/bgae047","url":null,"abstract":"Ral-binding/interacting protein (RLIP) acts as a transporter that responds to stress and provides protection, specifically against glutathione-electrophile conjugates and xenobiotic toxins. Its increased presence in malignant cells, especially in cancer, emphasizes its crucial antiapoptotic function. This is achieved by selectively regulating the cellular levels of proapoptotic oxidized lipid byproducts. Suppressing the progression of tumors in human xenografts can be achieved by effectively inhibiting RLIP, a transporter in the mercapturic acid pathway, without involving chemotherapy. Utilizing ovarian cancer (OC) cell lines (MDAH2774, OVCAR4, and OVCAR8), we observed that agents targeting RLIP, such as RLIP antisense and RLIP antibodies, not only substantially impeded the viability of OC cells but also remarkably increased their sensitivity to carboplatin. To delve further into the cytotoxic synergy between RLIP antisense, RLIP antibodies, and carboplatin, we conducted investigations in both cell culture and xenografts of OC cells. The outcomes revealed that RLIP depletion via phosphorothioate antisense led to rapid and sustained remissions in established subcutaneous human ovary xenografts. Furthermore, RLIP inhibition by RLIP antibodies exhibited comparable efficacy to antisense and enhanced the effectiveness of carboplatin in MDAH2774 OC xenografts. These investigations underscore RLIP as a central carrier crucial for supporting the survival of cancer cells, positioning it as a suitable focus for cancer treatment.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":"696-707"},"PeriodicalIF":3.3,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141757313","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}

引用次数: 0

Stem cells, Notch-1 signaling, and oxidative stress: a hellish trio in cancer development and progression within the airways. Is there a role for natural compounds? 干细胞、Notch-1 信号传导和氧化应激：气道内癌症发展和恶化的地狱三重奏。天然化合物能发挥作用吗？

IF 3.3 3区医学

Carcinogenesis Pub Date : 2024-09-11 DOI: 10.1093/carcin/bgae049

Giuseppina Chiappara, Serena Di Vincenzo, Caterina Cascio, Elisabetta Pace

引用次数: 0

PPP1r18 promotes tumor progression in esophageal squamous cell carcinoma by regulating the calcineurin-mediated ERK pathway. PPP1r18 通过调节钙神经蛋白介导的 ERK 通路促进食管鳞状细胞癌的肿瘤进展。

IF 3.3 3区医学

Carcinogenesis Pub Date : 2024-09-11 DOI: 10.1093/carcin/bgae028

Changhao Ren, Linfeng Wu, Shaoyuan Zhang, Kangwei Qi, Yifei Zhang, Jiacheng Xu, Yuanyuan Ruan, Mingxiang Feng

{"title":"PPP1r18 promotes tumor progression in esophageal squamous cell carcinoma by regulating the calcineurin-mediated ERK pathway.","authors":"Changhao Ren, Linfeng Wu, Shaoyuan Zhang, Kangwei Qi, Yifei Zhang, Jiacheng Xu, Yuanyuan Ruan, Mingxiang Feng","doi":"10.1093/carcin/bgae028","DOIUrl":"10.1093/carcin/bgae028","url":null,"abstract":"Esophageal cancer is one of the most common malignant tumors, and the 5-year overall survival rate is only 20%. Esophageal squamous cell carcinoma (ESCC) is the primary histological type of esophageal carcinoma in China. Protein phosphatase 1 regulatory subunit 18 (PPP1r18) is one of the actin-regulatory proteins and is able to bind to protein phosphatase 1 catalytic subunit alpha (PPP1CA). Yet, little is known about the role of PPP1r18 in ESCC. This study aimed to elucidate the biological functions of PPP1r18 in the ESCC progression. Clinical samples first confirmed that PPP1r18 expression was upregulated in ESCC, and PPP1r18 was correlated with tumor invasion depth, lymph node metastasis, distant metastasis and reduced overall survival. We then observed that PPP1r18 overexpression enhanced cell proliferation in vitro and in vivo. Mechanistically, PPP1r18 regulated tumor progression of ESCC through activating the calcineurin-mediated ERK pathway, rather than binding to PPP1CA. Collectively, our results suggest that PPP1r18 promotes ESCC progression by regulating the calcineurin-mediated ERK pathway. PPP1r18 might be a potential target for the diagnosis and treatment of ESCC.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":"673-684"},"PeriodicalIF":3.3,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140875954","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}

引用次数: 0

Sevoflurane inhibits lung cancer development by promoting FUS1 transcription via downregulating IRF6. 七氟烷通过下调IRF6促进FUS1转录，从而抑制肺癌发展

IF 3.3 3区医学

Carcinogenesis Pub Date : 2024-08-12 DOI: 10.1093/carcin/bgae034

Pei Zhou, Lei Yang, Xinyu Ma, Qiuguo Li

{"title":"Sevoflurane inhibits lung cancer development by promoting FUS1 transcription via downregulating IRF6.","authors":"Pei Zhou, Lei Yang, Xinyu Ma, Qiuguo Li","doi":"10.1093/carcin/bgae034","DOIUrl":"10.1093/carcin/bgae034","url":null,"abstract":"Lung cancer is a major contributor to cancer deaths worldwide and is on the rise. Although surgical resection has been widely used as a standard therapy for lung cancer patients, the relapse rate after surgery is high. It is still unclear whether there is a potential drug that can reduce the probability of postsurgical recurrence in lung cancer patients. We used 5 typical lung cancer cell lines as well as 41 lung cancer tissue samples and paracancer tissue samples to investigate the expression levels of interferon regulatory factor 6 (IRF6) and tumor suppressor candidate 2 (TUSC2, also known as FUS1). We also treated lung cancer cells (H322 and A549) with different concentrations of sevoflurane to study its influence on lung cancer cell tumorigenesis. Lentivirus-mediated gain-of-function studies of IRF6 and FUS1 were applied to validate the role of IRF6 and FUS1 in lung cancer. Next, we used short hairpin RNA-mediated loss of function of IRF6 and luciferase, chromatin immunoprecipitation assays to validate the regulatory role of IRF6 on FUS1. Our findings reported that IRF6 was upregulated in lung cancer tissues, while FUS1 was downregulated. Functional assays revealed that sevoflurane inhibits lung cancer development by downregulating IRF6 expression. Luciferase and chromatin immunoprecipitation-quantitative real-time PCR assays uncovered that IRF6 represses FUS1 transcriptional expression in lung cancer cells. We have shown that sevoflurane prevents lung cancer development by downregulating IRF6 to stimulate FUS1 transcription, indicating that sevoflurane can be used as the potential anesthetic drug in surgical resection to reduce postoperative tumor relapse in lung cancer patients.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":"543-555"},"PeriodicalIF":3.3,"publicationDate":"2024-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141178096","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}

引用次数: 0

Diverse functions of Tribbles homolog 3 in cancers and its potential as a therapeutic target. TRIB3 在癌症中的多种功能及其作为治疗靶点的潜力。

IF 3.3 3区医学

Carcinogenesis Pub Date : 2024-08-12 DOI: 10.1093/carcin/bgae042

Shiying Lei, Jiajun Sun, Yifang Xie, Xiaojuan Xiao, Xiaofeng He, Sheng Lin, Huifang Zhang, Zineng Huang, Haiqin Wang, Xusheng Wu, Hongling Peng, Jing Liu

{"title":"Diverse functions of Tribbles homolog 3 in cancers and its potential as a therapeutic target.","authors":"Shiying Lei, Jiajun Sun, Yifang Xie, Xiaojuan Xiao, Xiaofeng He, Sheng Lin, Huifang Zhang, Zineng Huang, Haiqin Wang, Xusheng Wu, Hongling Peng, Jing Liu","doi":"10.1093/carcin/bgae042","DOIUrl":"10.1093/carcin/bgae042","url":null,"abstract":"Currently, cancer is the second leading cause of death worldwide, and potential targeted drugs and molecular pathways for cancer development and progression have been a hot research topic worldwide. In recent years, the importance of the kinase superfamily in diseases has been well demonstrated by studies on various molecular mechanisms of kinases and the successful application of their inhibitors in diseases. Pseudokinases are members of the kinase superfamily, which have been increasingly documented to play a crucial role in cancers year after year. As a member of pseudokinases, tribbles homolog 3 (TRIB3) also exerts diverse functions in different cancers through different interacting proteins and molecular pathways, especially in tumor immunity, stemness, drug resistance, metabolism, and autophagy. In addition, peptide drugs targeting TRIB3 have high specificity in preclinical studies, which shows great promise for TRIB3 application in diseases including cancers. In this review, we dissect diverse functions played by TRIB3 in different cancers, describing the underlying mechanisms in detail. Notably, inhibitors and agonists currently available for TRIB3 are discussed, indicating the potential for TRIB3 as a therapeutic target.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":"527-542"},"PeriodicalIF":3.3,"publicationDate":"2024-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141431485","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}

引用次数: 0

CacyBP promotes the development of lung adenocarcinoma by regulating OTUD5. CacyBP 通过调控 OTUD5 促进肺腺癌的发展。

IF 3.3 3区医学

Carcinogenesis Pub Date : 2024-08-12 DOI: 10.1093/carcin/bgae023

Mixue Bai, Kun Lu, Yingying Che, Lin Fu

{"title":"CacyBP promotes the development of lung adenocarcinoma by regulating OTUD5.","authors":"Mixue Bai, Kun Lu, Yingying Che, Lin Fu","doi":"10.1093/carcin/bgae023","DOIUrl":"10.1093/carcin/bgae023","url":null,"abstract":"Lung cancer is the most common and lethal malignancy, with lung adenocarcinoma accounting for approximately 40% of all cases. Despite some progress in understanding the pathogenesis of this disease and developing new therapeutic approaches, the current treatments for lung adenocarcinoma remain ineffective due to factors such as high tumour heterogeneity and drug resistance. Therefore, there is an urgent need to identify novel therapeutic targets. Calcyclin-binding protein (CacyBP) can regulate a variety of physiological processes by binding to different proteins, but its function in lung adenocarcinoma is unknown. Here, we show that CacyBP is highly expressed in lung adenocarcinoma tissues, and high CacyBP expression correlates with poorer patient survival. Moreover, overexpression of CacyBP promoted the proliferation, migration and invasion of lung adenocarcinoma cell lines. Further mechanistic studies revealed that CacyBP interacts with the tumour suppressor ovarian tumour (OTU) deubiquitinase 5 (OTUD5), enhances the ubiquitination and proteasomal degradation of OTUD5 and regulates tumourigenesis via OTUD5. In conclusion, our study reveals a novel mechanism by which CacyBP promotes tumourigenesis by increasing the ubiquitination level and proteasome-dependent degradation of OTUD5, providing a potential target for the treatment of lung adenocarcinoma.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":"595-606"},"PeriodicalIF":3.3,"publicationDate":"2024-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140334839","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}

引用次数: 0