Carcinogenesis最新文献_第10页

CircCDK17 promotes the proliferation and metastasis of ovarian cancer cells by sponging miR-22-3p to regulate CD147 expression. CircCDK17通过海绵miR-22-3p调节CD147的表达，促进卵巢癌细胞的增殖和转移。

IF 4.7 3区医学

Carcinogenesis Pub Date : 2024-02-12 DOI: 10.1093/carcin/bgad079

Bin Qu, Lisha Sun, Ping Xiao, Haoming Shen, Yuxi Ren, Jing Zhang

{"title":"CircCDK17 promotes the proliferation and metastasis of ovarian cancer cells by sponging miR-22-3p to regulate CD147 expression.","authors":"Bin Qu, Lisha Sun, Ping Xiao, Haoming Shen, Yuxi Ren, Jing Zhang","doi":"10.1093/carcin/bgad079","DOIUrl":"10.1093/carcin/bgad079","url":null,"abstract":"Ovarian cancer (OC) is a common malignancy in women of reproductive age. Circular RNAs (circRNAs) are emerging players in OC progression. We investigated the function and mechanism of circular RNA hsa_circ_0027803 (circCDK17) in OC pathogenesis. Real‑time PCR (RT-qPCR) and western blot were utilized for gene and protein expression analysis, respectively. Cell counting kit‑8 (CCK-8), EdU and Transwell assays investigated OC cell proliferation, migration and invasion. The associations between circCDK17, miR-22-3p and CD147 were examined by dual-luciferase reporter and RNA-protein immunoprecipitation (RIP) assays. The in vivo model of OC nude mice was constructed to explore the role of circCDK17. CircCDK17 was increased in OC tissue and cells, and patients with higher expression of circCDK17 had a shorter survival. CircCDK17 downregulation inhibited OC cell proliferation, migration and invasion, and reduced epithelial-mesenchymal transition (EMT)-related markers. In vivo experiments showed that circCDK17 silencing inhibited OC tumor growth and metastasis. CircCDK17 depletion reduced CD147 level via sponging miR-22-3p. MiR-22-3p knockdown overturned effect of circCDK17 depletion on OC cell proliferation, migration and invasion. Meanwhile, overexpressed CD147 restored functions of circCDK17 downregulation on OC development. CircCDK17 is an important molecule that regulates OC pathogenic process through miR-22-3p/CD147.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":null,"pages":null},"PeriodicalIF":4.7,"publicationDate":"2024-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89716952","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

LncRNA CCAT1 participates in pancreatic ductal adenocarcinoma progression by forming a positive feedback loop with c-Myc. lncRNACCAT1通过与c-Myc形成正反馈回路参与胰腺导管腺癌的进展。

IF 4.7 3区医学

Carcinogenesis Pub Date : 2024-02-12 DOI: 10.1093/carcin/bgad076

Chundong Cheng, Zonglin Liu, Danxi Liu, Hua Chen, Yongwei Wang, Bei Sun

{"title":"LncRNA CCAT1 participates in pancreatic ductal adenocarcinoma progression by forming a positive feedback loop with c-Myc.","authors":"Chundong Cheng, Zonglin Liu, Danxi Liu, Hua Chen, Yongwei Wang, Bei Sun","doi":"10.1093/carcin/bgad076","DOIUrl":"10.1093/carcin/bgad076","url":null,"abstract":"Long noncoding RNAs (lncRNAs) play fundamental roles in cancer development; however, the underlying mechanisms for a large proportion of lncRNAs in pancreatic ductal adenocarcinoma (PDAC) have not been elucidated. The expression of colon cancer-associated transcript-1 (CCAT1) in PDAC specimens and cell lines was measured by quantitative real-time polymerase chain reaction (qRT-PCR). The function of CCAT1 was examined in vitro and in vivo. The interactions among CCAT1, miR-24-3p and c-Myc were determined by bioinformatics analysis, RNA immunoprecipitation (RIP), dual-luciferase reporter assay, and rescue experiments. CCAT1 was significantly increased in PDAC, positively correlated with PDAC progression and predicted a worse prognosis. Furthermore, CCAT1 enhanced Adenosine triphosphate (ATP) production to facilitate PDAC cell proliferation, colony formation and motility in vitro and tumor growth in vivo. CCAT1 may serve as an miR-24-3p sponge, thereby counteracting its repression by c-Myc expression. Reciprocally, c-Myc may act as a transcription factor to alter CCAT1 expression by directly targeting its promoter region, thus forming a positive feedback loop with CCAT1. Collectively, these results demonstrate that a positive feedback loop of CCAT1/miR-24-3p/c-Myc is involved in PDAC development, which may serve as a biomarker and therapeutic target for PDAC.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":null,"pages":null},"PeriodicalIF":4.7,"publicationDate":"2024-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71478314","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

S. Perwez Hussain, 1960-2023. S. Perwez Hussain，1960-2023 年。

IF 4.7 3区医学

Carcinogenesis Pub Date : 2024-01-02 DOI: 10.1093/carcin/bgad092

Stefan Ambs

引用次数: 0

Association between new plasma inflammatory markers and risk of colorectal neoplasms in individuals over 50 years old. 50 岁以上人群新血浆炎症标志物与结直肠肿瘤风险之间的关系。

IF 4.7 3区医学

Carcinogenesis Pub Date : 2023-12-30 DOI: 10.1093/carcin/bgad064

Jia-Yi Su, Yun Wang, Shang-Shang Wu, Wen-Kun Li, Cheng-Yao Wang, Jiu-Yue Ma, Yu-Ting Qiu, Min-Si Zhou, Zhan Wang, Peng Li, Chun-Tao Liu, Jing Wu

引用次数: 0

KCNN1 promotes proliferation and metastasis of breast cancer via ERLIN2-mediated stabilization and K63-dependent ubiquitination of Cyclin B1. KCNN1通过ERLIN2-介导的细胞周期蛋白B1的稳定化和K63-依赖性泛素化促进癌症的增殖和转移。

IF 3.3 3区医学

Carcinogenesis Pub Date : 2023-12-30 DOI: 10.1093/carcin/bgad070

Bin Xiao, Qin Xiang, Zihua Deng, Daxiang Chen, Shunhong Wu, Yanxia Zhang, Yaru Liang, Shi Wei, Guoqing Luo, Linhai Li

{"title":"KCNN1 promotes proliferation and metastasis of breast cancer via ERLIN2-mediated stabilization and K63-dependent ubiquitination of Cyclin B1.","authors":"Bin Xiao, Qin Xiang, Zihua Deng, Daxiang Chen, Shunhong Wu, Yanxia Zhang, Yaru Liang, Shi Wei, Guoqing Luo, Linhai Li","doi":"10.1093/carcin/bgad070","DOIUrl":"10.1093/carcin/bgad070","url":null,"abstract":"Potassium Calcium-Activated Channel Subfamily N1 (KCNN1), an integral membrane protein, is thought to regulate neuronal excitability by contributing to the slow component of synaptic after hyperpolarization. However, the role of KCNN1 in tumorigenesis has been rarely reported, and the underlying molecular mechanism remains unclear. Here, we report that KCNN1 functions as an oncogene in promoting breast cancer cell proliferation and metastasis. KCNN1 was overexpressed in breast cancer tissues and cells. The pro-proliferative and pro-metastatic effects of KCNN1 were demonstrated by CCK8, clone formation, Edu assay, wound healing assay and transwell experiments. Transcriptomic analysis using KCNN1 overexpressing cells revealed that KCNN1 could regulate key signaling pathways affecting the survival of breast cancer cells. KCNN1 interacts with ERLIN2 and enhances the effect of ERLIN2 on Cyclin B1 stability. Overexpression of KCNN1 promoted the protein expression of Cyclin B1, enhanced its stability and promoted its K63 dependent ubiquitination, while knockdown of KCNN1 had the opposite effects on Cyclin B1. Knockdown (or overexpression) ERLNI2 partially restored Cyclin B1 stability and K63 dependent ubiquitination induced by overexpression (or knockdown) of KCNN1. Knockdown (or overexpression) ERLIN2 also partially neutralizes the effects of overexpression (or knockdown) KCNN1-induced breast cancer cell proliferation, migration and invasion. In paired breast cancer clinical samples, we found a positive expression correlations between KCNN1 and ERLIN2, KCNN1 and Cyclin B1, as well as ERLIN2 and Cyclin B1. In conclusion, this study reveals, for the first time, the role of KCNN1 in tumorigenesis and emphasizes the importance of KCNN1/ERLIN2/Cyclin B1 axis in the development and metastasis of breast cancer.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2023-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10818095/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41192039","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

m6A-modified circASXL1 promotes proliferation and migration of ovarian cancer through the miR-320d/RACGAP1 axis. m6A-修饰的circASXL1通过miR-320d/RACGAP1轴促进卵巢癌症的增殖和迁移。

IF 4.7 3区医学

Carcinogenesis Pub Date : 2023-12-30 DOI: 10.1093/carcin/bgad066

Qi Tian, Qingling Mu, Shuang Liu, Kui Huang, Yi Tang, Pu Zhang, Jing Zhao, Chuqiang Shu

{"title":"m6A-modified circASXL1 promotes proliferation and migration of ovarian cancer through the miR-320d/RACGAP1 axis.","authors":"Qi Tian, Qingling Mu, Shuang Liu, Kui Huang, Yi Tang, Pu Zhang, Jing Zhao, Chuqiang Shu","doi":"10.1093/carcin/bgad066","DOIUrl":"10.1093/carcin/bgad066","url":null,"abstract":"Ovarian cancer (OC) is one of the most common malignant tumors in women. Circular RNAs (circRNAs) can potentially regulate the development of OC. Therefore, this study investigated the role of circASXL1 in OC progression. Cell functions were assessed by MTT, colony formation, wound healing, and transwell assays. RIP and dual luciferase reporter assays confirmed the relationship between miR-320d and circASXL1 or RACGAP1. MeRIP was utilized to detect m6A levels. Xenograft tumor was established for in vivo experiments. CircASXL1 and RACGAP1 levels were increased in OC tissues and cells, whereas miR-320d expression was decreased. Upregulation of circASXL1 was associated with poor prognosis in OC patients. CircASXL1 silencing suppressed OC cell proliferation, migration and invasion in vitro and in vivo. Mechanistically, METTL3/IGF2BP1-mediated m6A modification maintained circASXL1 stability and upregulated its expression. CircASXL1 was a ceRNA that sequestrated miR-320d from RACGAP1, leading to increased RACGAP1 expression. CircASXL1 promoted OC cell proliferation, migration and invasion via the miR-320d/RACGAP1 axis. Therefore, m6A-modified circASXL1 acts as an oncogene in OC by targeting miR-320d and activating RACGAP1/PI3K/Akt pathway, which provides novel promising biomarkers for OC diagnosis.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":null,"pages":null},"PeriodicalIF":4.7,"publicationDate":"2023-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41105522","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

Aqueous extracts of Ocimum gratissimum mitigate colitis and protect against AOM/DSS-induced colorectal cancer in mice. 牛膝水提取物减轻小鼠结肠炎和对AOM/DSS-诱导的大肠癌癌症的保护作用。

IF 4.7 3区医学

Carcinogenesis Pub Date : 2023-12-30 DOI: 10.1093/carcin/bgad074

Jer-Yuh Liu, Fang-Ling Tsai, Ya-Ling Chuang, Je-Chiuan Ye

{"title":"Aqueous extracts of Ocimum gratissimum mitigate colitis and protect against AOM/DSS-induced colorectal cancer in mice.","authors":"Jer-Yuh Liu, Fang-Ling Tsai, Ya-Ling Chuang, Je-Chiuan Ye","doi":"10.1093/carcin/bgad074","DOIUrl":"10.1093/carcin/bgad074","url":null,"abstract":"In this study, we explored the in vivo effects of Ocimum gratissimum aqueous extracts (OGE) on colorectal cancer (CRC) development provoked by azoxymethane/dextran sodium sulfate (AOM/DSS). The results showed a significant reduction in the tumor load and tumor number for the OGEH group that received continued administration of OGE compared to the AOM/DSS group, with P values of <0.01, but this was not observed in the OGEHs group that received separated administration of OGE. All groups except the control group exhibited aberrant crypt foci (ACF) and adenocarcinoma of lesion pathology in colon, and both conditions were significantly reduced in the OGEH group (P < 0.01) as compared to the AOM/DSS group. Subsequent investigation into whether OGE exhibits eliminative effects on DSS-induced severe colitis (SC) in mice showed that the disease activity index score was significantly reduced in the OGE-treated groups (P < 0.01), also colon colitis histological score was reversed. These data suggest that OGE may be potentially effective in preventing CRC when administered throughout the promotional stages of carcinogenesis by inhibiting inflammatory SC.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":null,"pages":null},"PeriodicalIF":4.7,"publicationDate":"2023-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49674596","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

Construction and identification of lncRNA/circRNA-coregulated ceRNA networks in gemcitabine-resistant bladder carcinoma. 吉西他滨耐药膀胱癌中lncRNA/circRNA协同调节的ceRNA网络的构建和鉴定。

IF 4.7 3区医学

Carcinogenesis Pub Date : 2023-12-30 DOI: 10.1093/carcin/bgad065

Jingjing Pan, Xiaojuan Xie, Jinxiu Sheng, Chenxi Ju, Shuaijie Sun, Fangfang Cui, Wen Zhai, Liang Ming

{"title":"Construction and identification of lncRNA/circRNA-coregulated ceRNA networks in gemcitabine-resistant bladder carcinoma.","authors":"Jingjing Pan, Xiaojuan Xie, Jinxiu Sheng, Chenxi Ju, Shuaijie Sun, Fangfang Cui, Wen Zhai, Liang Ming","doi":"10.1093/carcin/bgad065","DOIUrl":"10.1093/carcin/bgad065","url":null,"abstract":"Objectives: To explore the regulatory networks that underlie the development of chemoresistance in bladder cancer.Methods: We analyzed profiles of differentially expressed long non-coding RNAs (lncRNAs), circular RNAs (circRNAs), microRNAs (miRNAs) and messenger RNA (mRNAs) in gemcitabine-resistant/sensitive bladder cancer cells using next-generation sequencing data.Results: Hundreds of differentially expressed lncRNAs and miRNAs and thousands of circRNAs and mRNAs were identified. Bioinformatics analysis revealed the chromosomal localizations, classification and coexpression of mRNAs, as well as candidates for cis and trans regulation by lncRNAs. Furthermore, Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis of differentially expressed mRNAs and circRNAs indicated important functional roles of coregulated RNAs, thus establishing competing endogenous RNA (ceRNA) and protein-protein interactions networks that may underlie chemoresistance in bladder cancer. We demonstrated that lncRNA LINP1 can act as a ceRNA by inhibiting miR-193a-5p to increase TP73 expression; and that lncRNA ESRG and hsa_circ_0075881 can simultaneously bind miR-324-3p to increase ST6GAL1 expression. Modulation of ceRNA network components using ablation and overexpression approaches contributed to gemcitabine resistance in bladder cancer cells.Conclusions: These results elucidate mechanisms by which lncRNAs and circRNAs coregulate the development of bladder cancer cell resistance to gemcitabine, thus laying the foundation for future research to identify biomarkers and disease targets.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":null,"pages":null},"PeriodicalIF":4.7,"publicationDate":"2023-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41119636","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

Interplay between inflammasomes and PD-1/PD-L1 and their implications in cancer immunotherapy. 炎症小体与PD-1/PD-L1的相互作用及其在癌症免疫治疗中的意义。

IF 4.7 3区医学

Carcinogenesis Pub Date : 2023-12-30 DOI: 10.1093/carcin/bgad072

Zhongyu Jiao, Jun Zhang

引用次数: 0

Lnc-PKNOX1-1 inhibits tumor progression in cutaneous malignant melanoma by regulating NF-κB/IL-8 axis. Lnc-PKNOX1-1通过调节NF-κB/IL-8轴抑制皮肤恶性黑色素瘤的肿瘤进展。

IF 3.3 3区医学

Carcinogenesis Pub Date : 2023-12-30 DOI: 10.1093/carcin/bgad073

Anlan Hong, Meng Cao, Dongqing Li, Yixin Wang, Guoqiang Zhang, Fang Fang, Liang Zhao, Qiang Wang, Tong Lin, Yan Wang

{"title":"Lnc-PKNOX1-1 inhibits tumor progression in cutaneous malignant melanoma by regulating NF-κB/IL-8 axis.","authors":"Anlan Hong, Meng Cao, Dongqing Li, Yixin Wang, Guoqiang Zhang, Fang Fang, Liang Zhao, Qiang Wang, Tong Lin, Yan Wang","doi":"10.1093/carcin/bgad073","DOIUrl":"10.1093/carcin/bgad073","url":null,"abstract":"Cutaneous malignant melanoma is one of the most lethal cutaneous malignancies. Accumulating evidence has demonstrated the potential influence of long non-coding RNAs (lncRNAs) in biological behaviors of melanoma. Herein, we reported a novel lncRNA, lnc-PKNOX1-1 and systematically studied its functions and possible molecular mechanisms in melanoma. Reverse transcription-quantitative PCR assay showed that lnc-PKNOX1-1 was significantly decreased in melanoma cells and tissues. Low lnc-PKNOX1-1 expression was significantly correlated with invasive pathological type and Breslow thickness of melanoma. In vitro and in vivo experiments showed lnc-PKNOX1-1 dramatically inhibited melanoma cell proliferation, migration and invasion. Mechanically, protein microarray analysis suggested that interleukin-8 (IL-8) was negatively regulated by lnc-PKNOX1-1 in melanoma, which was confirmed by western blot and ELISA. Western blot analysis also showed that lnc-PKNOX1-1 could promote p65 phosphorylation at Ser536 in melanoma. Subsequent rescue assays proved IL-8 overexpression could partly reverse the tumor-suppressing function of lnc-PKNOX1-1 overexpression in melanoma cells, indicating that lnc-PKNOX1-1 suppressed the development of melanoma by regulating IL-8. Taken together, our study demonstrated the tumor-suppressing ability of lnc-PKNOX1-1 in melanoma, suggesting its potential as a novel diagnostic biomarker and therapeutic target for melanoma.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2023-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10818096/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41232525","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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