Carcinogenesis最新文献_第3页

Allura Red AC is a xenobiotic. Is it also a carcinogen? Allura Red AC 是一种异生物。它也是一种致癌物质吗？

IF 3.3 3区医学

Carcinogenesis Pub Date : 2024-10-10 DOI: 10.1093/carcin/bgae057

Lorne J Hofseth, James R Hebert, Elizabeth Angela Murphy, Erica Trauner, Athul Vikas, Quinn Harris, Alexander A Chumanevich

{"title":"Allura Red AC is a xenobiotic. Is it also a carcinogen?","authors":"Lorne J Hofseth, James R Hebert, Elizabeth Angela Murphy, Erica Trauner, Athul Vikas, Quinn Harris, Alexander A Chumanevich","doi":"10.1093/carcin/bgae057","DOIUrl":"10.1093/carcin/bgae057","url":null,"abstract":"Merriam-Webster and Oxford define a xenobiotic as any substance foreign to living systems. Allura Red AC (a.k.a., E129; FD&C Red No. 40), a synthetic food dye extensively used in manufacturing ultra-processed foods and therefore highly prevalent in our food supply, falls under this category. The surge in synthetic food dye consumption during the 70s and 80s was followed by an epidemic of metabolic diseases and the emergence of early-onset colorectal cancer in the 1990s. This temporal association raises significant concerns, particularly given the widespread inclusion of synthetic food dyes in ultra-processed products, notably those marketed toward children. Given its interactions with key contributors to colorectal carcinogenesis such as inflammatory mediators, the microbiome, and DNA damage, there is growing interest in understanding Allura Red AC's potential impact on colon health as a putative carcinogen. This review discusses the history of Allura Red AC, current research on its effects on the colon and rectum, potential mechanisms underlying its impact on colon health, and provides future considerations. Indeed, although no governing agencies classify Allura Red AC as a carcinogen, its interaction with key guardians of carcinogenesis makes it suspect and worthy of further molecular investigation. The goal of this review is to inspire research into the impact of synthetic food dyes on colon health.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":"711-720"},"PeriodicalIF":3.3,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11464682/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141916164","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

CDK12 is a promising therapeutic target for the transcription cycle and DNA damage response in metastatic osteosarcoma. CDK12 是转移性骨肉瘤转录周期和 DNA 损伤反应的一个很有前景的治疗靶点。

IF 3.3 3区医学

Carcinogenesis Pub Date : 2024-10-10 DOI: 10.1093/carcin/bgae051

Zihao Li, Xiaoyang Li, Nicole A Seebacher, Xu Liu, Wence Wu, Shengji Yu, Francis J Hornicek, Changzhi Huang, Zhenfeng Duan

{"title":"CDK12 is a promising therapeutic target for the transcription cycle and DNA damage response in metastatic osteosarcoma.","authors":"Zihao Li, Xiaoyang Li, Nicole A Seebacher, Xu Liu, Wence Wu, Shengji Yu, Francis J Hornicek, Changzhi Huang, Zhenfeng Duan","doi":"10.1093/carcin/bgae051","DOIUrl":"10.1093/carcin/bgae051","url":null,"abstract":"Osteosarcoma (OS) is a bone malignant tumor affecting children, adolescents, and young adults. Currently, osteosarcoma is treated with chemotherapy regimens established over 40 years ago. The investigation of novel therapeutic strategies for the treatment of osteosarcoma remains an important clinical need. Cyclin-dependent kinases (CDKs) have been considered promising molecular targets in cancer therapy. Among these, CDK12 has been shown to play a crucial role in the pathogenesis of malignancies, but its clinical significance and biological mechanisms in osteosarcoma remain unclear. In the present study, we aim to determine the expression and function of CDK12 and evaluate its prognostic and therapeutic value in metastatic osteosarcoma. We found that overexpression of CDK12 was associated with high tumor grade, tumor progression and reduced patient survival. The underlying mechanism revealed that knockdown of CDK12 expression with small interfering RNA or functional inhibition with the CDK12-targeting agent THZ531 effectively exhibited time- and dose-dependent cytotoxicity. Downregulation of CDK12 paused transcription by reducing RNAP II phosphorylation, interfered with DNA damage repair with increased γH2AX, and decreased cell proliferation through the PI3K-AKT pathway. This was accompanied by the promotion of apoptosis, as evidenced by enhanced Bax expression and reduced Bcl-xL expression. Furthermore, the CDK12 selective inhibitor THZ531 also hindered ex vivo 3D spheroid formation, growth of in vitro 2D cell colony, and prevented cell mobility. Our findings highlight the clinical importance of CDK12 as a potentially valuable prognostic biomarker and therapeutic target in metastatic osteosarcoma.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":"786-798"},"PeriodicalIF":3.3,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141854933","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

Intratumoral vitamin D signaling and lethal prostate cancer. 肿瘤内维生素 D 信号传导与致命性前列腺癌

IF 3.3 3区医学

Carcinogenesis Pub Date : 2024-10-10 DOI: 10.1093/carcin/bgae055

Jane B Vaselkiv, Irene M Shui, Sydney T Grob, Caroline I Ericsson, Isabel Giovannucci, Cheng Peng, Stephen P Finn, Lorelei A Mucci, Kathryn L Penney, Konrad H Stopsack

{"title":"Intratumoral vitamin D signaling and lethal prostate cancer.","authors":"Jane B Vaselkiv, Irene M Shui, Sydney T Grob, Caroline I Ericsson, Isabel Giovannucci, Cheng Peng, Stephen P Finn, Lorelei A Mucci, Kathryn L Penney, Konrad H Stopsack","doi":"10.1093/carcin/bgae055","DOIUrl":"10.1093/carcin/bgae055","url":null,"abstract":"High circulating vitamin D levels and supplementation may lower prostate cancer mortality. To probe for direct effects of vitamin D signaling in the primary tumor, we assessed how activation of intratumoral vitamin D signaling in prostate cancer is associated with lethal prostate cancer during long-term follow-up. Among 404 participants with primary prostate cancer in the Health Professionals Follow-up Study and the Physicians' Health Study, we defined a gene score of expected activated intratumoral vitamin D signaling consisting of transcriptionally upregulated (CYP27A1, CYP2R1, RXRA, RXRB, and VDR) and downregulated genes (CYP24A1 and DHCR7). We contrasted vitamin D signaling in tumors that progressed to lethal disease (metastases/prostate cancer-specific death, n = 119) over up to three decades of follow-up with indolent tumors that remained nonmetastatic for >8 years post-diagnosis (n = 285). The gene score was downregulated in tumor tissue compared with tumor-adjacent histologically normal tissue of the same men. Higher vitamin D gene scores were inversely associated with lethal prostate cancer (odds ratio for highest versus lowest quartile: 0.46, 95% confidence interval: 0.21-0.99) in a dose-response fashion and after adjusting for clinical and pathologic factors. This association appeared strongest among men with high predicted plasma 25-hydroxyvitamin D3 and men with body mass index ≥25 kg/m2. Findings were replicated with broader gene sets. These data support the hypothesis that active intratumoral vitamin D signaling is associated with better prostate cancer outcomes and provide further rationale for testing how vitamin D-related interventions after diagnosis could improve prostate cancer survival through effects on the tumor.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":"735-744"},"PeriodicalIF":3.3,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11464699/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141906007","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

ETS1 deficiency in macrophages suppresses colorectal cancer progression by reducing the F4/80+TIM4+ macrophage population. 巨噬细胞中 ETS1 的缺失通过减少 F4/80+TIM4+ 巨噬细胞群抑制结直肠癌的进展

IF 3.3 3区医学

Carcinogenesis Pub Date : 2024-10-10 DOI: 10.1093/carcin/bgae058

Yuanyuan Cao, Anning Guo, Muxin Li, Xinghua Ma, Xiaofeng Bian, YiRong Chen, Caixia Zhang, Shijia Huang, Wei Zhao, Shuli Zhao

{"title":"ETS1 deficiency in macrophages suppresses colorectal cancer progression by reducing the F4/80+TIM4+ macrophage population.","authors":"Yuanyuan Cao, Anning Guo, Muxin Li, Xinghua Ma, Xiaofeng Bian, YiRong Chen, Caixia Zhang, Shijia Huang, Wei Zhao, Shuli Zhao","doi":"10.1093/carcin/bgae058","DOIUrl":"10.1093/carcin/bgae058","url":null,"abstract":"Tumor-associated macrophages (TAMs) take on pivotal and complex roles in the tumor microenvironment (TME); however, their heterogeneity in the TME remains incompletely understood. ETS proto-oncogene 1 (ETS1) is a transcription factor that is mainly expressed in lymphocytes. However, its expression and immunoregulatory role in colorectal cancer (CRC)-associated macrophages remain unclear. In the study, the expression levels of ETS1 in CD68+ macrophages in the CRC microenvironment were significantly higher than those in matched paracarcinoma tissues. Importantly, ETS1 increased the levels of chemokines C-C motif chemokine ligand 2 (CCL2) and C-X-C motif chemokine ligand 10 (CXCL10) in lipopolysaccharide-stimulated THP-1 cells. It also boosted the migration and invasion of CRC cells during the in vitro co-culture. In the ETS1 conditional knockout mouse model, ETS1 deficiency in macrophages ameliorated the histological changes in DSS-induced ulcerative colitis mouse models and prolonged the survival in an azomethane/dextran sodium sulfate (AOM/DSS)-induced CRC model. ETS1 deficiency in macrophages substantially inhibited tumor formation, reduced F4/80+TIM4+ macrophages in the mesenteric lymph nodes, and decreased CCL2 and CXCL10 protein levels in tumor tissues. Moreover, ETS1 deficiency in macrophages effectively prevented liver metastasis of CRC and reduced the infiltration of TAMs into the metastasis sites. Subsequent studies have indicated that ETS1 upregulated the expression of T-cell immunoglobulin mucin receptor 4 in macrophages through the signal transducer and activator of the transcription 1 signaling pathway activated by the autocrine action of CCL2/CXCL10. Collectively, ETS1 deficiency in macrophages potentiates antitumor immune responses by repressing CCL2 and CXCL10 expression, shedding light on potential therapeutic strategies for CRC.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":"745-758"},"PeriodicalIF":3.3,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142003688","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

Machine learning based on biological context facilitates the identification of microvascular invasion in intrahepatic cholangiocarcinoma. 基于生物背景的机器学习有助于识别肝内胆管癌的微血管侵犯。

IF 3.3 3区医学

Carcinogenesis Pub Date : 2024-10-10 DOI: 10.1093/carcin/bgae052

Shuaishuai Xu, Mingyu Wan, Chanqi Ye, Ruyin Chen, Qiong Li, Xiaochen Zhang, Jian Ruan

{"title":"Machine learning based on biological context facilitates the identification of microvascular invasion in intrahepatic cholangiocarcinoma.","authors":"Shuaishuai Xu, Mingyu Wan, Chanqi Ye, Ruyin Chen, Qiong Li, Xiaochen Zhang, Jian Ruan","doi":"10.1093/carcin/bgae052","DOIUrl":"10.1093/carcin/bgae052","url":null,"abstract":"Intrahepatic cholangiocarcinoma is a rare disease associated with a poor prognosis, primarily due to early recurrence and metastasis. An important feature of this condition is microvascular invasion (MVI). However, current predictive models based on imaging have limited efficacy in this regard. This study employed a random forest model to construct a predictive model for MVI identification and uncover its biological basis. Single-cell transcriptome sequencing, whole exome sequencing, and proteome sequencing were performed. The area under the curve of the prediction model in the validation set was 0.93. Further analysis indicated that MVI-associated tumor cells exhibited functional changes related to epithelial-mesenchymal transition and lipid metabolism due to alterations in the nuclear factor-kappa B and mitogen-activated protein kinase signaling pathways. Tumor cells were also differentially enriched for the interleukin-17 signaling pathway. There was less infiltration of SLC30A1+ CD8+ T cells expressing cytotoxic genes in MVI-associated intrahepatic cholangiocarcinoma, whereas there was more infiltration of myeloid cells with attenuated expression of the major histocompatibility complex II pathway. Additionally, MVI-associated intercellular communication was closely related to the SPP1-CD44 and ANXA1-FPR1 pathways. These findings resulted in a brilliant predictive model and fresh insights into MVI.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":"721-734"},"PeriodicalIF":3.3,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141859124","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

Inhibition of Benzo[a]pyrene-induced DNA Adduct in Buccal Cells of Smokers by Black Raspberry Lozenges. 黑覆盆子润喉糖抑制吸烟者口腔细胞中苯并[a]芘诱导的 DNA 加合物

IF 3.3 3区医学

Carcinogenesis Pub Date : 2024-10-05 DOI: 10.1093/carcin/bgae067

Kun-Ming Chen, Nicolle M Krebs, Yuan-Wan Sun, Dongxiao Sun, Jiangang Liao, Lisa Reinhart, Jacek Krzeminski, Shantu Amin, Gary Stoner, Susan R Mallery, Karam El-Bayoumy

{"title":"Inhibition of Benzo[a]pyrene-induced DNA Adduct in Buccal Cells of Smokers by Black Raspberry Lozenges.","authors":"Kun-Ming Chen, Nicolle M Krebs, Yuan-Wan Sun, Dongxiao Sun, Jiangang Liao, Lisa Reinhart, Jacek Krzeminski, Shantu Amin, Gary Stoner, Susan R Mallery, Karam El-Bayoumy","doi":"10.1093/carcin/bgae067","DOIUrl":"https://doi.org/10.1093/carcin/bgae067","url":null,"abstract":"Using LC-MS/MS analysis we previously showed for the first time (Carcinogenesis 43:746-753, 2022) that levels of DNA damage-induced by benzo[a]pyrene (B[a]P), an oral carcinogen and tobacco smoke (TS) constituent, were significantly higher in buccal cells of smokers than those in non-smokers; these results suggest the potential contribution of B[a]P in the development of oral squamous cell carcinoma (OSCC) in humans. Treating cancers, including OSCC at late stages even with improved targeted therapies, continues to be a major challenge. Thus interception/prevention remains a preferable approach for OSCC management and control. In previous preclinical studies we and others demonstrated the protective effects of black raspberry (BRB) against carcinogen-induced DNA damage and OSCC. Thus, to translate preclinical findings we tested the hypothesis, in a Phase 0 clinical study, that BRB administration reduces DNA damage induced by B[a]P in buccal cells of smokers. After enrolling 27 smokers, baseline buccal cells were collected before the administration of BRB lozenges (5/day for 8 weeks, 1 gm BRB powder/lozenge) at baseline, at the middle and the end of BRB administration. The last samples were collected at four weeks after BRB cessation (washout period). B[a]P-induced DNA damage (BPDE-N2-dG) was evaluated by LC-MS/MS. BRB administration resulted in a significant reduction in DNA damage: 26.3% at the midpoint (p = 0.01506) compared to baseline, 36.1% at the end of BRB administration (p = 0.00355), and 16.6% after BRB cessation (p = 0.007586). Our results suggest the potential benefits of BRB as a chemopreventive agent against the development of TS-initiated OSCC.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142379126","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

Absence of lung tumor promotion with reduced tumor size in mice after inhalation of copper welding fumes. 小鼠吸入铜焊烟雾后，肺部肿瘤不再增大，肿瘤体积缩小。

IF 3.3 3区医学

Carcinogenesis Pub Date : 2024-09-11 DOI: 10.1093/carcin/bgae048

Patti C Zeidler-Erdely, Vamsi Kodali, Lauryn M Falcone, Robert Mercer, Stephen S Leonard, Aleksandr B Stefaniak, Lindsay Grose, Rebecca Salmen, Taylor Trainor-DeArmitt, Lori A Battelli, Walter McKinney, Samuel Stone, Terence G Meighan, Ella Betler, Sherri Friend, Kristen R Hobbie, Samantha Service, Michael Kashon, James M Antonini, Aaron Erdely

{"title":"Absence of lung tumor promotion with reduced tumor size in mice after inhalation of copper welding fumes.","authors":"Patti C Zeidler-Erdely, Vamsi Kodali, Lauryn M Falcone, Robert Mercer, Stephen S Leonard, Aleksandr B Stefaniak, Lindsay Grose, Rebecca Salmen, Taylor Trainor-DeArmitt, Lori A Battelli, Walter McKinney, Samuel Stone, Terence G Meighan, Ella Betler, Sherri Friend, Kristen R Hobbie, Samantha Service, Michael Kashon, James M Antonini, Aaron Erdely","doi":"10.1093/carcin/bgae048","DOIUrl":"10.1093/carcin/bgae048","url":null,"abstract":"Welding fumes are a Group 1 (carcinogenic to humans) carcinogen as classified by the International Agency for Research on Cancer. The process of welding creates inhalable fumes rich in iron (Fe) that may also contain known carcinogenic metals such as chromium (Cr) and nickel (Ni). Epidemiological evidence has shown that both mild steel (Fe-rich) and stainless steel (Fe-rich + Cr + Ni) welding fume exposure increases lung cancer risk, and experimental animal data support these findings. Copper-nickel (CuNi) welding processes have not been investigated in the context of lung cancer. Cu is intriguing, however, given the role of Cu in carcinogenesis and cancer therapeutics. This study examines the potential for a CuNi fume to induce mechanistic key characteristics of carcinogenesis in vitro and to promote lung tumorigenesis, using a two-stage mouse bioassay, in vivo. Male A/J mice, initiated with 3-methylcholanthrene (MCA; 10 µg/g), were exposed to CuNi fumes or air by whole-body inhalation for 9 weeks (low deposition-LD and high deposition-HD) and then sacrificed at 30 weeks. In BEAS-2B cells, the CuNi fume-induced micronuclei and caused DNA damage as measured by γ-H2AX. The fume exhibited high reactivity and a dose-response in cytotoxicity and oxidative stress. In vivo, MCA/CuNi HD and LD significantly decreased lung tumor size and adenomas. MCA/CuNi HD exposure significantly decreased gross-evaluated tumor number. In summary, the CuNi fume in vitro exhibited characteristics of a carcinogen, but in vivo, the exposure resulted in smaller tumors, fewer adenomas, less hyperplasia severity, and with HD exposure, less overall lung lesions/tumors.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":"630-641"},"PeriodicalIF":3.3,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141757312","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 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