Oncogenesis最新文献_第7页

WDR4 promotes the progression and lymphatic metastasis of bladder cancer via transcriptional down-regulation of ARRB2. WDR4通过ARRB2的转录下调促进膀胱癌症的进展和淋巴转移。

IF 6.2 2区医学

Oncogenesis Pub Date : 2023-10-02 DOI: 10.1038/s41389-023-00493-z

Guoli Wang, Xin He, Huiqi Dai, Lingyi Lin, Wenmin Cao, Yao Fu, Wenli Diao, Meng Ding, Qing Zhang, Wei Chen, Hongqian Guo

引用次数: 0

AIFM2 promotes hepatocellular carcinoma metastasis by enhancing mitochondrial biogenesis through activation of SIRT1/PGC-1α signaling. AIFM2通过激活SIRT1/PGC-1α信号增强线粒体生物发生，促进肝细胞癌转移。

IF 6.2 2区医学

Oncogenesis Pub Date : 2023-09-21 DOI: 10.1038/s41389-023-00491-1

Sanxing Guo, Fengying Li, Yixuan Liang, Yufei Zheng, Yingyi Mo, Deyao Zhao, Zhixiong Jiang, Mengmeng Cui, Lixia Qi, Jiaxing Chen, Lixin Wan, Guoyong Chen, Sidong Wei, Qi Yang, Junqi Liu

{"title":"AIFM2 promotes hepatocellular carcinoma metastasis by enhancing mitochondrial biogenesis through activation of SIRT1/PGC-1α signaling.","authors":"Sanxing Guo, Fengying Li, Yixuan Liang, Yufei Zheng, Yingyi Mo, Deyao Zhao, Zhixiong Jiang, Mengmeng Cui, Lixia Qi, Jiaxing Chen, Lixin Wan, Guoyong Chen, Sidong Wei, Qi Yang, Junqi Liu","doi":"10.1038/s41389-023-00491-1","DOIUrl":"10.1038/s41389-023-00491-1","url":null,"abstract":"AIFM2 is a crucial NADH oxidase involved in the regulation of cytosolic NAD+. However, the role of AIFM2 in the progression of human cancers remains largely unexplored. Here, we elucidated the clinical implications, biological functions, and molecular mechanisms of AIFM2 in hepatocellular carcinoma (HCC). We found that AIFM2 is significantly upregulated in HCC, which is most probably caused by DNA hypomethylation and downregulation of miR-150-5p. High expression of AIFM2 is markedly associated with poor survival in patients with HCC. Knockdown of AIFM2 significantly impaired, while forced expression of AIFM2 enhanced the metastasis of HCC both in vitro and in vivo. Mechanistically, increased mitochondrial biogenesis and oxidative phosphorylation by activation of SIRT1/PGC-1α signaling contributed to the promotion of metastasis by AIFM2 in HCC. In conclusion, AIFM2 upregulation plays a crucial role in the promotion of HCC metastasis by activating SIRT1/PGC-1α signaling, which strongly suggests that AIFM2 could be targeted for the treatment of HCC.","PeriodicalId":19489,"journal":{"name":"Oncogenesis","volume":"12 1","pages":"46"},"PeriodicalIF":6.2,"publicationDate":"2023-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10514190/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41125830","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: 1

Discovery of neddylation E2s inhibitors with therapeutic activity. 具有治疗活性的类黄酮化E2s抑制剂的发现。

IF 6.2 2区医学

Oncogenesis Pub Date : 2023-09-16 DOI: 10.1038/s41389-023-00490-2

Maa Mamun, Ying Liu, Yin-Ping Geng, Yi-Chao Zheng, Ya Gao, Jian-Gang Sun, Long-Fei Zhao, Li-Juan Zhao, Hong-Min Liu

引用次数: 0

Biological differences underlying sex and gender disparities in bladder cancer: current synopsis and future directions. 膀胱癌中潜在的生理差异和性别差异:现状概述和未来发展方向。

IF 6.2 2区医学

Oncogenesis Pub Date : 2023-09-04 DOI: 10.1038/s41389-023-00489-9

Bhavisha Doshi, Sarah R Athans, Anna Woloszynska

{"title":"Biological differences underlying sex and gender disparities in bladder cancer: current synopsis and future directions.","authors":"Bhavisha Doshi, Sarah R Athans, Anna Woloszynska","doi":"10.1038/s41389-023-00489-9","DOIUrl":"10.1038/s41389-023-00489-9","url":null,"abstract":"Sex and gender disparities in bladder cancer have long been a subject of interest to the cancer research community, wherein men have a 4 times higher incidence rate than women, and female patients often present with higher-grade disease and experience worse outcomes. Despite the known differences in disease incidence and clinical outcomes between male and female bladder cancer patients, clinical management remains the same. In this review, we critically analyze studies that report on the biological differences between men and women and evaluate how these differences contribute to sex and gender disparities in bladder cancer. Distinct characteristics of the male and female immune systems, differences in circulating hormone levels and hormone receptor expression, and different genetic and epigenetic alterations are major biological factors that all likely contribute to disparate incidence rates and outcomes for male and female bladder cancer patients. Future preclinical and clinical studies in this area should employ experimental approaches that account for and consider sex and gender disparities in bladder cancer, thereby facilitating the development of precision medicine for the effective treatment of bladder cancer in all patients.","PeriodicalId":19489,"journal":{"name":"Oncogenesis","volume":"12 1","pages":"44"},"PeriodicalIF":6.2,"publicationDate":"2023-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10477245/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10171203","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

Correction: Non-enzymatic heparanase enhances gastric tumor proliferation via TFEB-dependent autophagy. 更正:非酶促肝素酶通过tfeb依赖性自噬促进胃肿瘤增殖。

IF 6.2 2区医学

Oncogenesis Pub Date : 2023-08-18 DOI: 10.1038/s41389-023-00487-x

Min Yang, Bo Tang, Sumin Wang, Li Tang, Dalin Wen, Israel Vlodavsky, Shi-Ming Yang

引用次数: 0

Glucocorticoid receptor-induced non-muscle caldesmon regulates metastasis in castration-resistant prostate cancer. 糖皮质激素受体诱导的非肌肉caldesmon调节去势抵抗性前列腺癌的转移。

IF 6.2 2区医学

Oncogenesis Pub Date : 2023-08-12 DOI: 10.1038/s41389-023-00485-z

Verneri Virtanen, Kreetta Paunu, Antti Kukkula, Saana Niva, Ylva Junila, Mervi Toriseva, Terhi Jokilehto, Sari Mäkelä, Riikka Huhtaniemi, Matti Poutanen, Ilkka Paatero, Maria Sundvall

{"title":"Glucocorticoid receptor-induced non-muscle caldesmon regulates metastasis in castration-resistant prostate cancer.","authors":"Verneri Virtanen, Kreetta Paunu, Antti Kukkula, Saana Niva, Ylva Junila, Mervi Toriseva, Terhi Jokilehto, Sari Mäkelä, Riikka Huhtaniemi, Matti Poutanen, Ilkka Paatero, Maria Sundvall","doi":"10.1038/s41389-023-00485-z","DOIUrl":"10.1038/s41389-023-00485-z","url":null,"abstract":"Lethal prostate cancer (PCa) is characterized by the presence of metastases and development of resistance to therapies. Metastases form in a multi-step process enabled by dynamic cytoskeleton remodeling. An actin cytoskeleton regulating gene, CALD1, encodes a protein caldesmon (CaD). Its isoform, low-molecular-weight CaD (l-CaD), operates in non-muscle cells, supporting the function of filaments involved in force production and mechanosensing. Several factors, including glucocorticoid receptor (GR), have been identified as regulators of l-CaD in different cell types, but the regulation of l-CaD in PCa has not been defined. PCa develops resistance in response to therapeutic inhibition of androgen signaling by multiple strategies. Known strategies include androgen receptor (AR) alterations, modified steroid synthesis, and bypassing AR signaling, for example, by GR upregulation. Here, we report that in vitro downregulation of l-CaD promotes epithelial phenotype and reduces spheroid growth in 3D, which is reflected in vivo in reduced formation of metastases in zebrafish PCa xenografts. In accordance, CALD1 mRNA expression correlates with epithelial-to-mesenchymal transition (EMT) transcripts in PCa patients. We also show that CALD1 is highly co-expressed with GR in multiple PCa data sets, and GR activation upregulates l-CaD in vitro. Moreover, GR upregulation associates with increased l-CaD expression after the development of resistance to antiandrogen therapy in PCa xenograft mouse models. In summary, GR-regulated l-CaD plays a role in forming PCa metastases, being clinically relevant when antiandrogen resistance is attained by the means of bypassing AR signaling by GR upregulation.","PeriodicalId":19489,"journal":{"name":"Oncogenesis","volume":"12 1","pages":"42"},"PeriodicalIF":6.2,"publicationDate":"2023-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10423232/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9988903","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

SLC26A3/NHERF2-IκB/NFκB/p65 feedback loop suppresses tumorigenesis and metastasis in colorectal cancer. SLC26A3/ nherf2 - i - κ b / nf - κ b /p65反馈回路抑制结直肠癌的肿瘤发生和转移

IF 6.2 2区医学

Oncogenesis Pub Date : 2023-08-12 DOI: 10.1038/s41389-023-00488-w

Chunlin Lin, Penghang Lin, Huayan Lin, Hengxin Yao, Songyi Liu, Ruofan He, Hui Chen, Zuhong Teng, Robert M Hoffman, Jianxin Ye, Guangwei Zhu

{"title":"SLC26A3/NHERF2-IκB/NFκB/p65 feedback loop suppresses tumorigenesis and metastasis in colorectal cancer.","authors":"Chunlin Lin, Penghang Lin, Huayan Lin, Hengxin Yao, Songyi Liu, Ruofan He, Hui Chen, Zuhong Teng, Robert M Hoffman, Jianxin Ye, Guangwei Zhu","doi":"10.1038/s41389-023-00488-w","DOIUrl":"10.1038/s41389-023-00488-w","url":null,"abstract":"Colorectal cancer (CRC) is a formidable disease due to the intricate mechanisms that drive its proliferation and metastasis. Despite significant progress in cancer research, the integration of these mechanisms that influence cancer cell behavior remains elusive. Therefore, it is imperative to comprehensively elucidate the underlying mechanisms driving CRC proliferation and metastasis. In this study, we reported a novel role of SLC26A3 in suppressing CRC progression. We found that SLC26A3 expression was downregulated in CRC, which was proportionally correlated with survival. Our in vivo and in vitro experiments demonstrated that up-regulation of SLC26A3 inhibited CRC proliferation and metastasis, while down-regulation of SLC26A3 promoted CRC progression by modulating the expression level of IκB. Furthermore, we identified NHERF2 as a novel interacting protein of SLC26A3 responsible for stabilizing the IκB protein and removing ubiquitination modification. Mechanistically, SLC26A3 augmented the interaction between NHERF2 and IκB, subsequently reducing its degradation. This process inhibited the dissociation of p65 from the IκB/p65/p50 complex and reduced the translocation of p65 from the cytoplasm to the nucleus. Moreover, our investigation revealed that NF-κB/p65 directly bound to the promoter of SLC26A3, leading to a decline in its mRNA expression. Thus, SLC26A3 impeded the nuclear translocation of NF-κB/p65, enhancing the transcription of SLC26A3 and establishing a positive regulatory feedback loop in CRC cells. Collectively, these results suggest that a SLC26A3/NHERF2-IκB/NF-κB/p65 signaling loop suppresses proliferation and metastasis in CRC cells. These findings propose a novel SLC26A3-driven signaling loop that regulates proliferation and metastasis in CRC, providing promising therapeutic interventions and prognostic targets for the management of CRC.","PeriodicalId":19489,"journal":{"name":"Oncogenesis","volume":"12 1","pages":"41"},"PeriodicalIF":6.2,"publicationDate":"2023-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10423209/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10000486","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: 1

Loss of Pkd1 limits susceptibility to colitis and colorectal cancer. Pkd1的缺失限制了对结肠炎和结直肠癌癌症的易感性。

IF 6.2 2区医学

Oncogenesis Pub Date : 2023-08-05 DOI: 10.1038/s41389-023-00486-y

Anna S Nikonova, Alexander Y Deneka, Flaviane N Silva, Shabnam Pirestani, Rossella Tricarico, Anna A Kiseleva, Yan Zhou, Emmanuelle Nicolas, Douglas B Flieder, Sergei I Grivennikov, Erica A Golemis

{"title":"Loss of Pkd1 limits susceptibility to colitis and colorectal cancer.","authors":"Anna S Nikonova, Alexander Y Deneka, Flaviane N Silva, Shabnam Pirestani, Rossella Tricarico, Anna A Kiseleva, Yan Zhou, Emmanuelle Nicolas, Douglas B Flieder, Sergei I Grivennikov, Erica A Golemis","doi":"10.1038/s41389-023-00486-y","DOIUrl":"10.1038/s41389-023-00486-y","url":null,"abstract":"Colorectal cancer (CRC) is one of the most common cancers, with an annual incidence of ~135,000 in the US, associated with ~50,000 deaths. Autosomal dominant polycystic kidney disease (ADPKD), associated with mutations disabling the PKD1 gene, affects as many as 1 in 1000. Intriguingly, some studies have suggested that individuals with germline mutations in PKD1 have reduced incidence of CRC, suggesting a genetic modifier function. Using mouse models, we here establish that loss of Pkd1 greatly reduces CRC incidence and tumor growth induced by loss of the tumor suppressor Apc. Growth of Pkd1-/-;Apc-/- organoids was reduced relative to Apc-/- organoids, indicating a cancer cell-intrinsic activity, even though Pkd1 loss enhanced activity of pro-oncogenic signaling pathways. Notably, Pkd1 loss increased colon barrier function, with Pkd1-deficient animals resistant to DSS-induced colitis, associated with upregulation of claudins that decrease permeability, and reduced T cell infiltration. Notably, Pkd1 loss caused greater sensitivity to activation of CFTR, a tumor suppressor in CRC, paralleling signaling relations in ADPKD. Overall, these data and other data suggest germline and somatic mutations in PKD1 may influence incidence, presentation, and treatment response in human CRC and other pathologies involving the colon.","PeriodicalId":19489,"journal":{"name":"Oncogenesis","volume":"12 1","pages":"40"},"PeriodicalIF":6.2,"publicationDate":"2023-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10403611/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9946275","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

Retraction Note: Acetyl-CoA synthetase 3 promotes bladder cancer cell growth under metabolic stress. 备注:乙酰辅酶a合成酶3促进代谢应激下膀胱癌细胞生长。

IF 6.2 2区医学

Oncogenesis Pub Date : 2023-07-26 DOI: 10.1038/s41389-023-00484-0

Jianhao Zhang, Hongjian Duan, Zhipeng Feng, Xinwei Han, Chaohui Gu

引用次数: 0

Correction: Targeting IL-3Rα on tumor-derived endothelial cells blunts metastatic spread of triple-negative breast cancer via extracellular vesicle reprogramming. 校正:将IL-3Rα靶向肿瘤来源的内皮细胞，通过细胞外囊泡重编程使三阴性乳腺癌的转移性扩散减弱。

IF 6.2 2区医学

Oncogenesis Pub Date : 2023-07-25 DOI: 10.1038/s41389-023-00483-1

Tatiana Lopatina, Cristina Grange, Claudia Cavallari, Victor Navarro-Tableros, Giusy Lombardo, Arturo Rosso, Massimo Cedrino, Margherita Alba Carlotta Pomatto, Malvina Koni, Francesca Veneziano, Isabella Castellano, Giovanni Camussi, Maria Felice Brizzi

引用次数: 0