Oncogenesis最新文献_第5页

USP32 facilitates non-small cell lung cancer progression via deubiquitinating BAG3 and activating RAF-MEK-ERK signaling pathway. USP32 通过去泛素化 BAG3 和激活 RAF-MEK-ERK 信号通路促进非小细胞肺癌的进展。

IF 5.9 2区医学

Oncogenesis Pub Date : 2024-07-19 DOI: 10.1038/s41389-024-00528-z

Shuang Li, Lina Yang, Xiaoyan Ding, Hongxiao Sun, Xiaolei Dong, Fanghao Yang, Mengjun Wang, Huhu Zhang, Ya Li, Bing Li, Chunyan Liu

{"title":"USP32 facilitates non-small cell lung cancer progression via deubiquitinating BAG3 and activating RAF-MEK-ERK signaling pathway.","authors":"Shuang Li, Lina Yang, Xiaoyan Ding, Hongxiao Sun, Xiaolei Dong, Fanghao Yang, Mengjun Wang, Huhu Zhang, Ya Li, Bing Li, Chunyan Liu","doi":"10.1038/s41389-024-00528-z","DOIUrl":"10.1038/s41389-024-00528-z","url":null,"abstract":"The regulatory significance of ubiquitin-specific peptidase 32 (USP32) in tumor is significant, nevertheless, the biological roles and regulatory mechanisms of USP32 in non-small cell lung cancer (NSCLC) remain unclear. According to our research, USP32 was strongly expressed in NSCLC cell lines and tissues and was linked to a bad prognosis for NSCLC patients. Interference with USP32 resulted in a significant inhibition of NSCLC cell proliferation, migration potential, and EMT development; on the other hand, USP32 overexpression had the opposite effect. To further elucidate the mechanism of action of USP32 in NSCLC, we screened H1299 cells for interacting proteins and found that USP32 interacts with BAG3 (Bcl2-associated athanogene 3) and deubiquitinates and stabilizes BAG3 in a deubiquitinating activity-dependent manner. Functionally, restoration of BAG3 expression abrogated the antitumor effects of USP32 silencing. Furthermore, USP32 increased the phosphorylation level of the RAF/MEK/ERK signaling pathway in NSCLC cells by stabilizing BAG3. In summary, these findings imply that USP32 is critical to the development of NSCLC and could offer a theoretical framework for the clinical diagnosis and management of NSCLC patients in the future.","PeriodicalId":19489,"journal":{"name":"Oncogenesis","volume":"13 1","pages":"27"},"PeriodicalIF":5.9,"publicationDate":"2024-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11271578/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141727512","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

YAP/TAZ interacts with RBM39 to confer resistance against indisulam. YAP/TAZ 与 RBM39 相互作用，赋予茚虫威抗性。

IF 5.9 2区医学

Oncogenesis Pub Date : 2024-07-15 DOI: 10.1038/s41389-024-00527-0

Toshinori Ando, Kento Okamoto, Yume Ueda, Nanako Kataoka, Tomoaki Shintani, Souichi Yanamoto, Mutsumi Miyauchi, Mikihito Kajiya

{"title":"YAP/TAZ interacts with RBM39 to confer resistance against indisulam.","authors":"Toshinori Ando, Kento Okamoto, Yume Ueda, Nanako Kataoka, Tomoaki Shintani, Souichi Yanamoto, Mutsumi Miyauchi, Mikihito Kajiya","doi":"10.1038/s41389-024-00527-0","DOIUrl":"10.1038/s41389-024-00527-0","url":null,"abstract":"The Hippo pathway and its downstream effectors, Yes-associated protein/transcriptional coactivator with PDZ-binding motif (YAP/TAZ), are essential for cell growth and organ development. Emerging evidence revealed that the Hippo pathway and YAP/TAZ are frequently dysregulated by multiple genetic alterations in solid cancers including head and neck squamous cell carcinoma (HNSCC); however, the YAP/TAZ-nuclear interactome remains unclear. RNA-binding motif protein 39 (RBM39) enhances transcriptional activity of several transcription factors and also regulates mRNA splicing. Indisulam degrading RBM39 induces alternative splicing, leading to cell death. However, clinical trials of indisulam have failed to show effectiveness. Therefore, clarifying the resistance mechanism against splicing inhibitors is urgently required. In this study, we identified RBM39 as a novel YAP/TAZ-interacting molecule by proteome analysis. RBM39 promoted YAP/TAZ transcriptional activity. We further elucidated that indisulam reduces RBM39/YAP/TAZ-mediated integrin or collagen expression, thereby inactivating focal adhesion kinase (FAK) important for cell survival. Moreover, indisulam also induced alternative splicing of cell cycle- or DNA metabolism-related genes. YAP/TAZ hyperactivation delayed indisulam-induced RBM39 degradation, which restored the integrin/collagen expression to activate FAK, and alternative splicing, thereby conferring resistance against indisulam in vitro and in vivo. Our findings may aid to develop a novel cancer therapy focusing on YAP/TAZ/RBM39 interaction.","PeriodicalId":19489,"journal":{"name":"Oncogenesis","volume":"13 1","pages":"25"},"PeriodicalIF":5.9,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11247092/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141616903","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

Gemcitabine as chemotherapy of head and neck cancer in Fanconi anemia patients. 吉西他滨作为范可尼贫血症患者头颈癌的化疗药物。

IF 5.9 2区医学

Oncogenesis Pub Date : 2024-07-11 DOI: 10.1038/s41389-024-00525-2

Anne M van Harten, Ronak Shah, D Vicky de Boer, Marijke Buijze, Maaike Kreft, Ji-Ying Song, Lisa M Zürcher, Heinz Jacobs, Ruud H Brakenhoff

{"title":"Gemcitabine as chemotherapy of head and neck cancer in Fanconi anemia patients.","authors":"Anne M van Harten, Ronak Shah, D Vicky de Boer, Marijke Buijze, Maaike Kreft, Ji-Ying Song, Lisa M Zürcher, Heinz Jacobs, Ruud H Brakenhoff","doi":"10.1038/s41389-024-00525-2","DOIUrl":"10.1038/s41389-024-00525-2","url":null,"abstract":"Fanconi anemia (FA) is a rare hereditary disease resulting from an inactivating mutation in the FA/BRCA pathway, critical for the effective repair of DNA interstrand crosslinks (ICLs). The disease is characterized by congenital abnormalities, progressing bone marrow failure, and an increased risk of developing malignancies early in life, in particular head and neck squamous cell carcinoma (HNSCC). While ICL-inducing cisplatin combined with radiotherapy is a mainstay of HNSCC treatment, cisplatin is contra-indicated for FA-HNSCC patients. This dilemma necessitates the identification of novel treatment modalities tolerated by FA-HNSCC patients. To identify druggable targets, an siRNA-based genetic screen was previously performed in HNSCC-derived cell lines from FA and non-FA tumor origin. Here, we report that the Ribonucleotide Reductase (RNR) complex, consisting of the RRM1 and RRM2 subunits, was identified as a therapeutic target for both, FA and non-FA HNSCC. While non-FA HNSCC cells responded differentially to RNR depletion, FA-HNSCC cells were consistently found hypersensitive. This insight was confirmed pharmacologically using 2', 2'-difluoro 2'deoxycytidine (dFdC), also known as gemcitabine, a clinically used nucleotide analog that is a potent inhibitor of the RNR complex. Importantly, while cisplatin exposure displayed severe, long-lasting toxicity on the hematopoietic stem and progenitor compartments in Fancg-/- mice, gemcitabine was well tolerated and had only a mild, transient impact. Taken together, our data implicate that gemcitabine-based chemoradiotherapy could serve as an alternative HNSCC treatment in Fanconi patients, and deserves clinical testing.","PeriodicalId":19489,"journal":{"name":"Oncogenesis","volume":"13 1","pages":"26"},"PeriodicalIF":5.9,"publicationDate":"2024-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11239817/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141590964","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

Involvement of Kindlin-1 in cutaneous squamous cell carcinoma. 皮肤鳞状细胞癌中 Kindlin-1 的参与。

IF 5.9 2区医学

Oncogenesis Pub Date : 2024-07-09 DOI: 10.1038/s41389-024-00526-1

Giovana Carrasco, Ifigeneia Stavrou, Mairi Treanor-Taylor, Henry Beetham, Martin Lee, Roza Masalmeh, Artur Carreras-Soldevila, David Hardman, Miguel O Bernabeu, Alex von Kriegsheim, Gareth J Inman, Adam Byron, Valerie G Brunton

{"title":"Involvement of Kindlin-1 in cutaneous squamous cell carcinoma.","authors":"Giovana Carrasco, Ifigeneia Stavrou, Mairi Treanor-Taylor, Henry Beetham, Martin Lee, Roza Masalmeh, Artur Carreras-Soldevila, David Hardman, Miguel O Bernabeu, Alex von Kriegsheim, Gareth J Inman, Adam Byron, Valerie G Brunton","doi":"10.1038/s41389-024-00526-1","DOIUrl":"10.1038/s41389-024-00526-1","url":null,"abstract":"Kindler syndrome (KS) is a rare genodermatosis resulting from loss-of-function mutations in FERMT1, the gene that encodes Kindlin-1. KS patients have a high propensity to develop aggressive and metastatic cutaneous squamous cell carcinoma (cSCC). Here we show in non-KS-associated patients that elevation of FERMT1 expression is increased in actinic keratoses compared to normal skin, with a further increase in cSCC supporting a pro-tumorigenic role in this population. In contrast, we show that loss of Kindlin-1 leads to increased SCC tumor growth in vivo and in 3D spheroids, which was associated with the development of a hypoxic tumor environment and increased glycolysis. The metalloproteinase Mmp13 was upregulated in Kindlin-1-depleted tumors, and increased expression of MMP13 was responsible for driving increased invasion of the Kindlin-1-depleted SCC cells. These results provide evidence that Kindlin-1 loss in SCC can promote invasion through the upregulation of MMP13, and offer novel insights into how Kindlin-1 loss leads to the development of a hypoxic environment that is permissive for tumor growth.","PeriodicalId":19489,"journal":{"name":"Oncogenesis","volume":"13 1","pages":"24"},"PeriodicalIF":5.9,"publicationDate":"2024-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11233684/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141563991","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

USP21-mediated G3BP1 stabilization accelerates proliferation and metastasis of esophageal squamous cell carcinoma via activating Wnt/β-Catenin signaling. USP21 介导的 G3BP1 稳定通过激活 Wnt/β-Catenin 信号加速了食管鳞状细胞癌的增殖和转移。

IF 5.9 2区医学

Oncogenesis Pub Date : 2024-06-21 DOI: 10.1038/s41389-024-00524-3

Jiazhong Guo, Yunpeng Zhao, Huacong Sui, Lei Liu, Fanrong Liu, Lingxiao Yang, Fengyuan Gao, Jinfu Wang, Yilin Zhu, Lingbing Li, Xiangqing Song, Peng Li, Zhongxian Tian, Peichao Li, Xiaogang Zhao

{"title":"USP21-mediated G3BP1 stabilization accelerates proliferation and metastasis of esophageal squamous cell carcinoma via activating Wnt/β-Catenin signaling.","authors":"Jiazhong Guo, Yunpeng Zhao, Huacong Sui, Lei Liu, Fanrong Liu, Lingxiao Yang, Fengyuan Gao, Jinfu Wang, Yilin Zhu, Lingbing Li, Xiangqing Song, Peng Li, Zhongxian Tian, Peichao Li, Xiaogang Zhao","doi":"10.1038/s41389-024-00524-3","DOIUrl":"10.1038/s41389-024-00524-3","url":null,"abstract":"Lacking effective therapeutic targets heavily restricts the improvement of clinical prognosis for patients diagnosed with esophageal squamous cell carcinoma (ESCC). Ubiquitin Specific Peptidase 21 (USP21) is dysregulated in plenty of human cancers, however, its potential function and relevant molecular mechanisms in ESCC malignant progression as well as its value in clinical translation remain largely unknown. Here, in vitro and in vivo experiments revealed that aberrant upregulation of USP21 accelerated the proliferation and metastasis of ESCC in a deubiquitinase-dependent manner. Mechanistically, we found that USP21 binds to, deubiquitinates, and stabilizes the G3BP Stress Granule Assembly Factor 1 (G3BP1) protein, which is required for USP21-mediated ESCC progression. Further molecular studies demonstrated that the USP21/G3BP1 axis played a tumor-promoting role in ESCC progression by activating the Wnt/β-Catenin signaling pathway. Additionally, disulfiram (DSF), an inhibitor against USP21 deubiquitylation activity, markedly abolished the USP21-mediated stability of G3BP1 protein and significantly displayed an anti-tumor effect on USP21-driving ESCC progression. Finally, the regulatory axis of USP21/G3BP1 was demonstrated to be aberrantly activated in ESCC tumor tissues and closely associated with advanced clinical stages and unfavorable prognoses, which provides a promising therapeutic strategy targeting USP21/G3BP1 axis for ESCC patients.","PeriodicalId":19489,"journal":{"name":"Oncogenesis","volume":"13 1","pages":"23"},"PeriodicalIF":5.9,"publicationDate":"2024-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11192907/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141437268","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

Activated platelet-derived exosomal LRG1 promotes multiple myeloma cell growth. 活化的血小板衍生外泌体 LRG1 可促进多发性骨髓瘤细胞的生长。

IF 6.2 2区医学

Oncogenesis Pub Date : 2024-06-13 DOI: 10.1038/s41389-024-00522-5

Meng Gao, Hang Dong, Siyi Jiang, Fangping Chen, Yunfeng Fu, Yanwei Luo

{"title":"Activated platelet-derived exosomal LRG1 promotes multiple myeloma cell growth.","authors":"Meng Gao, Hang Dong, Siyi Jiang, Fangping Chen, Yunfeng Fu, Yanwei Luo","doi":"10.1038/s41389-024-00522-5","DOIUrl":"10.1038/s41389-024-00522-5","url":null,"abstract":"The hypercoagulable state is a hallmark for patients with multiple myeloma (MM) and is associated with disease progression. Activated platelets secrete exosomes and promote solid tumor growth. However, the role of platelet-derived exosomes in MM is not fully clear. We aim to study the underlying mechanism of how platelet-derived exosomes promote MM cell growth. Flow cytometry, Western blot, proteome analysis, co-immunoprecipitation, immunofluorescence staining, and NOD/SCID mouse subcutaneous transplantation model were performed to investigate the role of exosomal LRG1 on multiple myeloma cell growth. Peripheral blood platelets in MM patients were in a highly activated state, and platelet-rich plasma from MM patients significantly promoted cell proliferation and decreased apoptotic cells in U266 and RPMI8226 cells. Leucine-rich-alpha-2-glycoprotein 1 (LRG1) was significantly enriched in MM platelet-derived exosomes. Blocking LRG1 in recipient cells using LRG1 antibody could significantly eliminate the proliferation-promoting effect of platelet-derived exosomes on MM cells. And high exosomal LRG1 was associated with poor prognosis of patients with MM. Mechanistic studies revealed that LRG1 interacted with Olfactomedin 4 (OLFM4) to accelerate MM progression by activating the epithelial-to-mesenchymal transition (EMT) signaling pathway and promoting angiogenesis. Our results revealed that blocking LRG1 is a promising therapeutic strategy for the treatment of MM.","PeriodicalId":19489,"journal":{"name":"Oncogenesis","volume":"13 1","pages":"21"},"PeriodicalIF":6.2,"publicationDate":"2024-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11176168/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141317934","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

Comprehensive multi-omics analysis of breast cancer reveals distinct long-term prognostic subtypes. 乳腺癌多组学综合分析揭示了不同的长期预后亚型。

IF 6.2 2区医学

Oncogenesis Pub Date : 2024-06-13 DOI: 10.1038/s41389-024-00521-6

Abhibhav Sharma, Julia Debik, Bjørn Naume, Hege Oma Ohnstad, Tone F Bathen, Guro F Giskeødegård

{"title":"Comprehensive multi-omics analysis of breast cancer reveals distinct long-term prognostic subtypes.","authors":"Abhibhav Sharma, Julia Debik, Bjørn Naume, Hege Oma Ohnstad, Tone F Bathen, Guro F Giskeødegård","doi":"10.1038/s41389-024-00521-6","DOIUrl":"10.1038/s41389-024-00521-6","url":null,"abstract":"Breast cancer (BC) is a leading cause of cancer-related death worldwide. The diverse nature and heterogeneous biology of BC pose challenges for survival prediction, as patients with similar diagnoses often respond differently to treatment. Clinically relevant BC intrinsic subtypes have been established through gene expression profiling and are implemented in the clinic. While these intrinsic subtypes show a significant association with clinical outcomes, their long-term survival prediction beyond 5 years often deviates from expected clinical outcomes. This study aimed to identify naturally occurring long-term prognostic subgroups of BC based on an integrated multi-omics analysis. This study incorporates a clinical cohort of 335 untreated BC patients from the Oslo2 study with long-term follow-up (>12 years). Multi-Omics Factor Analysis (MOFA+) was employed to integrate transcriptomic, proteomic, and metabolomic data obtained from the tumor tissues. Our analysis revealed three prominent multi-omics clusters of BC patients with significantly different long-term prognoses (p = 0.005). The multi-omics clusters were validated in two independent large cohorts, METABRIC and TCGA. Importantly, a lack of prognostic association to long-term follow-up above 12 years in the previously established intrinsic subtypes was shown for these cohorts. Through a systems-biology approach, we identified varying enrichment levels of cell-cycle and immune-related pathways among the prognostic clusters. Integrated multi-omics analysis of BC revealed three distinct clusters with unique clinical and biological characteristics. Notably, these multi-omics clusters displayed robust associations with long-term survival, outperforming the established intrinsic subtypes.","PeriodicalId":19489,"journal":{"name":"Oncogenesis","volume":"13 1","pages":"22"},"PeriodicalIF":6.2,"publicationDate":"2024-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11176181/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141317935","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

DAB2IP inhibits glucose uptake by modulating HIF-1α ubiquitination under hypoxia in breast cancer. DAB2IP 在乳腺癌缺氧状态下通过调节 HIF-1α 泛素化抑制葡萄糖摄取

IF 6.2 2区医学

Oncogenesis Pub Date : 2024-06-11 DOI: 10.1038/s41389-024-00523-4

Hongliang Dong, Weiyi Jia, Weijian Meng, Rui Zhang, Zhihong Qi, Zhuo Chen, Sophia Xie, Jiang Min, Liang Liu, Jie Shen

{"title":"DAB2IP inhibits glucose uptake by modulating HIF-1α ubiquitination under hypoxia in breast cancer.","authors":"Hongliang Dong, Weiyi Jia, Weijian Meng, Rui Zhang, Zhihong Qi, Zhuo Chen, Sophia Xie, Jiang Min, Liang Liu, Jie Shen","doi":"10.1038/s41389-024-00523-4","DOIUrl":"10.1038/s41389-024-00523-4","url":null,"abstract":"Metabolic reprogramming has become increasingly important in tumor biology research. The glucose metabolic pathway is a major energy source and is often dysregulated in breast cancer. DAB2IP is widely reported to be a tumor suppressor that acts as a scaffold protein to suppress tumor malignancy in breast cancer. Interestingly, DAB2IP has also been found to be a potential regulator of glucose uptake; however, the exact mechanism remains unclear. In this study, we found that DAB2IP inhibited glucose uptake under hypoxia conditions in breast cancer cells by suppressing HIF-1α signals. Mechanically, DAB2IP interacted with the E3 ubiquitin ligase STUB1 via its PER domain, thus triggering STUB1 mediated HIF-1α ubiquitylation and degradation, and inhibit glucose metabolism and tumor progression. Deleting the PER domain abrogated the DAB2IP-related inhibitory effects on glucose uptake, intracellular ATP production, and lactic acid production in breast cancer cells. These findings elucidate the biological roles of DAB2IP in cancer-related glucose metabolism as well as a novel mechanism by which STUB1-driven HIF-1α ubiquitylated degradation is regulated in breast cancer.","PeriodicalId":19489,"journal":{"name":"Oncogenesis","volume":"13 1","pages":"20"},"PeriodicalIF":6.2,"publicationDate":"2024-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11166643/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141306489","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: PI3K/Akt pathway and Nanog maintain cancer stem cells in sarcomas. 撤稿说明：PI3K/Akt通路和Nanog可维持肉瘤中的癌症干细胞。

IF 6.2 2区医学

Oncogenesis Pub Date : 2024-05-29 DOI: 10.1038/s41389-024-00519-0

Changhwan Yoon, Jun Lu, Brendan C Yi, Kevin K Chang, M Celeste Simon, Sandra Ryeom, Sam S Yoon

引用次数: 0

Retraction Note: Platelet-derived growth factor receptor-α and -β promote cancer stem cell phenotypes in sarcomas. 撤稿说明：血小板衍生生长因子受体-α和-β可促进肉瘤中癌症干细胞表型的形成。

IF 6.2 2区医学

Oncogenesis Pub Date : 2024-05-29 DOI: 10.1038/s41389-024-00520-7

Kevin K Chang, Changhwan Yoon, Brendan C Yi, William D Tap, M Celeste Simon, Sam S Yoon

引用次数: 0