Oncogene最新文献_第4页

The complex roles of IL-36 and IL-38 in cancer: friends or foes?

IF 6.9 1区医学

Oncogene Pub Date : 2025-03-08 DOI: 10.1038/s41388-025-03293-4

Méabh Finucane, Elizabeth Brint, Aileen Houston

{"title":"The complex roles of IL-36 and IL-38 in cancer: friends or foes?","authors":"Méabh Finucane, Elizabeth Brint, Aileen Houston","doi":"10.1038/s41388-025-03293-4","DOIUrl":"10.1038/s41388-025-03293-4","url":null,"abstract":"The interleukin-36 (IL-36) family comprises of three pro-inflammatory receptor agonists (IL-36α, IL-36β and IL-36γ), two anti-inflammatory receptor antagonists (IL-36RA and IL-38) along with the IL-36 receptor (IL-36R). Part of the IL-1 cytokine superfamily, the IL-36 family was discovered in the early 2000s due to the homology of its member sequences to the IL-1 cytokines. As pro- and anti-inflammatory cytokines, respectively, IL-36α, IL-36β, IL-36γ and IL-38 aid in maintaining homoeostasis by reciprocally regulating the body’s response to damage and disease through IL-36R-associated signalling. With the significant roles of IL-36α, IL-36β and IL-36γ in regulating the immune response realised, interest has grown in investigating their roles in cancer. While initial studies indicated solely tumour-suppressing roles, more recent work has identified tumour-promoting roles in cancer, suggesting a more complex dual functionality of the IL-36 cytokines. The activity of IL-38 in cancer is similarly complex, with the receptor antagonist displaying distinct tumour-suppressive roles, particularly in colorectal cancer (CRC), in addition to broad tumour-promoting roles in various other malignancies. This review provides a comprehensive overview of the IL-36 and IL-38 cytokines, their activation and IL-36R signalling, the physiological functions of these cytokines, and their activity in cancer.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":"44 13","pages":"851-861"},"PeriodicalIF":6.9,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41388-025-03293-4.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143586384","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Cellular polarity pilots breast cancer progression and immunosuppression

IF 6.9 1区医学

Oncogene Pub Date : 2025-03-08 DOI: 10.1038/s41388-025-03324-0

Jie Huang, Shufeng Luo, Juan Shen, Maya Lee, Rachel Chen, Shenglin Ma, Lun-Quan Sun, Jian Jian Li

{"title":"Cellular polarity pilots breast cancer progression and immunosuppression","authors":"Jie Huang, Shufeng Luo, Juan Shen, Maya Lee, Rachel Chen, Shenglin Ma, Lun-Quan Sun, Jian Jian Li","doi":"10.1038/s41388-025-03324-0","DOIUrl":"10.1038/s41388-025-03324-0","url":null,"abstract":"Disrupted cellular polarity (DCP) is a hallmark of solid cancer, the malignant disease of epithelial tissues, which occupies ~90% of all human cancers. DCP has been identified to affect not only the cancer cell’s aggressive behavior but also the migration and infiltration of immune cells, although the precise mechanism of DCP-affected tumor-immune cell interaction remains unclear. This review discusses immunosuppressive tumor microenvironments (TME) caused by DCP-driven tumor cell proliferation with DCP-impaired immune cell functions. We will revisit the fundamental roles of cell polarity (CP) proteins in sustaining mammary luminal homeostasis, epithelial transformation, and breast cancer progression. Then, the current data on CP involvement in immune cell activation, maturation, migration, and tumor infiltration are evaluated. The CP status on the immune effector cells and their targeted tumor cells are highlighted in tumor immune regulation, including the antigen presentation and the formation of immune synapses (IS). CP-regulated antigen presentation and delivery and the formation of IS between the immune cells, especially between the immune effectors and tumor cells, will be addressed. Alterations of CP on the tumor cells, infiltrated immune effector cells, or both are discussed with these aspects. We conclude that CP-mediated tumor aggressiveness coupled with DCP-impaired immune cell disability may decide the degree of immunosuppressive status and responsiveness to immune checkpoint blockade (ICB). Further elucidating the dynamics of CP- or DCP-mediated immune regulation in TME will provide more critical insights into tumor-immune cell dynamics, which is required to invent more effective approaches for cancer immunotherapy.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":"44 12","pages":"783-793"},"PeriodicalIF":6.9,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41388-025-03324-0.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143586403","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Transcriptional reprogramming triggered by neonatal UV radiation or Lkb1 loss prevents BRAF^V600E-induced growth arrest in melanocytes. 新生儿紫外线辐射或Lkb1缺失引发的转录重编程可防止BRAFV600E诱导的黑色素细胞生长停滞。

IF 6.9 1区医学

Oncogene Pub Date : 2025-03-08 DOI: 10.1038/s41388-025-03339-7

Kimberley McGrail, Paula Granado-Martínez, Roberto Orsenigo, Ginevra Caratù, Paula Nieto, Holger Heyn, Berta Ferrer, Javier Hernández-Losa, Eva Muñoz-Couselo, Vicenç García-Patos, Juan A Recio

{"title":"Transcriptional reprogramming triggered by neonatal UV radiation or Lkb1 loss prevents BRAFV600E-induced growth arrest in melanocytes.","authors":"Kimberley McGrail, Paula Granado-Martínez, Roberto Orsenigo, Ginevra Caratù, Paula Nieto, Holger Heyn, Berta Ferrer, Javier Hernández-Losa, Eva Muñoz-Couselo, Vicenç García-Patos, Juan A Recio","doi":"10.1038/s41388-025-03339-7","DOIUrl":"https://doi.org/10.1038/s41388-025-03339-7","url":null,"abstract":"The mechanisms behind UVB-initiated, neonatal-specific melanoma linked to BRAFV600E are not well understood, particularly regarding its role in growth arrest. We found that, beyond mutations, neonatal UV irradiation or Lkb1 loss promotes a cell-autonomous transcriptional reprogramming that prevents BRAFV600E-induced growth arrest, leading to melanoma development. Using UVB-dependent and independent mouse models, genomic analyses, clinical data, and single-cell transcriptomics, we identified a transcriptional program that bypasses growth arrest, promoting melanoma. In humans, many of these genes are linked to poor survival and are upregulated in melanoma progression and other RAS pathway-driven tumors. Reconstitution experiments showed these genes cooperate with BRAFV600E in melanocyte transformation, dedifferentiation, and drug resistance. Depleting gene products like UPP1 highlights their potential as therapeutic targets. Our findings reveal that BRAFV600E-mutated melanomas can develop independently of nevus progression and identify novel targets for treatment.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143586387","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Integrated single-cell and spatial transcriptomic profiling reveals that CD177⁺ Tregs enhance immunosuppression through apoptosis and resistance to immunotherapy in hepatocellular carcinoma.

IF 6.9 1区医学

Oncogene Pub Date : 2025-03-07 DOI: 10.1038/s41388-025-03330-2

Yuan Liang, Lei Qiao, Qufei Qian, Rui Zhang, Yu Li, Xiaozhang Xu, Zibo Xu, Qingfa Bu, Hao Wang, Xiangyu Li, Tianning Huang, Jinren Zhou, Ling Lu, Qiuyang Chen

{"title":"Integrated single-cell and spatial transcriptomic profiling reveals that CD177+ Tregs enhance immunosuppression through apoptosis and resistance to immunotherapy in hepatocellular carcinoma.","authors":"Yuan Liang, Lei Qiao, Qufei Qian, Rui Zhang, Yu Li, Xiaozhang Xu, Zibo Xu, Qingfa Bu, Hao Wang, Xiangyu Li, Tianning Huang, Jinren Zhou, Ling Lu, Qiuyang Chen","doi":"10.1038/s41388-025-03330-2","DOIUrl":"https://doi.org/10.1038/s41388-025-03330-2","url":null,"abstract":"Regulatory T cells (Tregs), an immunosuppressive subpopulation of CD4+ T cells, are prevalent in tumor tissues, where they impede effective antitumor immune responses and represent potential targets for immunotherapy. However, targeting tumor-infiltrating Treg cells (TiTregs) remains challenging. In this study, we identified CD177 as a biomarker specifically expressed in TiTregs but not in adjacent or peripheral Treg cells through single-cell transcriptome sequencing combined with a stringent screening strategy. These CD177+ TiTregs exhibited distinct transcriptional profiles characterized by enhanced immunosuppressive capabilities and were correlated with poor patient prognosis. Mechanistically, the apoptosis-related transcription factor REL drove the differentiation of CD177+ TiTregs, accompanied by apoptosis and enhanced immunosuppression. Furthermore, using a CD177 Treg conditional knockout mouse model, we demonstrated that inhibiting CD177 in Tregs significantly impaired their immunosuppressive function and inhibited the progression of hepatocellular carcinoma (HCC) in vitro. Our results underscore the critical role of CD177+ TiTregs in cancer immunology and highlight their potential as novel therapeutic targets in HCC.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143586405","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

A mitochondrial outer membrane protein TOMM20 maintains protein stability of androgen receptor and regulates AR transcriptional activity in prostate cancer cells.

IF 6.9 1区医学

Oncogene Pub Date : 2025-03-06 DOI: 10.1038/s41388-025-03328-w

Linglong Yin, Yi Dai, Yue Wang, Shiwen Liu, Yubing Ye, Yongming Fu, Yuchong Peng, Ruizheng Tan, Li Fang, Haoran Suo, Xuli Qi, Bowen Yuan, Yingxue Gao, Youhong Liu, Xiong Li

{"title":"A mitochondrial outer membrane protein TOMM20 maintains protein stability of androgen receptor and regulates AR transcriptional activity in prostate cancer cells.","authors":"Linglong Yin, Yi Dai, Yue Wang, Shiwen Liu, Yubing Ye, Yongming Fu, Yuchong Peng, Ruizheng Tan, Li Fang, Haoran Suo, Xuli Qi, Bowen Yuan, Yingxue Gao, Youhong Liu, Xiong Li","doi":"10.1038/s41388-025-03328-w","DOIUrl":"10.1038/s41388-025-03328-w","url":null,"abstract":"Prostate cancer (PCa) is an androgen-dependent malignancy, with HSP90 and HSP70 serving as classical molecular chaperones that maintain androgen receptor (AR) protein stability and regulate its transcriptional activation. Surprisingly, our study identified TOMM20, a mitochondrial outer membrane protein, as a potential molecular chaperone with similar roles to HSP90/HSP70. We found that TOMM20 expression is elevated in PCa tissues and cell lines and positively correlates with AR levels. RNA-seq analysis revealed that TOMM20 knockdown significantly reduced the mRNA levels of AR-regulated genes. Additionally, the protein level of KLK3 (PSA) decreased, and AR binding to the androgen response element (ARE) of the KLK3 promoter was diminished following TOMM20 knockdown, leading to decreased KLK3 gene transcription. Furthermore, TOMM20 depletion reduced both cytoplasmic and nuclear AR protein levels and facilitated AR degradation via an E3 ubiquitin ligase SKP2-mediated ubiquitin-proteasome pathway, independent of heat shock proteins (HSPs). To our knowledge, this is the first report demonstrating that TOMM20, a mitochondrial outer translocase protein, stabilizes AR protein and enhances its transcriptional activity, while its knockdown promotes AR degradation through the SKP2-mediated ubiquitin-proteasome pathway. These findings suggest that TOMM20 may serve as a potential biomarker for PCa progression and a promising therapeutic target for drug development.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143567823","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Long non-coding RNA-MIR181A1HG acts as an oncogene and contributes to invasion and metastasis in gastric cancer.

IF 6.9 1区医学

Oncogene Pub Date : 2025-03-05 DOI: 10.1038/s41388-025-03323-1

Jieming Zhang, Xiangyang Wei, Yanci Xie, Siyang Peng, Ping Yang, Yidong Chen, Xiaodong Huang, Jieke Wu, Linjie Hong, Zheng Guo, Xiaoting Huang, Zhizhao Lin, Fachao Zhi, Side Liu, Li Xiang, Jianjiao Lin, Aimin Li, Jide Wang

{"title":"Long non-coding RNA-MIR181A1HG acts as an oncogene and contributes to invasion and metastasis in gastric cancer.","authors":"Jieming Zhang, Xiangyang Wei, Yanci Xie, Siyang Peng, Ping Yang, Yidong Chen, Xiaodong Huang, Jieke Wu, Linjie Hong, Zheng Guo, Xiaoting Huang, Zhizhao Lin, Fachao Zhi, Side Liu, Li Xiang, Jianjiao Lin, Aimin Li, Jide Wang","doi":"10.1038/s41388-025-03323-1","DOIUrl":"https://doi.org/10.1038/s41388-025-03323-1","url":null,"abstract":"Dysregulation of long non-coding RNAs (lncRNA) plays an essential role in cancer development and progression. However, their functions and mechanisms of action in gastric cancer (GC) remain largely unknown. Gene expression in GC was evaluated using quantitative real-time PCR, western blotting, immunofluorescence, immunohistochemistry, and RNA in situ hybridization. The impact of MIR181A1HG on GC cells was explored in vitro and in vivo using cell proliferation, migration, invasion assays and animal models. Biotinylated RNA pull-down, RNA immunoprecipitation, co-immunoprecipitation, chromatin immunoprecipitation, and luciferase reporter assays were performed to evaluate the molecular interactions. LncRNA-MIR181A1HG was upregulated in GC and associated with malignant progression. MIR181A1HG physically interacts with ELAVL1 to regulate epithelial-mesenchymal transition (EMT) in GC cells. MIR181A1HG intron-derived miR-181a-5p/miR-181b-5p triggers MIR181A1HG transcription through binding to and destabilizing SOCS3 messenger RNA. Specifically, SOCS3 interacts with NFATC2 and downregulated SOCS3 enhances the NFATC2-mediated transcriptional activation of the MIR181A1HG promoter. Collectively, MIR181A1HG, activated by miR-181a-5p/miR-181b-5p-SOCS3-NFATC2 positive feedback loop, contributes to GC progression through stabilizing ELAVL1. MIR181A1HG expression correlates positively with ELAVL1, miR-181a-5p, miR-181b-5p, and NFATC2 and negatively with SOCS3 in fresh GC samples. These data demonstrate that MIR181A1HG plays an important role in tumor progression by promoting invasion, metastasis, and EMT, indicating its potential as a prognostic biomarker in GC.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143567825","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

ITGB1/FERMT1 mechanoactivation enhances CD44 characteristic stemness in oral squamous cell carcinoma via ubiquitin-dependent CK1α degradation.

IF 6.9 1区医学

Oncogene Pub Date : 2025-03-05 DOI: 10.1038/s41388-025-03317-z

Xiang Li, Hui Zhao, Erhui Jiang, Pan Liu, Yang Chen, Yue Wang, Ji Li, Yufei Wu, Zhenan Liu, Zhengjun Shang

{"title":"ITGB1/FERMT1 mechanoactivation enhances CD44 characteristic stemness in oral squamous cell carcinoma via ubiquitin-dependent CK1α degradation.","authors":"Xiang Li, Hui Zhao, Erhui Jiang, Pan Liu, Yang Chen, Yue Wang, Ji Li, Yufei Wu, Zhenan Liu, Zhengjun Shang","doi":"10.1038/s41388-025-03317-z","DOIUrl":"https://doi.org/10.1038/s41388-025-03317-z","url":null,"abstract":"Cancer stem cells (CSCs) contribute to chemotherapy resistance and poor prognosis, posing significant challenges in the treatment of oral squamous cell carcinoma. The extracellular matrix (ECM)-constructed microenvironment remodels the niche of CSCs. Yet mechanisms by which biophysical properties of ECM relate to CSCs remain undefined. Here, our findings link ECM mechanical stimuli to CSCs phenotype transition, and propose that ECM stiffening mechanoactivates tumor cells to dedifferentiate and acquire CD44+ stem cell-like characteristics through noncanonical mechanotransduction. ITGB1 senses and transduces biomechanical signals, while FERMT1 acts as an intracellular mechanotransduction downstream, activating CSCs. Mechanistically, FERMT1 promotes the proteasomal degradation of CK1α by E3 ubiquitin ligase MIB1, thereby triggering Wnt signaling pathway. Combining targeted ECM softening with mechanotransduction inhibition strategy significantly attenuates tumor stemness and chemoresistance in vivo. Therefore, our findings highlight the role of ECM in regulating CSCs via biomechanical-dependent manner, suggesting the ECM/ITGB1/FERMT1/Wnt axis as a promising therapeutic target for CSCs therapy.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143567824","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

WTAP-mediated m⁶A methylation of PHF19 facilitates cell cycle progression by remodeling the accessible chromatin landscape in t(8;21) AML.

IF 6.9 1区医学

Oncogene Pub Date : 2025-03-04 DOI: 10.1038/s41388-025-03329-9

Yu-Qing Li, Di Liu, Li-Li Wang, Yang-Liu Shao, Hui-Sheng Zhou, Ya-Lei Hu, Kai-Li Min, Chun-Ji Gao, Dai-Hong Liu, Jie Zhou, Ji Lin, Xiao-Ning Gao

{"title":"WTAP-mediated m6A methylation of PHF19 facilitates cell cycle progression by remodeling the accessible chromatin landscape in t(8;21) AML.","authors":"Yu-Qing Li, Di Liu, Li-Li Wang, Yang-Liu Shao, Hui-Sheng Zhou, Ya-Lei Hu, Kai-Li Min, Chun-Ji Gao, Dai-Hong Liu, Jie Zhou, Ji Lin, Xiao-Ning Gao","doi":"10.1038/s41388-025-03329-9","DOIUrl":"10.1038/s41388-025-03329-9","url":null,"abstract":"Wilms' tumor 1-associated protein (WTAP) is a key N6-methyladenosine (m6A) methyltransferase that is upregulated in t(8;21) acute myeloid leukemia (AML) under hypoxia inducible factor 1α-mediated transcriptional activation, promoting leukemogenesis through transcriptome-wide m6A modifications. However, the specific substrates and intrinsic regulatory mechanisms of WTAP are not well understood. Here, we provide evidence that PHD finger protein 19 (PHF19) overexpression is regulated by WTAP-mediated m6A modification and promotes cell cycle progression by altering chromatin accessibility. At the same time, high expression of PHF19 and WTAP in t(8;21) AML patients indicates a worse prognosis. Furthermore, inhibition of PHF19 expression significantly suppresses the growth of t(8;21) AML cells in both in vitro and in vivo. Mechanistically, WTAP enhances the stability of PHF19 mRNA by binding to m6A sites in the 3'-untranslated region, thereby upregulating PHF19 expression. Conversely, WTAP suppression reduces m6A modification levels on the PHF19 transcript, leading to increased instability. Knockdown of PHF19 precipitates loss of H3K27 trimethylation and enhanced chromatin accessibility, ultimately resulting in upregulated expression of genes involved in the cell cycle and DNA damage checkpoints. Therefore, WTAP/m6A-dependent PHF19 upregulation accelerates leukemia progression by coordinating m6A modification and histone methylation, establishing its status as a novel therapeutic target for t(8;21) AML.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143557382","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Retraction Note: Dynamin 2 mediates PDGFRα-SHP-2-promoted glioblastoma growth and invasion 撤稿说明：Dynamin 2介导PDGFRα-SHP-2促进胶质母细胞瘤的生长和侵袭。

IF 6.9 1区医学

Oncogene Pub Date : 2025-03-03 DOI: 10.1038/s41388-025-03313-3

H Feng, KW Liu, P Guo, P Zhang, T Cheng, MA McNiven, GR Johnson, B Hu, SY Cheng

引用次数: 0

Editorial Expression of Concern: Epithelial–mesenchymal transition of ovarian cancer cells is sustained by Rac1 through simultaneous activation of MEK1/2 and Src signaling pathways

IF 6.9 1区医学

Oncogene Pub Date : 2025-03-03 DOI: 10.1038/s41388-025-03333-z

D. Fang, H. Chen, J. Y. Zhu, W. Wang, Y. Teng, H. -F Ding, Q. Jing, S. -B Su, S. Huang

引用次数: 0