Oncogene最新文献_第2页

PPM1D activity promotes cellular transformation by preventing senescence and cell death. PPM1D 的活性通过防止衰老和细胞死亡来促进细胞转化。

IF 6.9 1区医学

Oncogene Pub Date : 2024-09-05 DOI: 10.1038/s41388-024-03149-3

Miroslav Stoyanov, Andra S Martinikova, Katerina Matejkova, Klara Horackova, Petra Zemankova, Kamila Burdova, Zuzana Zemanova, Petra Kleiblova, Zdenek Kleibl, Libor Macurek

{"title":"PPM1D activity promotes cellular transformation by preventing senescence and cell death.","authors":"Miroslav Stoyanov, Andra S Martinikova, Katerina Matejkova, Klara Horackova, Petra Zemankova, Kamila Burdova, Zuzana Zemanova, Petra Kleiblova, Zdenek Kleibl, Libor Macurek","doi":"10.1038/s41388-024-03149-3","DOIUrl":"https://doi.org/10.1038/s41388-024-03149-3","url":null,"abstract":"Cell cycle checkpoints, oncogene-induced senescence and programmed cell death represent intrinsic barriers to tumorigenesis. Protein phosphatase magnesium-dependent 1 (PPM1D) is a negative regulator of the tumour suppressor p53 and has been implicated in termination of the DNA damage response. Here, we addressed the consequences of increased PPM1D activity resulting from the gain-of-function truncating mutations in exon 6 of the PPM1D. We show that while control cells permanently exit the cell cycle and reside in senescence in the presence of DNA damage caused by ionising radiation or replication stress induced by the active RAS oncogene, RPE1-hTERT and BJ-hTERT cells carrying the truncated PPM1D continue proliferation in the presence of DNA damage, form micronuclei and accumulate genomic rearrangements revealed by karyotyping. Further, we show that increased PPM1D activity promotes cell growth in the soft agar and formation of tumours in xenograft models. Finally, expression profiling of the transformed clones revealed dysregulation of several oncogenic and tumour suppressor pathways. Our data support the oncogenic potential of PPM1D in the context of exposure to ionising radiation and oncogene-induced replication stress.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":null,"pages":null},"PeriodicalIF":6.9,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142140700","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

Sorafenib-mediated cleavage of p62 initiates cellular senescence as a mechanism to evade its anti-hepatocellular carcinoma efficacy. 索拉非尼介导的p62裂解引发细胞衰老是一种逃避其抗肝细胞癌疗效的机制。

IF 6.9 1区医学

Oncogene Pub Date : 2024-09-04 DOI: 10.1038/s41388-024-03142-w

Jiaying Du, Dongsheng Bai, Chunyang Gu, Jiawei Zhao, Chen Zhou, Yuxiang Wang, Yue Zhao, Na Lu

{"title":"Sorafenib-mediated cleavage of p62 initiates cellular senescence as a mechanism to evade its anti-hepatocellular carcinoma efficacy.","authors":"Jiaying Du, Dongsheng Bai, Chunyang Gu, Jiawei Zhao, Chen Zhou, Yuxiang Wang, Yue Zhao, Na Lu","doi":"10.1038/s41388-024-03142-w","DOIUrl":"https://doi.org/10.1038/s41388-024-03142-w","url":null,"abstract":"Hepatocellular carcinoma (HCC) stands as one of the most aggressively advancing and lethal malignancies. Sorafenib is presently endorsed as a primary therapy for advanced liver cancer, but its resistance presents a formidable challenge. Previous studies have implicated a connection between post-sorafenib discontinuation rebound and the development of drug resistance, yet the underlying mechanism remains elusive. In this study, we discerned that Sorafenib induced a senescent phenotype in HCC cells and caused a cleavage of ubiquitin-binding protein p62. Mechanistic studies establish that truncated p62 drives cellular senescence by promoting proteasome-dependent degradation of 4EBP1. Furthermore, truncated p62 induced specific ubiquitination of 4EBP1. Crucially, virtual drug screening uncovered that dacinostat inhibited cellular senescence by blocking sorafenib-induced p62 cleavage. In summary, our findings imply that truncated p62 from sorafenib cleavage promotes senescence via 4EBP1 degradation. The prevention of p62 cleavage could emerge as a crucial strategy for impeding the sorafenib-induced cellular senescence.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":null,"pages":null},"PeriodicalIF":6.9,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142133389","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

Synergistic effects of combined BET and FAK inhibition against Vestibular Schwannomas in NF2-related Schwannomatosis. 联合抑制 BET 和 FAK 对 NF2 相关性前庭神经丛神经瘤的协同作用

IF 6.9 1区医学

Oncogene Pub Date : 2024-08-29 DOI: 10.1038/s41388-024-03144-8

Maria A González-Rodriguez, Scott Troutman, Simon Bayle, Daniel K Lester, Matthew Grove, Derek Duckett, Michael S Kareta, Joseph L Kissil

{"title":"Synergistic effects of combined BET and FAK inhibition against Vestibular Schwannomas in NF2-related Schwannomatosis.","authors":"Maria A González-Rodriguez, Scott Troutman, Simon Bayle, Daniel K Lester, Matthew Grove, Derek Duckett, Michael S Kareta, Joseph L Kissil","doi":"10.1038/s41388-024-03144-8","DOIUrl":"https://doi.org/10.1038/s41388-024-03144-8","url":null,"abstract":"Neurofibromatosis type 2 (NF2) is a rare disorder that causes vestibular schwannomas (VS), meningiomas and ependymomas. To date, there is no FDA approved drug-based treatment for NF2. We have previously identified that BET inhibition can selectively reduce growth of the NF2-null schwannoma and Schwann cells in vitro and tumorigenesis in vivo and, separately, reported that inhibition of Focal Adhesion Kinase 1 (FAK1) via crizotinib has antiproliferative effects in NF2-null Schwann cells. The current study was aimed at determining whether combined BET and FAK inhibition can synergize and to identify the mechanisms of action. A panel of normal and NF2-null Schwann and schwannoma cell lines were used to characterize the effects of combined BET and FAK inhibition in vitro and in vivo using pharmacological and genetic approaches. The mechanism of action was explored by chromatin immunoprecipitation, ChIP-PCR, western blotting, and functional approaches. We find that combined BET and FAK inhibition are synergistic and inhibit the proliferation of NF2-null schwannoma and Schwann cell lines in vitro and in vivo, by arresting cells in the G1/S and G2/M phases of the cell cycle. Further, we identify the mechanism of action through the downregulation of FAK1 transcription by BET inhibition, which potentiates inhibition of FAK by 100-fold. Our findings suggest that combined targeting of BET and FAK1 may offer a potential therapeutic option for the treatment of NF2-related schwannomas.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":null,"pages":null},"PeriodicalIF":6.9,"publicationDate":"2024-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142110418","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

Bioinformatics advances in eccDNA identification and analysis. eccDNA鉴定和分析中的生物信息学进展。

IF 6.9 1区医学

Oncogene Pub Date : 2024-08-29 DOI: 10.1038/s41388-024-03138-6

Fuyu Li, Wenlong Ming, Wenxiang Lu, Ying Wang, Xianjun Dong, Yunfei Bai

引用次数: 0

Editorial Expression of Concern: p38 MAPK inhibition enhances PS-341 (bortezomib)-induced cytotoxicity against multiple myeloma cells. 社论关注：抑制 p38 MAPK 可增强 PS-341（硼替佐米）诱导的多发性骨髓瘤细胞毒性。

IF 6.9 1区医学

Oncogene Pub Date : 2024-08-29 DOI: 10.1038/s41388-024-03147-5

Teru Hideshima, Klaus Podar, Dharminder Chauhan, Kenji Ishitsuka, Constantine Mitsiades, Yu-Tzu Tai, Makoto Hamasaki, Noopur Raje, Hiromasa Hideshima, George Schreiner, Aaron N Nguyen, Tony Navas, Nikhil C Munshi, Paul G Richardson, Linda S Higgins, Kenneth C Anderson

引用次数: 0

m⁶A modification of lipoyltransferase 1 inhibits bladder cancer progression by activating cuproptosis. 脂肪酰基转移酶 1 的 m6A 修饰通过激活杯突酶抑制膀胱癌的进展。

IF 6.9 1区医学

Oncogene Pub Date : 2024-08-28 DOI: 10.1038/s41388-024-03139-5

Kaixuan Du, Yongbo Luo, Lei Zhang, Youmiao Zeng, Yiheng Dai, Mengda Ren, Wenbang Pan, Yuanhao Liu, Fengyan Tian, Lijie Zhou, Chaohui Gu

{"title":"m6A modification of lipoyltransferase 1 inhibits bladder cancer progression by activating cuproptosis.","authors":"Kaixuan Du, Yongbo Luo, Lei Zhang, Youmiao Zeng, Yiheng Dai, Mengda Ren, Wenbang Pan, Yuanhao Liu, Fengyan Tian, Lijie Zhou, Chaohui Gu","doi":"10.1038/s41388-024-03139-5","DOIUrl":"https://doi.org/10.1038/s41388-024-03139-5","url":null,"abstract":"Cuproptosis, a cell death process caused by copper ions, is mediated by protein lipidation related to lipoic acid metabolism. There is a close connection between cuproptosis and the progression and prognosis of various tumors. Here, we identified lipoyltransferase 1 (LIPT1), a key gene related to cuproptosis, was downregulated in bladder cancer (BLCA) and was associated with unfavorable patient prognosis. Restoring the LIPT1 expression in BLCA cells suppressed the proliferation and promoted cuproptosis. Moreover, the consequences of RNA sequencing and Bodipy staining showed that the metabolic pathway mediated by LIPT1 inhibited the accumulation of lipid droplets in cells, disrupted endoplasmic reticulum (ER) homeostasis, and promoted cell apoptosis. Additionally, overexpression of LIPT1 not only repressed the proliferation rate of BLCA cells in vitro but also in vivo. Mechanistically, YTH N6-Methyladenosine RNA Binding Protein F2 (YTHDF2) promoted the degradation of LIPT1 mRNA in a m6A-dependent manner. In summary, these conclusions reveal that LIPT1 promotes cuprotosis and ER stress to inhibit the progression of BLCA, indicating that LIPT1 will provide a powerful treatment direction and drug target for treating BLCA.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":null,"pages":null},"PeriodicalIF":6.9,"publicationDate":"2024-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142093654","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

S-p-bromobenzyl-glutathione cyclopentyl diester (BBGC) as novel therapeutic strategy to enhance trabectedin anti-tumor effect in soft tissue sarcoma preclinical models. S-对溴苄基谷胱甘肽环戊基二酯（BBGC）作为一种新型治疗策略，可增强曲贝替定在软组织肉瘤临床前模型中的抗肿瘤效果。

IF 6.9 1区医学

Oncogene Pub Date : 2024-08-28 DOI: 10.1038/s41388-024-03143-9

F Pantano, S Simonetti, M Iuliani, M J Guillen, C Cuevas, P Aviles, S Cavaliere, A Napolitano, A Cortellini, A Mazzocca, L Nibid, G Sabarese, G Perrone, M Gambarotti, A Righi, E Palmerini, S Stacchiotti, M Barisella, A Gronchi, S Valeri, M Sbaraglia, A P Dei Tos, G Tonini, B Vincenzi

{"title":"S-p-bromobenzyl-glutathione cyclopentyl diester (BBGC) as novel therapeutic strategy to enhance trabectedin anti-tumor effect in soft tissue sarcoma preclinical models.","authors":"F Pantano, S Simonetti, M Iuliani, M J Guillen, C Cuevas, P Aviles, S Cavaliere, A Napolitano, A Cortellini, A Mazzocca, L Nibid, G Sabarese, G Perrone, M Gambarotti, A Righi, E Palmerini, S Stacchiotti, M Barisella, A Gronchi, S Valeri, M Sbaraglia, A P Dei Tos, G Tonini, B Vincenzi","doi":"10.1038/s41388-024-03143-9","DOIUrl":"https://doi.org/10.1038/s41388-024-03143-9","url":null,"abstract":"Trabectedin, approved for the treatment of soft tissue sarcoma (STS), interferes with cell division and genetic transcription processes. Due to its strong anti-tumor activity in only certain histotypes, several studies on trabectedin combinations are currently ongoing to improve its efficacy. In this study, we aimed to investigate novel potential therapeutic strategies to enhance the anti-tumor effect of trabectedin using integrated in silico, in vitro, and in vivo approaches. For in silico analysis, we screened two public datasets, GSEA M5190 and TCGA SARC. Fibrosarcoma, leiomyosarcoma, dedifferentiated, and myxoid liposarcoma cell lines were used for in vitro studies. For in vivo experiments, fibrosarcoma orthotopic murine model was developed. In silico analysis identified Glo1 as the only druggable target upregulated after trabectedin treatment and correlated with poor prognosis. The specific Glo1 inhibitor, S-p-bromobenzylglutathione cyclopentyl diester (BBGC), increased trabectedin cytotoxicity in STS cells, and restored drug sensitivity in myxoid liposarcoma cells resistant to trabectedin. Moreover, the combined treatment with BBGC and trabectedin had a synergistic antitumor effect in vivo without any additional toxicity to mice. Based on these results, we believe that BBGC warrants further investigation to evaluate its potential clinical use in combination with trabectedin.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":null,"pages":null},"PeriodicalIF":6.9,"publicationDate":"2024-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142093655","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

RBM12 drives PD-L1-mediated immune evasion in hepatocellular carcinoma by increasing JAK1 mRNA translation. RBM12通过增加JAK1 mRNA的翻译来驱动肝细胞癌中PD-L1介导的免疫逃避。

IF 6.9 1区医学

Oncogene Pub Date : 2024-08-26 DOI: 10.1038/s41388-024-03140-y

Hexu Han, Qian Shi, Yue Zhang, Mingdong Ding, Xianzhong He, Cuixia Liu, Dakun Zhao, Yifan Wang, Yanping Du, Yichao Zhu, Yin Yuan, Siliang Wang, Huimin Guo, Qiang Wang

{"title":"RBM12 drives PD-L1-mediated immune evasion in hepatocellular carcinoma by increasing JAK1 mRNA translation.","authors":"Hexu Han, Qian Shi, Yue Zhang, Mingdong Ding, Xianzhong He, Cuixia Liu, Dakun Zhao, Yifan Wang, Yanping Du, Yichao Zhu, Yin Yuan, Siliang Wang, Huimin Guo, Qiang Wang","doi":"10.1038/s41388-024-03140-y","DOIUrl":"10.1038/s41388-024-03140-y","url":null,"abstract":"Immunosuppression characterizes the tumour microenvironment in HCC, and recent studies have implicated RNA-binding proteins (RBPs) in the development of HCC. Here, we conducted a screen and identified RBM12 as a key protein that increased the expression of PD-L1, thereby driving immune evasion in HCC. Furthermore, RBM12 was found to be significantly upregulated in HCC tissues and was associated with a poor prognosis for HCC patients. Through various molecular assays and high-throughput screening, we determined that RBM12 could directly bind to the JAK1 mRNA via its 4th-RRM (RNA recognition motif) domain and recruit EIF4A2 through its 2nd-RRM domain, enhancing the distribution of ribosomes on JAK1 mRNA, which promotes the translation of JAK1 and the subsequent upregulation of its expression. As a result, the activated JAK1/STAT1 pathway transcriptionally upregulates PD-L1 expression, facilitating immune evasion in HCC. In summary, our findings provide insights into the significant contribution of RBM12 to immune evasion in HCC, highlighting its potential as a therapeutic target in the future. This graphical abstract shows that elevated expression of RBM12 in HCC can augment PD-L1-mediated tumour immune evasion by increasing the efficiency of JAK1 mRNA translation.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":null,"pages":null},"PeriodicalIF":6.9,"publicationDate":"2024-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142073499","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

Targeting MERTK on tumour cells and macrophages: a potential intervention for sporadic and NF2-related meningioma and schwannoma tumours. 以肿瘤细胞和巨噬细胞上的 MERTK 为靶点：对散发性和 NF2 相关脑膜瘤和裂隙瘤的潜在干预。

IF 6.9 1区医学

Oncogene Pub Date : 2024-08-23 DOI: 10.1038/s41388-024-03131-z

Foram Dave, Kevin Herrera, Alex Lockley, Laurien L van de Weijer, Summer Henderson, Agbolahan A Sofela, Laura Hook, Claire L Adams, Emanuela Ercolano, David A Hilton, Emmanuel A Maze, Kathreena M Kurian, Sylwia Ammoun, C Oliver Hanemann

{"title":"Targeting MERTK on tumour cells and macrophages: a potential intervention for sporadic and NF2-related meningioma and schwannoma tumours.","authors":"Foram Dave, Kevin Herrera, Alex Lockley, Laurien L van de Weijer, Summer Henderson, Agbolahan A Sofela, Laura Hook, Claire L Adams, Emanuela Ercolano, David A Hilton, Emmanuel A Maze, Kathreena M Kurian, Sylwia Ammoun, C Oliver Hanemann","doi":"10.1038/s41388-024-03131-z","DOIUrl":"https://doi.org/10.1038/s41388-024-03131-z","url":null,"abstract":"Meningioma and schwannoma are common tumours of the nervous system. They occur sporadically or as part of the hereditary NF2-related schwannomatosis syndrome. There is an unmet need for new effective drug treatments for both tumour types. In this paper, we demonstrate overexpression/activation of TAM (TYRO3/AXL/MERTK) receptors (TAMs) and overexpression/release of ligand GAS6 in patient-derived meningioma tumour cells and tissue. For the first time, we reveal the formation of MERTK/TYRO3 heterocomplexes in meningioma and schwannoma tissue. We demonstrate the dependence of AXL and TYRO3 expression on MERTK in both tumour types, as well as interdependency of MERTK and AXL expression in meningioma. We show that MERTK and AXL contribute to increased proliferation and survival of meningioma and schwannoma cells, which we inhibited in vitro using the MERTK/FLT3 inhibitor UNC2025 and the AXL inhibitor BGB324. UNC2025 was effective in both tumour types with superior efficacy over BGB324. Finally, we found that TAMs are expressed by tumour-associated macrophages in meningioma and schwannoma tumours and that UNC2025 strongly depleted macrophages in both tumour types.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":null,"pages":null},"PeriodicalIF":6.9,"publicationDate":"2024-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142046967","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

Identification of a novel alternative splicing isoform of the Hippo kinase STK3/MST2 with impaired kinase and cell growth suppressing activities. 鉴定出一种新的河马激酶 STK3/MST2 替代剪接异构体，其激酶和细胞生长抑制活性受损。

IF 6.9 1区医学

Oncogene Pub Date : 2024-08-22 DOI: 10.1038/s41388-024-03104-2

Ana Maria Rodrigues, Ana Paula Zen Petisco Fiore, Gabriela D A Guardia, Rebeka Tomasin, André Azevedo Reis Teixeira, Ricardo Jose Giordano, Deborah Schechtman, Michele Pagano, Pedro A F Galante, Alexandre Bruni-Cardoso

{"title":"Identification of a novel alternative splicing isoform of the Hippo kinase STK3/MST2 with impaired kinase and cell growth suppressing activities.","authors":"Ana Maria Rodrigues, Ana Paula Zen Petisco Fiore, Gabriela D A Guardia, Rebeka Tomasin, André Azevedo Reis Teixeira, Ricardo Jose Giordano, Deborah Schechtman, Michele Pagano, Pedro A F Galante, Alexandre Bruni-Cardoso","doi":"10.1038/s41388-024-03104-2","DOIUrl":"https://doi.org/10.1038/s41388-024-03104-2","url":null,"abstract":"Mammalian Ste-20-like Kinases 1 and 2 (MST1/2) are core serine-threonine kinases of the Hippo pathway regulating several cellular processes, including cell cycle arrest and cell death. Here, we discovered a novel alternative splicing variant of the MST2 encoding gene, STK3, in malignant cells and tumor datasets. This variant, named STK3∆7 or MST2∆7 (for mRNA or protein, respectively), resulted from the skipping of exon 7. MST2∆7 exhibited increased ubiquitylation and interaction with the E3 ubiquitin-protein ligase CHIP compared to the full-length protein (MST2FL). Exon 7 in STK3 encodes a segment within the kinase domain, and its exclusion compromised MST2 interaction with and phosphorylation of MOB, a major MST1/2 substrate. Nevertheless, MST2∆7 was capable of interacting with MST1 and MST2FL. Unlike MST2FL, overexpression of MST2∆7 did not lead to increased cell death and growth arrest. Strikingly, we observed the exclusion of STK3 exon 7 in 3.2-15% of tumor samples from patients of several types of cancer, while STK3∆7 was seldomly found in healthy tissues. Our study identified a novel STK3 splicing variant with loss of function and the potential to disturb tissue homeostasis by impacting on MST2 activities in the regulation of cell death and quiescence.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":null,"pages":null},"PeriodicalIF":6.9,"publicationDate":"2024-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142036469","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