Cancer Science最新文献_第5页

SPOP Suppresses Hepatocellular Carcinoma Growth and Metastasis by Ubiquitination and Proteasomal Degradation of TRAF6 SPOP通过泛素化和蛋白酶体降解TRAF6抑制肝癌的生长和转移。

IF 4.5 2区医学

Cancer Science Pub Date : 2025-02-17 DOI: 10.1111/cas.70025

Wenyi Chang, Kaiying Feng, Peng Zhou, Deao Gong, Ke Wang, Ailong Huang, Kai Wang, Ni Tang

{"title":"SPOP Suppresses Hepatocellular Carcinoma Growth and Metastasis by Ubiquitination and Proteasomal Degradation of TRAF6","authors":"Wenyi Chang, Kaiying Feng, Peng Zhou, Deao Gong, Ke Wang, Ailong Huang, Kai Wang, Ni Tang","doi":"10.1111/cas.70025","DOIUrl":"10.1111/cas.70025","url":null,"abstract":"Tumor necrosis factor receptor-associated factor-6 (TRAF6) is a well-established upstream regulator of the IKK complex, essential for the modulation of the NF-κB (nuclear factor kappa B) signaling pathway. Aberrant activation of TRAF6 has been strongly implicated in the pathogenesis of various cancers, including hepatocellular carcinoma (HCC). The speckle type BTB/POZ protein (SPOP), an E3 ubiquitin ligase substrate-binding adapter, constitutes a significant component of the CUL3/SPOP/RBX1 complex, which is closely linked to tumorigenesis. In this study, we demonstrated that the E3 ubiquitin ligase SPOP shielded TRAF6 from proteasomal degradation, leading to the hyperactivation of the NF-κB pathway. Notably, a liver cancer-associated S119N mutation in SPOP resulted in a failure to mediate the ubiquitination and subsequent degradation of TRAF6. Moreover, both gain-of-function and loss-of-function experiments revealed that SPOP inhibits the proliferation and invasion of HCC cells through the TRAF6-NF-κB axis in vitro and in vivo. Taken together, our findings elucidate the underpinning mechanism by which SPOP negatively regulates the stability of the TRAF6 oncoprotein, thus offering a new therapeutic target for HCC intervention.","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"116 5","pages":"1295-1307"},"PeriodicalIF":4.5,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cas.70025","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143442542","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

Role of IL-34 in Tumors and Its Application to Regulate Inflammation IL-34在肿瘤中的作用及其在炎症调节中的应用

IF 4.5 2区医学

Cancer Science Pub Date : 2025-02-14 DOI: 10.1111/cas.70020

Yuichi Igarashi, Ken-ichiro Seino

{"title":"Role of IL-34 in Tumors and Its Application to Regulate Inflammation","authors":"Yuichi Igarashi, Ken-ichiro Seino","doi":"10.1111/cas.70020","DOIUrl":"10.1111/cas.70020","url":null,"abstract":"Interleukin (IL)-34 is a relatively recently discovered cytokine which binds to colony-stimulating factor-1 receptor (CSF-1R). So far, there has been no clear explanation as to why CSF-1R requires two ligands. While CSF-1 is ubiquitously expressed, the expression of IL-34 is relatively restricted. However, it has been revealed that IL-34 expression increases in various diseases and is associated with their pathology. Naturally, both IL-34 and CSF-1 stimulate CSF-1R, thereby contributing to the differentiation of monocytes into macrophages. In many cases, the induced macrophages significantly influence the disease pathology. In particular, we have demonstrated that IL-34 expression in cancer is deeply involved in tumor progression and therapeutic resistance. We have shown that the blockade of IL-34 significantly improved therapeutic efficacy such as chemotherapy, radiotherapy, and immune checkpoint blockade against IL-34-expressing cancers. Recently, since macrophages induced by IL-34 exhibit immunosuppressive properties, whereas IL-34 can enhance inflammation, there is growing interest in actively regulating inflammation utilizing IL-34. In this review article, we provide an overview of the characteristics and roles of IL-34 and discuss how it could be applied to future diagnostics and therapeutics.","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"116 5","pages":"1164-1170"},"PeriodicalIF":4.5,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cas.70020","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143415541","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

A Mutual Interaction Between GSTP1 and p53 Improves the Drug Resistance and Malignant Biology of Pancreatic Cancer GSTP1和p53的相互作用提高了胰腺癌的耐药和恶性生物学

IF 4.5 2区医学

Cancer Science Pub Date : 2025-02-14 DOI: 10.1111/cas.70019

Guosen Wang, Yi Cao, Tengcheng Hu, Zhengqing Cai, ChuanPing Chen, Qilong Geng, Xinyu Luo, Yang Liu, Weijie Wang, Jiabin Jin, Weiwei Sheng

{"title":"A Mutual Interaction Between GSTP1 and p53 Improves the Drug Resistance and Malignant Biology of Pancreatic Cancer","authors":"Guosen Wang, Yi Cao, Tengcheng Hu, Zhengqing Cai, ChuanPing Chen, Qilong Geng, Xinyu Luo, Yang Liu, Weijie Wang, Jiabin Jin, Weiwei Sheng","doi":"10.1111/cas.70019","DOIUrl":"10.1111/cas.70019","url":null,"abstract":"Glutathione S-transferase P1 (GSTP1), a classic tumor biomarker, plays a controversial role in cancer progression. However, its specific role in pancreatic cancer (PC) has rarely been investigated. In the present study, we investigated the function and relationship between GSTP1 and mutant/wild-type p53 (mtp53/wtp53) in PC in vitro and in vivo. Compared with paired adjacent normal pancreas tissue, GSTP1 was downregulated in PC tissue, which was closely correlated with lymph node metastasis, Union for International Cancer Control (UICC) stage, and a better outcome of PC patients, processes dependent on wtp53 rather than mtp53. Moreover, a mutual regulation between GSTP1 and p53 was found in wtp53 PC cells. GSTP1 overexpression inhibited cell proliferation and chemotherapy resistance in vitro via wtp53/p21 and Bax/Bcl2 signaling, which was significantly reversed by wtp53 silencing, and vice versa. Similarly, the coordination of GSTP1 and p53 regulated the invasion and migration of PC cells, which was accompanied by changes in epithelial-mesenchymal transition (EMT) signaling (E-cad, ZO-1 and MMP9). Moreover, GSTP1 overexpression inhibited tumor growth and liver metastasis in vivo, as did high wtp53 and low ki67 expression. Interestingly, GSTP1 did not coimmunoprecipitate with either mtp53 or wtp53 in vitro. However, the wtp53 protein, as a transcription factor, could bind to the GSTP1 DNA promoter to transactivate GSTP1 mRNA expression as demonstrated via a Chip assay. Additionally, GSTP1 promoted the translocation of wtp53 into the nucleus but not mtp53. These results suggest that the positive feedback regulation of GSTP1 and wtp53 plays a significant role in cell proliferation, drug resistance, cell invasion and metastasis in PC.","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"116 5","pages":"1268-1281"},"PeriodicalIF":4.5,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cas.70019","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143425995","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

Mefloquine Suppresses Metastasis in Renal Cell Carcinoma Through Targeting SPC25 甲氟喹通过靶向SPC25抑制肾癌转移。

IF 4.5 2区医学

Cancer Science Pub Date : 2025-02-13 DOI: 10.1111/cas.70001

Yongbo Wang, He Wang, Yipeng Xu, Jiawei Ling, Chuhong Zong, Yan Zhang, Xiaoxuan Guo, Guanan Zhao, Yuan Zhou, Jiahui Zhao, Pengrong Lou, Xigao Liu, Tengfei Xu, Qi Ma

{"title":"Mefloquine Suppresses Metastasis in Renal Cell Carcinoma Through Targeting SPC25","authors":"Yongbo Wang, He Wang, Yipeng Xu, Jiawei Ling, Chuhong Zong, Yan Zhang, Xiaoxuan Guo, Guanan Zhao, Yuan Zhou, Jiahui Zhao, Pengrong Lou, Xigao Liu, Tengfei Xu, Qi Ma","doi":"10.1111/cas.70001","DOIUrl":"10.1111/cas.70001","url":null,"abstract":"Renal cell carcinoma (RCC) is the third most common malignant tumor in the urinary system, often presenting with distant metastases at diagnosis. Approximately one-quarter of patients undergoing nephrectomy experience distant recurrence. Despite the recent advancements in combination-targeted and immune checkpoint inhibitor therapies, the development of new therapeutic strategies and the identification of biomarkers for metastatic risk remain crucial. The study found that high SPC25 expression is closely associated with poor clinical outcomes, and knocking down SPC25 significantly inhibits tumor cell proliferation and migration. Non-targeted metabolomics analysis also revealed that SPC25 knockdown reduces tumor cell activity, resulting in a low-invasive state. Additionally, this study utilized high-throughput molecular docking to screen small molecule drugs targeting SPC25, aiming to find drugs that inhibit RCC metastasis. The research discovered that mefloquine, at concentrations that do not significantly kill tumor cells, can markedly inhibit RCC metastasis. It was the first to report that mefloquine achieves its anti-metastatic effects by binding to SPC25 and inhibiting epithelial-mesenchymal transition. These results suggest that SPC25 has the potential to serve as an early biomarker for metastatic risk in RCC and highlight a novel strategy where mefloquine inhibits RCC metastasis through SPC25 binding, offering new avenues to improve the prognosis of RCC patients.","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"116 5","pages":"1239-1254"},"PeriodicalIF":4.5,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cas.70001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143415505","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

Single-Nucleus RNA Sequencing and Spatial Transcriptomics for Squamous Cell Carcinoma Arising From Ovarian Mature Teratoma 卵巢成熟畸胎瘤引起的鳞状细胞癌的单核RNA测序和空间转录组学研究。

IF 4.5 2区医学

Cancer Science Pub Date : 2025-02-13 DOI: 10.1111/cas.70022

Kosuke Yoshida, Akira Yokoi, Hironori Suzuki, Satoshi Tamauchi, Masami Kitagawa, Eri Inami, Jun Nakayama, Yutaro Mori, Koji Okamoto, Yutaka Suzuki, Hiroshi Yoshida, Tomoyasu Kato, Hiroaki Kajiyama, Yusuke Yamamoto

{"title":"Single-Nucleus RNA Sequencing and Spatial Transcriptomics for Squamous Cell Carcinoma Arising From Ovarian Mature Teratoma","authors":"Kosuke Yoshida, Akira Yokoi, Hironori Suzuki, Satoshi Tamauchi, Masami Kitagawa, Eri Inami, Jun Nakayama, Yutaro Mori, Koji Okamoto, Yutaka Suzuki, Hiroshi Yoshida, Tomoyasu Kato, Hiroaki Kajiyama, Yusuke Yamamoto","doi":"10.1111/cas.70022","DOIUrl":"10.1111/cas.70022","url":null,"abstract":"Squamous cell carcinoma arising from mature teratoma (SCC-MT) is a rare ovarian malignancy. The detailed molecular pathology of SCC-MT is not well understood. Moreover, the prognosis of the patients remains poor because no standard treatment has been established. In this study, we performed single-nucleus RNA sequencing and spatial transcriptomics using clinical SCC-MT samples to identify novel therapeutic candidates. snRNA-seq revealed three epithelial cell clusters, of which one was significantly associated with epidermis and keratinocyte development. Moreover, spatial transcriptomics revealed that the epithelial-mesenchymal transition was significantly inhibited, and the MYC and E2F targets were significantly activated in cancer spots on specimen sections. We focused on KLF5, which was one of the upregulated genes in cancer cells, and performed a functional analysis using NOSCC-1, a cell line derived from an SCC-MT. KLF5 downregulation significantly decreased cell proliferation and increased apoptosis. Furthermore, we previously identified miR-145-5p as a downregulated miRNA in SCC-MT. We demonstrated that miR-145-5p overexpression attenuated cell proliferation and decreased KLF5 expression. In conclusion, through multi-omics analyses, we identified unique gene expression profiles of SCC-MT and determined a role for KLF5 in SCC-MT development. Therefore, KLF5-related factors may be novel therapeutic targets, and further studies are needed to improve the diagnosis and treatment of SCC-MT.","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"116 5","pages":"1339-1351"},"PeriodicalIF":4.5,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cas.70022","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143415708","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

Cell Biology of Cancer Peritoneal Metastasis: Multiclonal Seeding and Peritoneal Tumor Microenvironment 肿瘤腹膜转移的细胞生物学：多克隆播种和腹膜肿瘤微环境。

IF 4.5 2区医学

Cancer Science Pub Date : 2025-02-13 DOI: 10.1111/cas.70021

Hideki Yamaguchi, Makoto Miyazaki

{"title":"Cell Biology of Cancer Peritoneal Metastasis: Multiclonal Seeding and Peritoneal Tumor Microenvironment","authors":"Hideki Yamaguchi, Makoto Miyazaki","doi":"10.1111/cas.70021","DOIUrl":"10.1111/cas.70021","url":null,"abstract":"Peritoneal metastasis, also known as peritoneal dissemination or carcinomatosis, refers to the spread of cancer to the peritoneum that lines the abdominal and pelvic cavities and covers the abdominal organs. Peritoneal metastasis typically occurs in advanced cancers of abdominal origin, most commonly gastrointestinal and gynecological cancers. Conventional chemotherapy has limited efficacy, and no effective molecular-targeted therapy is currently available for peritoneal metastasis. As a result, peritoneal metastasis is associated with poor outcomes and significantly reduced quality of life in patients with advanced cancers. This is largely due to a limited understanding of the molecular and cellular mechanisms underlying peritoneal metastasis. However, recent studies employing innovative approaches have provided novel insights into the mechanisms of peritoneal metastasis, contributing to the development of novel therapeutic strategies. In this review, we summarize recent findings on the cell biological aspects of peritoneal metastasis and potential therapeutic target molecules. In particular, we emphasize the importance of cancer cell clustering within the abdominal cavity, which drives multiclonal peritoneal seeding. We also focus on the interactions of cancer cells with mesothelial cells and cancer-associated fibroblasts within the peritoneal tumor microenvironment.","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"116 5","pages":"1171-1180"},"PeriodicalIF":4.5,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cas.70021","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143415498","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

Plasma tsRNA Signatures Serve as a Novel Biomarker for Bladder Cancer 血浆tsRNA标记可作为膀胱癌的新生物标志物

IF 4.5 2区医学

Cancer Science Pub Date : 2025-02-13 DOI: 10.1111/cas.70003

Xinyan Xu, Jinbang Chen, Ming Bai, TianYao Liu, Shoubin Zhan, Jiazheng Li, YuanChun Ma, Yulin Zhang, Liming Wu, Zihan Zhao, Siyang Liu, Xi Chen, Feng Fang, Hongqian Guo, Ying Sun, Rong Yang

{"title":"Plasma tsRNA Signatures Serve as a Novel Biomarker for Bladder Cancer","authors":"Xinyan Xu, Jinbang Chen, Ming Bai, TianYao Liu, Shoubin Zhan, Jiazheng Li, YuanChun Ma, Yulin Zhang, Liming Wu, Zihan Zhao, Siyang Liu, Xi Chen, Feng Fang, Hongqian Guo, Ying Sun, Rong Yang","doi":"10.1111/cas.70003","DOIUrl":"10.1111/cas.70003","url":null,"abstract":"Bladder cancer (BLCA) is one of the most common tumors of the urinary tract. The diagnosis of BLCA is mostly by invasive tests, which are damaging and unsuitable for early screening. Current non-invasive diagnostic modalities are insufficient in sensitivity and specificity. Therefore, novel diagnostic markers are urgently needed to facilitate early detection of bladder cancer. tRNA-derived small RNAs (tsRNAs) are considered to be novel and potentially biologically functional non-coding RNAs (ncRNAs). tsRNAs have been used to help early diagnosis of a variety of tumors. However, whether tsRNAs in BLCA are altered or involved in BLCA progression or regulation remains unclear. Here, we identified a group of up-regulated tsRNAs in BLCA by sequencing tsRNAs in the plasma of BLCA patients and normal controls and further screened two highly correlated tsRNAs with BLCA in the training set and validation set, which were named as tRF-1:28-chrM.Ser-TGA and tiRNA-1:34-Glu-CTC-1-M2. ROC analyses of the expression profiles of these two tsRNAs by the validation set identified a high diagnostic value. We also found that circulating tRF-1:28-chrM.Ser-TGA and tiRNA-1:34-Glu-CTC-1-M2 were specifically expressed and released by BLCA cells and were positively correlated with the degree of disease malignancy. In vitro and in vivo experiments revealed that the two tsRNAs exacerbated BLCA progression and played a role in promoting tumor lipid metabolism. Our study screened two plasma tsRNAs that could serve as valuable early screening and diagnostic biomarkers for BLCA and is also expected to provide potential novel molecular targets for the treatment of BLCA.","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"116 5","pages":"1255-1267"},"PeriodicalIF":4.5,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cas.70003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143415537","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 to “PRMT9 Promotes Hepatocellular Carcinoma Invasion and Metastasis via Activating PI3K/Akt/GSK-3β/Snail Signaling” 更正“PRMT9通过激活PI3K/Akt/GSK-3β/Snail信号传导促进肝细胞癌的侵袭和转移”。

IF 4.5 2区医学

Cancer Science Pub Date : 2025-02-12 DOI: 10.1111/cas.70004

引用次数: 0

Correction to “Tumor-derived Prevotella intermedia aggravates gastric cancer by enhancing Perilipin 3 expression” 更正“肿瘤源性中普雷沃氏菌通过增强Perilipin 3表达加重胃癌”。

IF 4.5 2区医学

Cancer Science Pub Date : 2025-02-12 DOI: 10.1111/cas.70005

引用次数: 0

STAT3 Inhibition Prevents Adaptive Resistance and Augments NK Cell Cytotoxicity to KRASG12C Inhibitors in Nonsmall Cell Lung Cancer STAT3抑制可阻止非小细胞肺癌患者对KRASG12C抑制剂的适应性耐药并增强NK细胞毒性

IF 4.5 2区医学

Cancer Science Pub Date : 2025-02-12 DOI: 10.1111/cas.70017

Zehao Pan, Yuxian Qian, Yajing Wang, Te Zhang, Xuming Song, Hanling Ding, Rutao Li, Yijian Zhang, Zi Wang, Hui Wang, Wenjie Xia, Lei Wei, Lin Xu, Gaochao Dong, Feng Jiang

{"title":"STAT3 Inhibition Prevents Adaptive Resistance and Augments NK Cell Cytotoxicity to KRASG12C Inhibitors in Nonsmall Cell Lung Cancer","authors":"Zehao Pan, Yuxian Qian, Yajing Wang, Te Zhang, Xuming Song, Hanling Ding, Rutao Li, Yijian Zhang, Zi Wang, Hui Wang, Wenjie Xia, Lei Wei, Lin Xu, Gaochao Dong, Feng Jiang","doi":"10.1111/cas.70017","DOIUrl":"10.1111/cas.70017","url":null,"abstract":"KRASG12C inhibitors exhibit conspicuous clinical response in KRASG12C-mutant lung cancer, yet adaptive resistance, the rapid onset of intrinsic resistance, dampens their therapeutic success. Rational combination strategies could tackle this challenging problem. A high-throughput screening of a pharmacological library with 423 compounds revealed that napabucasin, a signal transducer and activator of transcription 3 (STAT3) inhibitor, synergistically potentiated the growth inhibition effect of the KRASG12C inhibitor sotorasib in sensitive and resistant KRASG12C NSCLC cell lines. Functional assays further revealed that the coordinated targeting of KRAS with STAT3 improved the inhibitory effect on tumor growth and augmented the infiltration and activation of natural killer (NK) cells within the tumor microenvironment. Mechanistically, KRASG12C inhibition induced compensatory activation of STAT3, contingent on concomitant suppression of downstream ERK signaling, abrogated by napabucasin. Moreover, we unveiled and verified the binding site of phosphorylated STAT3 at the HLA-B promoter, an inhibitor ligand for NK cells. Our study dissected an unknown mechanism of adaptive resistance to KRASG12C inhibitors, with the STAT3 activation sustaining the regrowth of tumor cells under KRAS inhibition and up-regulating HLA-B transcription to dampen the cytotoxicity of infiltrated NK cells.","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"116 5","pages":"1375-1391"},"PeriodicalIF":4.5,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cas.70017","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143411318","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