Cancer Science最新文献_第2页

Hypoxia Inhibitor Improves Iodine Uptake Disorder in Thyroid Cancer Through the hsa_circ_0023990/miR-448/DNMT1/NIS Axis. 缺氧抑制剂通过hsa_circ_0023990/miR-448/DNMT1/NIS轴改善甲状腺癌碘摄取障碍

IF 5.7 2区医学

Cancer Science Pub Date : 2025-05-19 DOI: 10.1111/cas.70102

Ruiqin Gou, Shiqi Chen, Yangyang Lei, Pengqing Wu, Xuezhong Chen, Qing Zhang

{"title":"Hypoxia Inhibitor Improves Iodine Uptake Disorder in Thyroid Cancer Through the hsa_circ_0023990/miR-448/DNMT1/NIS Axis.","authors":"Ruiqin Gou, Shiqi Chen, Yangyang Lei, Pengqing Wu, Xuezhong Chen, Qing Zhang","doi":"10.1111/cas.70102","DOIUrl":"https://doi.org/10.1111/cas.70102","url":null,"abstract":"This research seeks to investigate how hypoxia inhibitors enhance iodine uptake in thyroid cancer cells. Clinical samples were gathered and assessed for hsa_circ_0023990, DNMT1, NIS, and their promoter methylation levels using RT-PCR, western blot, and methylation-specific PCR (MSP) techniques. The study involved examining the impact and mechanism of hsa_circ_0023990 on iodine uptake in differentiated thyroid carcinoma (DTC) cells through genetic manipulation. Luciferase reporter gene experiments were conducted to validate the interaction between hsa_circ_0023990, DNMT1, and miR-448. Xenograft tumors were established in nude mice for in vivo validation. The results showed that hsa_circ_0023990 was notably elevated in DTC and RAIR-DTC tissues. It was found that hsa_circ_0023990 could modulate NIS promoter methylation via the miR-448/DNMT1 signaling pathway, thereby influencing NIS expression. Hypoxia inhibitors effectively suppressed hsa_circ_0023990 expression in DTC cells, leading to increased NIS expression and enhanced iodine uptake. Subcutaneous transplantation experiments in animals further confirmed that hypoxia inhibitors could boost iodine absorption in tumor tissue and inhibit tumor growth through the hsa_circ_0023990/miR-448/DNMT1/NIS signaling axis. In conclusion, hypoxia inhibitors ameliorate iodine uptake dysfunction in thyroid cancer by acting on the hsa_circ_0023990/miR-448/DNMT1/NIS signaling pathway.","PeriodicalId":48943,"journal":{"name":"Cancer Science","volume":" ","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144095546","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

PSMD14/E2F1 Axis-Mediated CENPF Promotes the Metastasis of Triple-Negative Breast Cancer Through Inhibiting Ferroptosis. PSMD14/E2F1轴介导的CENPF通过抑制铁下沉促进三阴性乳腺癌转移。

IF 5.7 2区医学

Cancer Science Pub Date : 2025-05-14 DOI: 10.1111/cas.70064

Meifeng Zhou, Xianglu Li, Weifeng Wang, Jianyong Wu, Jindian Tan

{"title":"PSMD14/E2F1 Axis-Mediated CENPF Promotes the Metastasis of Triple-Negative Breast Cancer Through Inhibiting Ferroptosis.","authors":"Meifeng Zhou, Xianglu Li, Weifeng Wang, Jianyong Wu, Jindian Tan","doi":"10.1111/cas.70064","DOIUrl":"https://doi.org/10.1111/cas.70064","url":null,"abstract":"The metastasis of triple-negative breast cancer (TNBC) usually contributes to the failure of treatment. Centromere Protein F (CENPF) can induce proliferation and metastasis in TNBC. Nevertheless, the upstream mechanism of CENPF in BC remains unclear. Western blot and RT-qPCR were employed for testing the levels of PSMD14, E2F1, and CENPF, and cell migration was assessed using the Transwell assay. Additionally, the CCK8 assay was applied to investigate cell viability, and C11-BODIPY 581/591 was applied to assess the lipid ROS level. ChIP and dual luciferase assays were used to examine the association between E2F1 and the CENPF promoter. The interaction between PSMD14 and E2F1 was verified using Co-IP. Knockdown of CENPF could significantly inhibit migration and invasion in TNBC cells. In addition, the silencing of CENPF aggravated arachidonic acid metabolism-induced ferroptosis in TNBC cells. Meanwhile, E2F1 knockdown greatly inhibited the expressions of CENPF and attenuated TNBC cell invasion and migration by decreasing its binding with the CENPF promoter. More importantly, PSMD14 could suppress arachidonic acid metabolism-induced ferroptosis in TNBC cells through the E2F1/CENPF axis. The PSMD14/E2F1 axis-mediated CENPF could promote the metastasis of TNBC by inhibiting arachidonic acid metabolism-induced ferroptosis. This research might bring novel insights into discovering methods for alleviating tumor metastasis in TNBC.","PeriodicalId":48943,"journal":{"name":"Cancer Science","volume":" ","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144047995","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

PI3Kδ Inhibitor Parsaclisib in Japanese Patients With Relapsed or Refractory Follicular Lymphoma. PI3Kδ抑制剂Parsaclisib在日本复发或难治性滤泡性淋巴瘤患者中的应用

IF 5.7 2区医学

Cancer Science Pub Date : 2025-05-14 DOI: 10.1111/cas.70046

Noriko Fukuhara, Isao Yoshida, Takuro Ishiguro, Katsuya Fujimoto, Junya Kuroda, Toshiki Uchida, Ryusuke Yamamoto, Yoshiaki Ogawa, Yasushi Hiramatsu, Toshiro Ito, Seiichiro Katagiri, Tomonori Nakazato, Kazumi Suzukawa, Kenzo Kinami, Mi Zhou, Eiju Negoro

{"title":"PI3Kδ Inhibitor Parsaclisib in Japanese Patients With Relapsed or Refractory Follicular Lymphoma.","authors":"Noriko Fukuhara, Isao Yoshida, Takuro Ishiguro, Katsuya Fujimoto, Junya Kuroda, Toshiki Uchida, Ryusuke Yamamoto, Yoshiaki Ogawa, Yasushi Hiramatsu, Toshiro Ito, Seiichiro Katagiri, Tomonori Nakazato, Kazumi Suzukawa, Kenzo Kinami, Mi Zhou, Eiju Negoro","doi":"10.1111/cas.70046","DOIUrl":"https://doi.org/10.1111/cas.70046","url":null,"abstract":"Follicular lymphoma (FL) is the second most common subtype of non-Hodgkin lymphoma (NHL) in Japan, the United States, and Western Europe. Parsaclisib is a potent, selective next-generation PI3Kδ inhibitor that has demonstrated clinical efficacy and tolerability in phase II studies of patients with relapsed or refractory (R/R) B-cell NHL, including FL. We report results from CITADEL-213 (NCT04434937), a phase II study evaluating the efficacy and safety of parsaclisib in Japanese patients with R/R FL. Eligible patients were aged ≥ 18 years with histologically confirmed R/R FL (grade 1, 2, or 3a), had received two or more prior systemic therapies, and were ineligible for hematopoietic stem cell transplantation. Patients received parsaclisib 20 mg once daily for 8 weeks, followed by parsaclisib 2.5 mg once daily thereafter. The primary endpoint was the objective response rate (ORR). At the data cut-off (February 16, 2023), 42 patients had received treatment with parsaclisib, of whom 41 were evaluable for change in target tumor size. Median (range) age at baseline was 66.5 (52-87) years. ORR (95% confidence interval [CI]) was 88.1% (74.4-96.0), with 10 patients (23.8%) experiencing a complete response and 27 patients (64.3%) experiencing a partial response. Median (95% CI) duration of response was not reached (8.0 months-not estimable). The most common treatment-emergent adverse events (TEAEs) were diarrhea (28.6%; grade ≥ 3, 7.1%) and stomatitis (23.8%; grade ≥ 3, 11.9%); TEAEs led to parsaclisib discontinuation in five patients (11.9%). There were no fatal TEAEs. In conclusion, parsaclisib monotherapy demonstrated durable responses with a manageable safety profile in Japanese patients with R/R FL. Trial Registration: ClinicalTrials.gov, NCT04434937.","PeriodicalId":48943,"journal":{"name":"Cancer Science","volume":" ","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144038801","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Correction to "The Clinicopathological Characteristics of Muscle-Invasive Bladder Recurrence in Upper Tract Urothelial Carcinoma". 修正“上尿路上皮癌肌肉浸润性膀胱复发的临床病理特征”。

IF 5.7 2区医学

Cancer Science Pub Date : 2025-05-14 DOI: 10.1111/cas.70101

引用次数: 0

OCT-2 Is Associated With Pro-Metastatic Epigenomic Properties of Triple-Negative Breast Cancer Cells. OCT-2与三阴性乳腺癌细胞的前转移性表观基因组特性相关

IF 5.7 2区医学

Cancer Science Pub Date : 2025-05-14 DOI: 10.1111/cas.70093

Kazuki Ogikubo, Jun Nishida, Kei Takahashi-Yamashiro, Masato Morikawa, Shogo Ehata, Tetsuro Watabe, Kohei Miyazono, Daizo Koinuma

{"title":"OCT-2 Is Associated With Pro-Metastatic Epigenomic Properties of Triple-Negative Breast Cancer Cells.","authors":"Kazuki Ogikubo, Jun Nishida, Kei Takahashi-Yamashiro, Masato Morikawa, Shogo Ehata, Tetsuro Watabe, Kohei Miyazono, Daizo Koinuma","doi":"10.1111/cas.70093","DOIUrl":"https://doi.org/10.1111/cas.70093","url":null,"abstract":"Triple-negative breast cancer (TNBC) is a malignant type of breast cancer. Owing to the lack of expression of receptors that serve as molecular targets for standard therapy for breast cancer, conventional cytotoxic chemotherapy is the primary treatment option for TNBC. However, TNBC exhibits a high degree of genomic heterogeneity, rendering it resistant to chemotherapy. Therefore, there is an urgent need to identify novel therapeutic targets for the treatment of TNBC. Advances in massively parallel sequencing technology have enabled the identification of cancer cell-specific gene expression patterns and epigenetic alterations that regulate their expression. Cancer cell-specific super-enhancers (SEs) have been identified as effective therapeutic targets for cancer. In this study, we identified the functional roles of epigenetic changes and their regulatory mechanisms in TNBC cells. TNBC cell-specific SEs were formed near several genes that contribute to malignant cancer cell acquisition. We found that the transcription factor OCT-2 (encoded by POU2F2) was responsible for the formation of SEs and the expression of genes encoded in the vicinity of the SE regions. Overexpression of POU2F2 enhances the metastasis of TNBC cells in mice, and its expression is highly correlated to poor prognosis of TNBC patients. Our findings provide a new insight into cancer cell-specific epigenetic changes induced by OCT-2, which trigger the progression of TNBC, and suggest possible candidates that could be targeted for the treatment of TNBC.","PeriodicalId":48943,"journal":{"name":"Cancer Science","volume":" ","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143991621","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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 Distal Enhancer That Regulates TGF-β-Induced SNAI1 Expression. 调控TGF-β-诱导的SNAI1表达的远端增强子的鉴定

IF 5.7 2区医学

Cancer Science Pub Date : 2025-05-13 DOI: 10.1111/cas.70091

Hao Fu, Yuka Itoh, Tomoe Sawaguchi, Shigeo Otake, Chiho Omata, Masao Saitoh, Keiji Miyazawa

{"title":"Identification of a Distal Enhancer That Regulates TGF-β-Induced SNAI1 Expression.","authors":"Hao Fu, Yuka Itoh, Tomoe Sawaguchi, Shigeo Otake, Chiho Omata, Masao Saitoh, Keiji Miyazawa","doi":"10.1111/cas.70091","DOIUrl":"https://doi.org/10.1111/cas.70091","url":null,"abstract":"Snail is a zinc finger transcription factor encoded by the SNAI1 gene and triggers a cellular process termed epithelial-mesenchymal transition (EMT) upon its increased expression and/or functional activation. Snail expression and activity are regulated by various extracellular stimuli, including cytokines and environmental factors. Transforming growth factor-β (TGF-β) is a Snail inducer that functions via Smad3-mediated transcriptional activation. In the present study, we identified a distal enhancer that modulates TGF-β-induced SNAI1 expression. ChIP-seq and Hi-C analyses showed that the enhancer is located 46 kb downstream of the SNAI1 gene; in TGF-β-stimulated cells, it associates with Smad3 and interacts with the SNAI1 proximal promoter. Inhibiting the activity of the enhancer using CRISPRi attenuated TGF-β-induced SNAI1 expression, stress fiber formation, and cell motility enhancement, suggesting that the enhancer mediates TGF-β-induced EMT. The enhancer contains a Smad-binding CAGA motif and an activator protein-1 (AP-1) binding motif that function in transcriptional activation. Ras-responsive element binding protein 1 (RREB1), a transcription factor required for TGF-β-induced Snail expression, regulated the basal activity of the enhancer but not its inducibility by TGF-β. In contrast to the enhancer, the association of Smad3 with the proximal promoter was not evident. These findings suggest that the proximal promoter and the distal enhancer respond to distinct signaling cues, integrate them, and cooperatively function to drive SNAI1 expression.","PeriodicalId":48943,"journal":{"name":"Cancer Science","volume":" ","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144055322","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Upregulation of YY1/EZH2 and MLH1 as Therapeutic Targets for Adult T-Cell Leukemia/Lymphoma. 上调YY1/EZH2和MLH1作为成人t细胞白血病/淋巴瘤的治疗靶点

IF 5.7 2区医学

Cancer Science Pub Date : 2025-05-12 DOI: 10.1111/cas.70095

Takuya Shimizu, Takero Shindo, Hanako Ogawa, Kaori Teranaka, Akira Watanabe, Akifumi Takaori-Kondo

{"title":"Upregulation of YY1/EZH2 and MLH1 as Therapeutic Targets for Adult T-Cell Leukemia/Lymphoma.","authors":"Takuya Shimizu, Takero Shindo, Hanako Ogawa, Kaori Teranaka, Akira Watanabe, Akifumi Takaori-Kondo","doi":"10.1111/cas.70095","DOIUrl":"https://doi.org/10.1111/cas.70095","url":null,"abstract":"The clinical and genetic presentation of adult T-cell leukemia/lymphoma (ATLL) ranges from indolent to aggressive, making it difficult to identify common therapeutic targets. Inhibiting EZH1/2 suppresses ATLL through epigenetic modulation; however, the diverse genetic background of ATLL precludes its mode of action from being clearly elucidated. We conducted single-cell RNA sequencing (scRNA-seq) of primary ATLL cells and identified an epigenetic regulative axis. First, flow cytometry showed that the proliferative potential of CADM1+ HTLV-1-infected cells ranges from stable to treatment-required. Second, scRNA-seq identified a CCR4+CD48- cluster, the population of which increased in treatment-required patients. In silico promoter analysis of this cluster identified a transcription factor YY1 as a candidate regulator. Intracellular flow cytometry confirmed that YY1 and EZH2 were upregulated in acute-type. By contrast, MLH1 but not MSH2 within CADM1+ cells was downregulated in remitted ATLL (p < 0.05), suggesting that MLH1 is associated with YY1/EZH2. Notably, lentiviral YY1 knockdown and the EZH1/2 inhibitor valemetostat downregulated MLH1 in ATLL cell lines and primary ATLL cells. Finally, knockdown of YY1 or MLH1 suppressed the proliferation of ATLL cells. Our findings suggest that YY1/EZH2 overexpression in the ATLL subpopulation defines aggressiveness and that MLH1 downregulation through YY1/EZH2 inhibition may be an effective treatment for aggressive ATLL.","PeriodicalId":48943,"journal":{"name":"Cancer Science","volume":" ","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144051410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Immunosuppressive Effects of Multiple Myeloma-Derived Extracellular Vesicles Through T Cell Exhaustion. 多发性骨髓瘤源性细胞外囊泡通过T细胞衰竭的免疫抑制作用。

IF 5.7 2区医学

Cancer Science Pub Date : 2025-05-08 DOI: 10.1111/cas.70099

Shinya Hagiwara, Masaki Ri, Toru Ebina, Yoshiaki Marumo, Tomoyuki Nakamura, Kentaro Hirade, Takahiro Nakashima, Arisa Asano, Shiori Kinoshita, Tomotaka Suzuki, Tomoko Narita, Ayako Masaki, Hirokazu Komatsu, Shinsuke Iida

{"title":"Immunosuppressive Effects of Multiple Myeloma-Derived Extracellular Vesicles Through T Cell Exhaustion.","authors":"Shinya Hagiwara, Masaki Ri, Toru Ebina, Yoshiaki Marumo, Tomoyuki Nakamura, Kentaro Hirade, Takahiro Nakashima, Arisa Asano, Shiori Kinoshita, Tomotaka Suzuki, Tomoko Narita, Ayako Masaki, Hirokazu Komatsu, Shinsuke Iida","doi":"10.1111/cas.70099","DOIUrl":"https://doi.org/10.1111/cas.70099","url":null,"abstract":"Extracellular vehicles (EVs) are reported to be involved in several processes relating to tumor progression, including angiogenesis, osteolysis, and drug resistance in multiple myeloma (MM). However, the role of EVs in the immune-suppressive milieu of MM is poorly understood. Here, we investigated the effects of MM-derived EVs on T cells, focusing on markers of T cell exhaustion. Using activated peripheral blood mononuclear cells from healthy donors, we observed immunosuppressive effects such as upregulated expression of immune checkpoint markers on CD8+ T cells treated with MM-derived EVs. Proteomic analysis identified several proteins, such as IL-8, SLC1A5, PIN2, and FSP1, associated with regulation of T cell exhaustion and chronic inflammation. Surprisingly, sphingosine kinase 1 (SPHK1) was enriched in MM cell line-derived EVs, implicating SPHK1/S1P signaling in the immunosuppressive effect of MM EVs. Thus, MM-derived EVs may promote T cell exhaustion via upregulating the expression of immune checkpoint markers and thereby contribute to the formation of the immune-suppressive milieu of MM, resulting in impaired T cell activity.","PeriodicalId":48943,"journal":{"name":"Cancer Science","volume":" ","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144041456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Correction to "Mitogen-Activated Protein Kinase Inhibition Augments the T Cell Response Against HOXB7-Expressing Tumor Through Human Leukocyte Antigen Upregulation". 更正“丝裂原活化蛋白激酶抑制通过上调人白细胞抗原增强T细胞对表达hoxb7的肿瘤的反应”。

IF 5.7 2区医学

Cancer Science Pub Date : 2025-05-06 DOI: 10.1111/cas.70094

引用次数: 0

In Vitro Expansion and Transduction of Primary NK Cells Using Feeder Cells Expressing Costimulatory Molecules and IL-21. 用表达共刺激分子和IL-21的饲养细胞体外扩增和转导原代NK细胞。

IF 5.7 2区医学

Cancer Science Pub Date : 2025-05-05 DOI: 10.1111/cas.70090

Thi Bao Tram Tran, Thi Van Anh Bui, Thi Minh Thu Tran, Nguyen Minh Nguyen, Hoang Thien Phuc Nguyen, Thi Phuong Diem Tran, Duc Minh Quan Nguyen, Thai Minh Quan Ngo, Thanh Binh Nguyen, Els Verhoeyen, Nhat Thang Tran, Hoai-Nghia Nguyen, Le Son Tran

{"title":"In Vitro Expansion and Transduction of Primary NK Cells Using Feeder Cells Expressing Costimulatory Molecules and IL-21.","authors":"Thi Bao Tram Tran, Thi Van Anh Bui, Thi Minh Thu Tran, Nguyen Minh Nguyen, Hoang Thien Phuc Nguyen, Thi Phuong Diem Tran, Duc Minh Quan Nguyen, Thai Minh Quan Ngo, Thanh Binh Nguyen, Els Verhoeyen, Nhat Thang Tran, Hoai-Nghia Nguyen, Le Son Tran","doi":"10.1111/cas.70090","DOIUrl":"https://doi.org/10.1111/cas.70090","url":null,"abstract":"Natural Killer (NK) cells are an important population of the immune system, and NK cell-based therapy has shown great potential in the treatment of cancers. However, to apply NK cells clinically, producing a large number of cells with high cytotoxicity remains a challenge. Current strategies focus on employing different irradiated feeder cells to stimulate NK expansion, maturation, and cytotoxicity. While co-stimulatory signals play critical roles in promoting NK cell proliferation and activating their functions, the exploitation of these signals for expanding NK cells has not been fully explored. To identify the optimal engineered feeder cells for expanding umbilical cord blood-derived NK cells, we generated different feeder cells expressing the co-stimulatory molecules CD80, 4-1BBL, or membrane-bound IL-21 (mbIL21). We then evaluated the transduction efficacy of a chimeric antigen receptor (CAR) construct into expanded NK cells using various lentiviral vectors. Our results showed that CD80, in combination with 4-1BBL and mbIL21, induced the highest expansion of NK cells from cord blood. The expanded NK cells displayed higher cytotoxicity toward target cells compared to T cells following CAR transduction using BaEV lentivirus.","PeriodicalId":48943,"journal":{"name":"Cancer Science","volume":" ","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144052734","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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