Cancer gene therapy最新文献_第5页

Correction: A model of breast cancer meningeal metastases: characterization with in vivo molecular imaging 更正：乳腺癌脑膜转移模型：活体分子成像特征。

IF 4.8 3区医学

Cancer gene therapy Pub Date : 2024-11-26 DOI: 10.1038/s41417-024-00800-9

Darshini Kuruppu, Deepak Bhere, Christian T. Farrar, Khalid Shah, Anna-Liisa Brownell, Kenneth K. Tanabe

引用次数: 0

CCDC34 maintains stemness phenotype through β-catenin-mediated autophagy and promotes EGFR-TKI resistance in lung adenocarcinoma CCDC34通过β-catenin介导的自噬维持干性表型，并促进肺腺癌对表皮生长因子受体-TKI的耐药性。

IF 4.8 3区医学

Cancer gene therapy Pub Date : 2024-11-25 DOI: 10.1038/s41417-024-00843-y

Ping Yue, Yuchao He, Ran Zuo, Wenchen Gong, Yu Wang, Liwei Chen, Yi Luo, Yuanying Feng, Yuan Gao, Zhiyong Liu, Peng Chen, Hua Guo

{"title":"CCDC34 maintains stemness phenotype through β-catenin-mediated autophagy and promotes EGFR-TKI resistance in lung adenocarcinoma","authors":"Ping Yue, Yuchao He, Ran Zuo, Wenchen Gong, Yu Wang, Liwei Chen, Yi Luo, Yuanying Feng, Yuan Gao, Zhiyong Liu, Peng Chen, Hua Guo","doi":"10.1038/s41417-024-00843-y","DOIUrl":"10.1038/s41417-024-00843-y","url":null,"abstract":"Despite recent advances in treatment strategy, lung cancer remains the leading cause of cancer-related mortality worldwide, and it is a serious threat to human health. Lung adenocarcinoma (LUAD) is the most common histological type of lung cancer, and approximately 40–50% of patients with LUAD in Asian populations have epidermal growth factor receptor (EGFR) mutations. The use of EGFR tyrosine kinase inhibitors (EGFR-TKIs) has revolutionarily improved the prognosis of patients with EGFR-mutated LUAD. However, acquired drug resistance is the main cause of treatment failure. Therefore, new therapeutic strategies are necessary to address the resistance to EGFR-TKIs in patients with LUAD. Cancer stemness-related factors lead to multiple-drug resistance in cancer treatment, including EGFR–TKI resistance. Coiled-coil domain-containing 34 (CCDC34) serves as an oncogene in several types of cancer. However, the role and molecular mechanism of CCDC34 in the malignant progression of LUAD have not been reported to date. In the present study, we found that CCDC34 may be associated with LUAD stemness through weighted gene co-expression network analysis (WGCNA). Furthermore, we demonstrated that CCDC34 promoted LUAD stemness properties through β-catenin-mediated regulation of ATG5-induced autophagy, which was conducive to acquired EGFR-TKI resistance in LUAD in vitro and in vivo. Knockdown CCDC34 can synergistically inhibit tumor growth when combined with EGFR-TKIs. This study reveals a positive association between CCDC34 and the stemness phenotype of LUAD, providing new insights into overcoming EGFR-TKI resistance in LUAD by inhibiting CCDC34 expression.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"32 1","pages":"104-121"},"PeriodicalIF":4.8,"publicationDate":"2024-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142715498","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Soft tissue sarcomas at the single-cell and spatial resolution: new markers and targets 单细胞和空间分辨率的软组织肉瘤：新的标记和靶标。

IF 4.8 3区医学

Cancer gene therapy Pub Date : 2024-11-24 DOI: 10.1038/s41417-024-00856-7

Maxim E. Menyailo, Elena E. Kopantseva, Anna A. Khozyainova, Anastasia A. Korobeynikova, Evgeny V. Denisov

引用次数: 0

Establishment and characterization of the first immortalized vocal cord leukoplakia epithelial cell line 建立首个永生化声带白斑上皮细胞系并确定其特征。

IF 4.8 3区医学

Cancer gene therapy Pub Date : 2024-11-23 DOI: 10.1038/s41417-024-00859-4

Zi-Ming Fu, Yang-Yang Bao, Zhe Chen, Jiang-Tao Zhong, Heng-Chao Chen, Zai-Zai Cao, Shui-Hong Zhou

引用次数: 0

Reversible downregulation of MYC in a spheroid model of metastatic epithelial ovarian cancer 转移性上皮性卵巢癌球形模型中 MYC 的可逆下调。

IF 4.8 3区医学

Cancer gene therapy Pub Date : 2024-11-21 DOI: 10.1038/s41417-024-00850-z

Adrian Buensuceso, Matthew J. Borrelli, Yudith Ramos Valdés, Trevor G. Shepherd

{"title":"Reversible downregulation of MYC in a spheroid model of metastatic epithelial ovarian cancer","authors":"Adrian Buensuceso, Matthew J. Borrelli, Yudith Ramos Valdés, Trevor G. Shepherd","doi":"10.1038/s41417-024-00850-z","DOIUrl":"10.1038/s41417-024-00850-z","url":null,"abstract":"Upon detachment from the primary tumour, epithelial ovarian cancer cells can form multicellular aggregates, also referred to as spheroids, that have the capacity to establish metastases at distant sites. These structures exhibit numerous adaptations that may facilitate metastatic transit and promote tumorigenic potential. One such adaptation is the acquisition of dormancy, characterized by decreased proliferation and molecular features of quiescence. One of the most frequently dysregulated genes in cancer is MYC, which encodes a transcription factor that promotes cell proliferation. In this study, we demonstrate that MYC protein abundance and associated gene expression is significantly decreased in EOC spheroids compared to adherent cells. This downregulation occurs rapidly upon cell detachment and is proteasome-dependent. Moreover, MYC protein abundance and associated gene expression is restored upon spheroid reattachment to an adherent culture surface. Overall, our findings suggest that suppression of MYC activity is a common feature of EOC spheroids and may contribute to the reversible acquisition of dormancy.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"32 1","pages":"83-94"},"PeriodicalIF":4.8,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11772254/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142686230","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Oncolytic virus encoding 4-1BBL and IL15 enhances the efficacy of tumor-infiltrating lymphocyte adoptive therapy in HCC 编码4-1BBL和IL15的肿瘤溶解病毒可提高肿瘤浸润淋巴细胞采纳疗法对HCC的疗效。

IF 4.8 3区医学

Cancer gene therapy Pub Date : 2024-11-20 DOI: 10.1038/s41417-024-00853-w

Kai Ye, Yongfeng Yan, Rui Su, Qinghai Dai, Kunyan Qiao, Yu Cao, Jian Xu, Lihua Yan, Zhixiao Huo, Wei Liu, Yue Hu, Yu Zhu, Liang Xu, Yuqiang Mi

{"title":"Oncolytic virus encoding 4-1BBL and IL15 enhances the efficacy of tumor-infiltrating lymphocyte adoptive therapy in HCC","authors":"Kai Ye, Yongfeng Yan, Rui Su, Qinghai Dai, Kunyan Qiao, Yu Cao, Jian Xu, Lihua Yan, Zhixiao Huo, Wei Liu, Yue Hu, Yu Zhu, Liang Xu, Yuqiang Mi","doi":"10.1038/s41417-024-00853-w","DOIUrl":"10.1038/s41417-024-00853-w","url":null,"abstract":"Previous studies have found that oncolytic virus (OVs) can improve the efficacy of TIL adoptive therapy in oral cancer, colon cancer, and pancreatic cancer. However, the curative effect in hepatocellular carcinoma (HCC) is still unclear. Therefore, this study aims to explore the therapeutic effect and mechanism of OVs encoding 4-1BBL and IL15 (OV-4-1BBL/IL15) combined with TIL adoptive therapy on HCC. In this study, the role and immunological mechanism of armed OVs combined with TILs were evaluated by flow cytometry and ELISA in patient-derived xenograft and syngeneic mouse tumor models. Co-culturing with TILs can up-regulate the expression of antigen-presenting cell (APC) markers on the surface of OV-infected primary HCC cells, and promote the specific activation ability and tumor-killing ability of TILs. OV-4-1BBL/IL15 combined with TIL adoptive therapy could induce tumor volume reduction and anti-tumor immune memory in patient-derived xenograft and syngeneic mouse tumor models. Furthermore, OV combined with TIL adoptive therapy can endow tumor cells with aAPC characteristics, activate T cells at the same time, and reprogram tumor macrophages into anti-tumor phenotype. OV-4-1BBL/IL15 can stimulate the anti-tumor potential of TIL therapy in HCC, and possess broad clinical application prospects.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"32 1","pages":"71-82"},"PeriodicalIF":4.8,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41417-024-00853-w.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142680975","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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: SEMA7A-mediated juxtacrine stimulation of IGFBP-3 upregulates IL-17RB at pancreatic cancer invasive front 更正：SEMA7A介导的IGFBP-3并体刺激可上调胰腺癌浸润前沿的IL-17RB。

IF 4.8 3区医学

Cancer gene therapy Pub Date : 2024-11-20 DOI: 10.1038/s41417-024-00857-6

Yi-Ing Chen, Sui-Chih Tien, Yi-Ling Ko, Chin-Chun Chang, Min-Fen Hsu, Hung Jen Chien, Hsuan-Yu Peng, Yung-Ming Jeng, Yun-Wen Tien, Yu-Ting Chang, Ming-Chu Chang, Chun-Mei Hu

引用次数: 0

The antitumor peptide M1-20 induced the degradation of CDK1 through CUL4-DDB1-DCAF1-involved ubiquitination 抗肿瘤肽 M1-20 通过 CUL4-DDB1-DCAF1 参与的泛素化作用诱导 CDK1 降解。

IF 4.8 3区医学

Cancer gene therapy Pub Date : 2024-11-20 DOI: 10.1038/s41417-024-00855-8

Huitong Bu, Chaozhu Pei, Min Ouyang, Yan Chen, Li Yu, Xiaoqin Huang, Yongjun Tan

引用次数: 0

CEACAM6 facilitates gastric cancer progression through upregulating SLC27A2 CEACAM6 通过上调 SLC27A2 促进胃癌进展。

IF 4.8 3区医学

Cancer gene therapy Pub Date : 2024-11-19 DOI: 10.1038/s41417-024-00846-9

Xiaqiong Mao, Tongtai Liu, Shunying Yu, Yuqi Wei, Chunli Zhou, Xiaoyi Kuai

引用次数: 0

Serum small extracellular vesicles-derived BST2 as a biomarker for papillary thyroid microcarcinoma promotes lymph node metastasis 血清小细胞外囊泡衍生的BST2是甲状腺乳头状微癌促进淋巴结转移的生物标记物

IF 4.8 3区医学

Cancer gene therapy Pub Date : 2024-11-18 DOI: 10.1038/s41417-024-00854-9

Zhen Cao, Yuanyang Wang, Jianqiang Wu, Xiaoyue Tang, Zhihong Qian, Zejian Zhang, Rui Liu, Peng Liu, Zepeng Li, Xiequn Xu, Ziwen Liu

{"title":"Serum small extracellular vesicles-derived BST2 as a biomarker for papillary thyroid microcarcinoma promotes lymph node metastasis","authors":"Zhen Cao, Yuanyang Wang, Jianqiang Wu, Xiaoyue Tang, Zhihong Qian, Zejian Zhang, Rui Liu, Peng Liu, Zepeng Li, Xiequn Xu, Ziwen Liu","doi":"10.1038/s41417-024-00854-9","DOIUrl":"10.1038/s41417-024-00854-9","url":null,"abstract":"Papillary thyroid microcarcinoma (PTMC), although frequently indolent, could be aggressive in a few patients, leading to lymph node metastasis (LNM) and worsened prognosis. To explore the role of protein profiling of small extracellular vesicles (sEVs) in the auxiliary diagnosis and risk stratification of PTMC, proteins in serum sEVs isolated from PTMC patients with (N = 10) and without (N = 10) LNM and benign thyroid nodule (BN) patients (N = 9) were profiled via a bioinformatics-integrated data-independent acquisition proteomic technique. The performance of candidate proteins as diagnostic and prognostic biomarkers in PTMC was assessed via receiver operating characteristic analysis. We found that serum sEVs from PTMC patients promoted the proliferation and migration of human papillary thyroid cancer (PTC) cells and tube formation in human lymphatic endothelial cells (HLECs). SEV proteins from PTMC patients with and without LNM have differential expression profiles, with bone marrow stromal cell antigen 2 (BST2) being best associated with PTMC progression. Through knockdown and overexpression, we proved that the high expression of sEV-derived BST2 was bound up with higher proliferation and migration ability of PTC cells as well as stronger lymphangiogenesis in HLECs. This study brought insight into the differential sEV-protein profile with or without LNM in PTMC. The serum sEV-BST2 may contribute to PTMC progression and LNM and may have diagnostic, prognostic, and therapeutic implications.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"32 1","pages":"38-50"},"PeriodicalIF":4.8,"publicationDate":"2024-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11772248/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142667066","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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