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Nicotinamide N-methyltransferase negatively regulates metastasis-promoting property of cancer-associated fibroblasts in lung adenocarcinoma.
IF 20.1 1区 医学
Cancer Communications Pub Date : 2024-12-02 DOI: 10.1002/cac2.12633
Peiyu Wang, Guangxi Wang, Haoran Li, Yuyao Yuan, Haiming Chen, Shaodong Wang, Zewen Sun, Fanjie Meng, Yun Li, Fan Yang, Jun Wang, Kezhong Chen, Mantang Qiu
{"title":"Nicotinamide N-methyltransferase negatively regulates metastasis-promoting property of cancer-associated fibroblasts in lung adenocarcinoma.","authors":"Peiyu Wang, Guangxi Wang, Haoran Li, Yuyao Yuan, Haiming Chen, Shaodong Wang, Zewen Sun, Fanjie Meng, Yun Li, Fan Yang, Jun Wang, Kezhong Chen, Mantang Qiu","doi":"10.1002/cac2.12633","DOIUrl":"https://doi.org/10.1002/cac2.12633","url":null,"abstract":"<p><strong>Background: </strong>Recurrence and metastasis remain significant challenges in lung adenocarcinoma (LUAD) after radical resection. The mechanisms behind the recurrence and metastasis of LUAD remain elusive, and deregulated cellular metabolism is suspected to play a significant role. This study explores the metabolic and epigenetic regulation mediated by nicotinamide N-methyl transferase (NNMT) in LUAD.</p><p><strong>Methods: </strong>Untargeted metabolomic analyses were performed to detect metabolism irregularities. Single-cell RNA sequencing (RNA-seq) databases and multiplex immunofluorescence analysis were used to identify the location of NNMT within the tumor microenvironment. The biological functions of NNMT were investigated both in vitro and in vivo, with RNA-seq and chromatin immunoprecipitation-PCR providing insights into underlying mechanisms. Finally, single-cell RNA-seq data and immunohistochemistry of primary tumors were analyzed to validate the main findings.</p><p><strong>Results: </strong>Untargeted metabolomic analyses revealed metabolic aberrations in amino acids, organic acids, lipids, and nicotinamide pathways, which are linked to metastasis of non-small cell lung cancer. NNMT is a key enzyme in nicotinamide metabolism, and we found the bulk tissue mRNA level of NNMT gene was inversely associated with LUAD metastasis. NNMT was proved to be predominantly expressed in cancer-associated fibroblasts (CAFs) within the stromal regions of LUAD, and a low stromal NNMT expression was identified as a predictor of poor disease-free survival following radical resection of LUAD. The isolation and primary culture of CAFs from LUAD enabled in vitro and in vivo experiments, which confirmed that NNMT negatively regulated the metastasis-promoting properties of CAFs in LUAD. Mechanistically, the downregulation of NNMT led to an increase in intracellular methyl groups by reducing the activity of the methionine cycle, resulting in heightened methylation at H3K4me3. This alteration triggered the upregulation of genes involved in extracellular matrix remodeling in CAFs, including those encoding collagens, integrins, laminins, and matrix metalloproteinases, thereby facilitating cancer cell invasion and metastasis. Reanalysis of single-cell RNA-seq data and immunohistochemistry assays of primary LUAD tissues substantiated NNMT's negative regulation of these genes in CAFs.</p><p><strong>Conclusions: </strong>This study provides novel insights into the metabolic and epigenetic regulatory functions of NNMT in CAFs, expanding the current understanding of LUAD metastasis regulation and suggesting potential avenues for future research and therapeutic development.</p>","PeriodicalId":9495,"journal":{"name":"Cancer Communications","volume":" ","pages":""},"PeriodicalIF":20.1,"publicationDate":"2024-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142766580","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
Advances in cervical cancer: current insights and future directions.
IF 20.1 1区 医学
Cancer Communications Pub Date : 2024-11-29 DOI: 10.1002/cac2.12629
Miaochun Xu, Canhui Cao, Peng Wu, Xiaoyuan Huang, Ding Ma
{"title":"Advances in cervical cancer: current insights and future directions.","authors":"Miaochun Xu, Canhui Cao, Peng Wu, Xiaoyuan Huang, Ding Ma","doi":"10.1002/cac2.12629","DOIUrl":"https://doi.org/10.1002/cac2.12629","url":null,"abstract":"<p><p>In alignment with the World Health Organization's strategy to eliminate cervical cancer, substantial progress has been made in the treatment of this malignancy. Cervical cancer, largely driven by human papillomavirus (HPV) infection, is considered preventable and manageable because of its well-established etiology. Advancements in precision screening technologies, such as DNA methylation triage, HPV integration detection, liquid biopsies, and artificial intelligence-assisted diagnostics, have augmented traditional screening methods such as HPV nucleic acid testing and cytology. Therapeutic strategies aimed at eradicating HPV and reversing precancerous lesions have been refined as pivotal measures for disease prevention. The controversy surrounding surgery for early-stage cervical cancer revolves around identifying optimal candidates for minimally invasive and conservative procedures without compromising oncological outcomes. Recent clinical trials have yielded promising results for the development of systemic therapies for advanced cervical cancer. Immunotherapies, such as immune checkpoint inhibitors (ICIs), antibody-drug conjugates (ADCs), and targeted therapy have demonstrated significant effectiveness, marking a substantial advancement in cervical cancer management. Various combination therapies have been validated, and ongoing trials aim to enhance outcomes through the development of novel drugs and optimized combination regimens. The prospect of eradicating cervical cancer as the first malignancy to be eliminated is now within reach. In this review, we provide a comprehensive overview of the latest scientific insights, with a particular focus on precision managements for various stages of cervical disease, and explore future research directions in cervical cancer.</p>","PeriodicalId":9495,"journal":{"name":"Cancer Communications","volume":" ","pages":""},"PeriodicalIF":20.1,"publicationDate":"2024-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142749557","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
PTPN9 regulates HER3 phosphorylation during trastuzumab treatment and loss of PTPN9 is a potential biomarker for trastuzumab resistance in HER2 positive breast cancer. PTPN9 在曲妥珠单抗治疗过程中调节 HER3 磷酸化,而 PTPN9 的缺失是 HER2 阳性乳腺癌患者对曲妥珠单抗耐药的潜在生物标志物。
IF 20.1 1区 医学
Cancer Communications Pub Date : 2024-11-24 DOI: 10.1002/cac2.12632
Abul Azad, Maryam Arshad, Daniele Generali, Katharina Feldinger, Merel Gijsen, Carla Strina, Mariarosa Cappelletti, Daniele Andreis, Russell Leek, Syed Haider, Pirkko-Liisa Kellokumpu-Lehtinen, Ioannis Roxanis, Adrian Llewellyn Harris, Abeer Mahmoud Shaaban, Heikki Joensuu, Anthony Kong
{"title":"PTPN9 regulates HER3 phosphorylation during trastuzumab treatment and loss of PTPN9 is a potential biomarker for trastuzumab resistance in HER2 positive breast cancer.","authors":"Abul Azad, Maryam Arshad, Daniele Generali, Katharina Feldinger, Merel Gijsen, Carla Strina, Mariarosa Cappelletti, Daniele Andreis, Russell Leek, Syed Haider, Pirkko-Liisa Kellokumpu-Lehtinen, Ioannis Roxanis, Adrian Llewellyn Harris, Abeer Mahmoud Shaaban, Heikki Joensuu, Anthony Kong","doi":"10.1002/cac2.12632","DOIUrl":"https://doi.org/10.1002/cac2.12632","url":null,"abstract":"","PeriodicalId":9495,"journal":{"name":"Cancer Communications","volume":" ","pages":""},"PeriodicalIF":20.1,"publicationDate":"2024-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142709188","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
Ex vivo STAT3 phosphorylation in circulating immune cells: a novel biomarker for early cancer diagnosis and response to anti-PD-1 therapy. 循环免疫细胞中的体外 STAT3 磷酸化:早期癌症诊断和抗 PD-1 治疗反应的新型生物标记物。
IF 20.1 1区 医学
Cancer Communications Pub Date : 2024-11-20 DOI: 10.1002/cac2.12631
Sung-Woo Lee, Young Ju Kim, Saei Jeong, Kyung Na Rho, Jeong Eun Noh, Hee-Ok Kim, Hyun-Ju Cho, Yoo Duk Choi, Deok Hwan Yang, Eu Chang Hwang, Woo Kyun Bae, Sook Jung Yun, Ju Sik Yun, Cheol-Kyu Park, In-Jae Oh, Jae-Ho Cho
{"title":"Ex vivo STAT3 phosphorylation in circulating immune cells: a novel biomarker for early cancer diagnosis and response to anti-PD-1 therapy.","authors":"Sung-Woo Lee, Young Ju Kim, Saei Jeong, Kyung Na Rho, Jeong Eun Noh, Hee-Ok Kim, Hyun-Ju Cho, Yoo Duk Choi, Deok Hwan Yang, Eu Chang Hwang, Woo Kyun Bae, Sook Jung Yun, Ju Sik Yun, Cheol-Kyu Park, In-Jae Oh, Jae-Ho Cho","doi":"10.1002/cac2.12631","DOIUrl":"https://doi.org/10.1002/cac2.12631","url":null,"abstract":"","PeriodicalId":9495,"journal":{"name":"Cancer Communications","volume":" ","pages":""},"PeriodicalIF":20.1,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142680963","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
Anti-tumor drug supervision in China from 2010 to 2024: the evolution and prospect of drug review standards. 2010-2024年中国抗肿瘤药物监管:药品审评标准的演变与展望》。
IF 20.1 1区 医学
Cancer Communications Pub Date : 2024-11-20 DOI: 10.1002/cac2.12630
Ling Tang, Yuanyuan Song, Hong Zhang, Ruimin Hao, Xin Tong, Xing Ai, Jun Ma, Zhimin Yang
{"title":"Anti-tumor drug supervision in China from 2010 to 2024: the evolution and prospect of drug review standards.","authors":"Ling Tang, Yuanyuan Song, Hong Zhang, Ruimin Hao, Xin Tong, Xing Ai, Jun Ma, Zhimin Yang","doi":"10.1002/cac2.12630","DOIUrl":"https://doi.org/10.1002/cac2.12630","url":null,"abstract":"","PeriodicalId":9495,"journal":{"name":"Cancer Communications","volume":" ","pages":""},"PeriodicalIF":20.1,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142675158","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 IL-17A to manage immunotherapy-induced toxicity in melanoma. 以 IL-17A 为靶点,控制黑色素瘤免疫疗法引起的毒性。
IF 20.1 1区 医学
Cancer Communications Pub Date : 2024-11-13 DOI: 10.1002/cac2.12628
Kai Huang
{"title":"Targeting IL-17A to manage immunotherapy-induced toxicity in melanoma.","authors":"Kai Huang","doi":"10.1002/cac2.12628","DOIUrl":"https://doi.org/10.1002/cac2.12628","url":null,"abstract":"","PeriodicalId":9495,"journal":{"name":"Cancer Communications","volume":" ","pages":""},"PeriodicalIF":20.1,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142615171","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
Epigenomic exploration of disease status of EGFR-mutated non-small cell lung cancer using plasma cell-free DNA hydroxymethylomes. 利用血浆细胞游离 DNA 羟甲基组对表皮生长因子受体突变的非小细胞肺癌的疾病状态进行表观基因组学探索。
IF 20.1 1区 医学
Cancer Communications Pub Date : 2024-11-11 DOI: 10.1002/cac2.12606
Yong Peng, Jason Karpus, Jyoti D Patel, Everett E Vokes, Marina Chiara Garassino, Kirsteen Lugtu, Zhou Zhang, Wei Zhang, Mengjie Chen, Chuan He, Christine M Bestvina
{"title":"Epigenomic exploration of disease status of EGFR-mutated non-small cell lung cancer using plasma cell-free DNA hydroxymethylomes.","authors":"Yong Peng, Jason Karpus, Jyoti D Patel, Everett E Vokes, Marina Chiara Garassino, Kirsteen Lugtu, Zhou Zhang, Wei Zhang, Mengjie Chen, Chuan He, Christine M Bestvina","doi":"10.1002/cac2.12606","DOIUrl":"https://doi.org/10.1002/cac2.12606","url":null,"abstract":"","PeriodicalId":9495,"journal":{"name":"Cancer Communications","volume":" ","pages":""},"PeriodicalIF":20.1,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142615168","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
Discovery of a novel viroid-like circular RNA in colorectal cancer. 在结直肠癌中发现新型病毒样环状 RNA。
IF 20.1 1区 医学
Cancer Communications Pub Date : 2024-11-09 DOI: 10.1002/cac2.12626
Meini Wu, Wenliang Li, Ningzhu Hu, Changning Liu, Jianfang Li, Yanhan Li, Ning Xu, Jiandong Shi, Jing Sun, Jing Li, Yunzhang Hu
{"title":"Discovery of a novel viroid-like circular RNA in colorectal cancer.","authors":"Meini Wu, Wenliang Li, Ningzhu Hu, Changning Liu, Jianfang Li, Yanhan Li, Ning Xu, Jiandong Shi, Jing Sun, Jing Li, Yunzhang Hu","doi":"10.1002/cac2.12626","DOIUrl":"https://doi.org/10.1002/cac2.12626","url":null,"abstract":"","PeriodicalId":9495,"journal":{"name":"Cancer Communications","volume":" ","pages":""},"PeriodicalIF":20.1,"publicationDate":"2024-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142614992","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
FOXO1 or not FOXO1: that is the question. FOXO1 还是 FOXO1:这是一个问题。
IF 20.1 1区 医学
Cancer Communications Pub Date : 2024-11-07 DOI: 10.1002/cac2.12624
Maude Marchais, Marianne Mangeney
{"title":"FOXO1 or not FOXO1: that is the question.","authors":"Maude Marchais, Marianne Mangeney","doi":"10.1002/cac2.12624","DOIUrl":"https://doi.org/10.1002/cac2.12624","url":null,"abstract":"","PeriodicalId":9495,"journal":{"name":"Cancer Communications","volume":" ","pages":""},"PeriodicalIF":20.1,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142603059","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
Tryptophan 2,3-dioxygenase-positive matrix fibroblasts fuel breast cancer lung metastasis via kynurenine-mediated ferroptosis resistance of metastatic cells and T cell dysfunction. 色氨酸-2,3-二氧合酶阳性基质成纤维细胞通过犬尿氨酸介导的转移细胞铁蛋白沉积抗性和 T 细胞功能障碍助长乳腺癌肺转移。
IF 20.1 1区 医学
Cancer Communications Pub Date : 2024-11-01 Epub Date: 2024-09-02 DOI: 10.1002/cac2.12608
Yongcan Liu, Shanchun Chen, Xueying Wan, Rui Wang, Haojun Luo, Chao Chang, Peijin Dai, Yubi Gan, Yuetong Guo, Yixuan Hou, Yan Sun, Yong Teng, Xiaojiang Cui, Manran Liu
{"title":"Tryptophan 2,3-dioxygenase-positive matrix fibroblasts fuel breast cancer lung metastasis via kynurenine-mediated ferroptosis resistance of metastatic cells and T cell dysfunction.","authors":"Yongcan Liu, Shanchun Chen, Xueying Wan, Rui Wang, Haojun Luo, Chao Chang, Peijin Dai, Yubi Gan, Yuetong Guo, Yixuan Hou, Yan Sun, Yong Teng, Xiaojiang Cui, Manran Liu","doi":"10.1002/cac2.12608","DOIUrl":"10.1002/cac2.12608","url":null,"abstract":"<p><strong>Background: </strong>Tumor metastasis is a major threat to cancer patient survival. The organ-specific niche plays a pivotal role in tumor organotropic metastasis. Fibroblasts serve as a vital component of the metastatic microenvironment, but how heterogeneous metastasis-associated fibroblasts (MAFs) promote organotropic metastasis is poorly characterized. Here, we aimed to decipher the heterogeneity of MAFs and elucidate the distinct roles of these fibroblasts in pulmonary metastasis formation in breast cancer.</p><p><strong>Methods: </strong>Mouse models of breast cancer pulmonary metastasis were established using an in vivo selection method of repeated injections of metastatic cells purified from the mouse lung. Single-cell RNA-sequencing (scRNA-seq) was employed to investigate the heterogeneity of MAFs. Transgenic mice were used to examine the contribution of tryptophan 2,3-dioxygenase-positive matrix fibroblasts (TDO2<sup>+</sup> MFs) in lung metastasis.</p><p><strong>Results: </strong>We uncovered 3 subtypes of MAFs in the lung metastatic microenvironment, and their transcriptome profiles changed dynamically as lung metastasis evolved. As the predominant subtype, MFs were exclusively marked by platelet-derived growth factor receptor alpha (PDGFRA) and mainly located on the edge of the metastasis, and T cells were enriched around MFs. Notably, high MF signatures were significantly associated with poor survival in breast cancer patients. Lung metastases were markedly diminished, and the suppression of T cells was dramatically attenuated in MF-depleted experimental metastatic mouse models. We found that TDO2<sup>+</sup> MFs controlled pulmonary metastasis by producing kynurenine (KYN), which upregulated ferritin heavy chain 1 (FTH1) level in disseminated tumor cells (DTCs), enabling DTCs to resist ferroptosis. Moreover, TDO2<sup>+</sup> MF-secreted chemokines C-C motif chemokine ligand 8 (CCL8) and C-C motif chemokine ligand 11 (CCL11) recruited T cells. TDO2<sup>+</sup> MF-derived KYN induced T cell dysfunction. Conditional knockout of Tdo2 in MFs diminished lung metastasis and enhanced immune activation.</p><p><strong>Conclusions: </strong>Our study reveals crucial roles of TDO2<sup>+</sup> MFs in promoting lung metastasis and DTCs' immune evasion in the metastatic niche. It suggests that targeting the metabolism of lung-specific stromal cells may be an effective treatment strategy for breast cancer patients with lung metastasis.</p>","PeriodicalId":9495,"journal":{"name":"Cancer Communications","volume":" ","pages":"1261-1286"},"PeriodicalIF":20.1,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cac2.12608","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142104686","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
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