Cellular Oncology最新文献

{"title":"Fibroblast subtypes in pancreatic cancer and pancreatitis: from mechanisms to therapeutic strategies.","authors":"Huizhen Huang, Wanyi Lu, Xiuli Zhang, Jiachun Pan, Feng Cao, Li Wen","doi":"10.1007/s13402-023-00874-x","DOIUrl":"10.1007/s13402-023-00874-x","url":null,"abstract":"<p><p>Excessive fibrosis is a predominant feature of pancreatic stroma and plays a crucial role in the development and progression of pancreatic ductal adenocarcinoma (PDAC) and chronic pancreatitis (CP). Emerging evidence showed diversity and heterogeneity of fibroblasts play crucial and somewhat contradictory roles, the interactions between fibroblasts and pancreatic cells or infiltrating immune cells are of great importance during PDAC and CP progression, with some promising therapeutic strategies being tested. Therefore, in this review, we describe the classification of fibroblasts and their functions in PDAC and pancreatitis, the mechanisms by which fibroblasts mediate the development and progression of PDAC and CP through direct or indirect interaction between fibroblast and pancreatic parenchymal cells, or by remodeling the pancreatic immune microenvironment mediates the development and progression of PDAC and CP. Finally, we summarized the current therapeutic strategies and agents that directly target subtypes of fibroblasts or interfere with their essential functions.</p>","PeriodicalId":49223,"journal":{"name":"Cellular Oncology","volume":" ","pages":"383-396"},"PeriodicalIF":6.6,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10291873","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}

{"title":"Plasma cell signatures predict prognosis and treatment efficacy for lung adenocarcinoma.","authors":"Long Shu, Jun Tang, Shuang Liu, Yongguang Tao","doi":"10.1007/s13402-023-00883-w","DOIUrl":"10.1007/s13402-023-00883-w","url":null,"abstract":"<p><strong>Purpose: </strong>This study aims to identify key genes regulating tumor infiltrating plasma cells (PC) and provide new insights for innovative immunotherapy.</p><p><strong>Methods: </strong>Key genes related to PC were identified using machine learning in lung adenocarcinoma (LUAD) patients. A prognostic model called PC scores was developed using TCGA data and validated with GEO cohorts. We assessed the molecular background, immune features, and drug sensitivity of the high PC scores group. Real-time PCR was utilized to assess the expression of hub genes in both localized LUAD patients and LUAD cell lines.</p><p><strong>Results: </strong>We constructed PC scores based on seventeen PC-related hub genes (ELOVL6, MFI2, FURIN, DOK1, ERO1LB, CLEC7A, ZNF431, KIAA1324, NUCB2, TXNDC11, ICAM3, CR2, CLIC6, CARNS1, P2RY13, KLF15, and SLC24A4). Higher age, TNM stage, and PC scores independently predicted shorter overall survival. The AUC value of PC scores for one year, three years, and five years of overall survival were 0.713, 0.716, and 0.690, separately. The nomogram model that integrated age, stage, and PC scores showed significantly higher predictive value than stage alone (P < 0.01). High PC scores group exhibited an immune suppressing microenvironment with lower B, CD8 + T, CD4 + T, and dendritic cell infiltration. Docetaxel, gefitinib, and erlotinib had lower IC50 in high PC groups (P < 0.001). After validation through the local cohort and in vitro experiments, we ultimately confirmed three key potential targets: MFI2, KLF15, and CLEC7A.</p><p><strong>Conclusion: </strong>We proposed a prediction mode which can effectively identify high-risk LUAD patients and found three novel genes closely correlated with PC tumor infiltration.</p>","PeriodicalId":49223,"journal":{"name":"Cellular Oncology","volume":" ","pages":"555-571"},"PeriodicalIF":6.6,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41183947","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}

{"title":"Cancer/testis-45A1 promotes cervical cancer cell tumorigenesis and drug resistance by activating oncogenic SRC and downstream signaling pathways.","authors":"Mei Meng, Yan Guo, Yu Chen, Xu Li, Bin Zhang, Zhijia Xie, Juntao Liu, Zhe Zhao, Yuxi Liu, Tong Zhang, Yingnan Qiao, Bingxue Shang, Quansheng Zhou","doi":"10.1007/s13402-023-00891-w","DOIUrl":"10.1007/s13402-023-00891-w","url":null,"abstract":"<p><strong>Background: </strong>Cancer/testis antigen-45A1 (CT45A1) is overexpressed in various types of cancer but is not expressed in healthy women. The role of CT45A1 in cervical cancer has not yet been described in the literature.</p><p><strong>Purpose: </strong>The aim of this research was to study the role of CT45A1 in cervical cancer progression and drug resistance, elucidate the mechanisms underlying CT45A1-mediated tumorigenesis and investigate CT45A1 as a biomarker for cervical cancer diagnosis, prognostic prediction, and targeted therapy.</p><p><strong>Methods: </strong>The CT45A1 levels in the tumors from cervical cancer patients were measured using immunohistochemical staining. The role and mechanisms underlying CT45A1-mediated cervical cancer cell tumor growth, invasion, and drug resistance were studied using xenograft mice, cervical cancer cells, immunohistochemistry, RNA-seq, real-time qPCR, Chromatin immunoprecipitation and Western blotting.</p><p><strong>Results: </strong>CT45A1 levels were notably high in the tumor tissues of human cervical cancer patients compared to the paracancerous tissues (p < 0.001). Overexpression of CT45A1 was closely associated with poor prognosis in cervical cancer patients. CT45A1 promoted cervical cancer cell tumor growth, invasion, neovascularization, and drug resistance. Mechanistically, CT45A1 promoted the expression of 128 pro-tumorigenic genes and concurrently activated key signaling pathways, including the oncogenic SRC, ERK, CREB, and YAP/TAZ signaling pathways. Furthermore, CT45A1-mediated tumorigenesis and drug resistance were markedly inhibited by the small molecule lycorine.</p><p><strong>Conclusion: </strong>CT45A1 promotes cervical cancer cell tumorigenesis, neovascularization, and drug resistance by activating oncogenic SRC and downstream tumorigenic signaling pathways. These findings provide new insight into the pathogenesis of cervical cancer and offer a new platform for the development of novel therapeutics against cervical cancer.</p>","PeriodicalId":49223,"journal":{"name":"Cellular Oncology","volume":" ","pages":"657-676"},"PeriodicalIF":6.6,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11090944/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71487969","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}

{"title":"High-plex spatial transcriptomic profiling reveals distinct immune components and the HLA class I/DNMT3A/CD8 modulatory axis in mismatch repair-deficient endometrial cancer.","authors":"Jingjing Guo, Baijie Tang, Jing Fu, Xuan Zhu, Wenlong Xie, Nan Wang, Zhiyong Ding, Zhentao Song, Yue Yang, Gang Xu, Xue Xiao","doi":"10.1007/s13402-023-00885-8","DOIUrl":"10.1007/s13402-023-00885-8","url":null,"abstract":"<p><strong>Purpose: </strong>Tumors bearing mismatch repair deficiency (MMRd) are characterized by a high load of neoantigens and are believed to trigger immunogenic reactions upon immune checkpoint blockade treatment such as anti-PD-1/PD-L1 therapy. However, the mechanisms are still ill-defined, as multiple cancers with MMRd exhibit variable responses to immune checkpoint inhibitors (ICIs). In endometrial cancer (EC), a distinct tumor microenvironment (TME) exists that may correspond to treatment-related efficacies. We aimed to characterize EC patients with aberrant MMR pathways to identify molecular subtypes predisposed to respond to ICI therapies.</p><p><strong>Methods: </strong>We applied digital spatial profiling, a high-plex spatial transcriptomic approach covering over 1,800 genes, to obtain a highly resolved TME landscape in 45 MMRd-EC patients. We cross-validated multiple biomarkers identified using immunohistochemistry and multiplexed immunofluorescence using in-study and independent cohorts totaling 123 MMRd-EC patients and validated our findings using external TCGA data from microsatellite instability endometrial cancer (MSI-EC) patients.</p><p><strong>Results: </strong>High-plex spatial profiling identified a 14-gene signature in the MMRd tumor-enriched regions stratifying tumors into \"hot\", \"intermediate\" and \"cold\" groups according to their distinct immune profiles, a finding highly consistent with the corresponding CD8 + T-cell infiltration status. Our validation studies further corroborated an existing coregulatory network involving HLA class I and DNMT3A potentially bridged through dynamic crosstalk incorporating CCL5.</p><p><strong>Conclusion: </strong>Our study confirmed the heterogeneous TME status within MMRd-ECs and showed that these ECs can be stratified based on potential biomarkers such as HLA class I, DNMT3A and CD8 in pathological settings for improved ICI therapeutic efficacy in this subset of patients.</p>","PeriodicalId":49223,"journal":{"name":"Cellular Oncology","volume":" ","pages":"573-585"},"PeriodicalIF":6.6,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11090934/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41240238","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}

{"title":"From basic research to clinical application: targeting fibroblast activation protein for cancer diagnosis and treatment.","authors":"Zeyu Zhang, Jinxin Tao, Jiangdong Qiu, Zhe Cao, Hua Huang, Jianchun Xiao, Taiping Zhang","doi":"10.1007/s13402-023-00872-z","DOIUrl":"10.1007/s13402-023-00872-z","url":null,"abstract":"<p><strong>Purpose: </strong>This study aims to review the multifaceted roles of a membrane protein named Fibroblast Activation Protein (FAP) expressed in tumor tissue, including its molecular functionalities, regulatory mechanisms governing its expression, prognostic significance, and its crucial role in cancer diagnosis and treatment.</p><p><strong>Methods: </strong>Articles that have uncovered the regulatory role of FAP in tumor, as well as its potential utility within clinical realms, spanning diagnosis to therapeutic intervention has been screened for a comprehensive review.</p><p><strong>Results: </strong>Our review reveals that FAP plays a pivotal role in solid tumor progression by undertaking a multitude of enzymatic and nonenzymatic roles within the tumor stroma. The exclusive presence of FAP within tumor tissues highlights its potential as a diagnostic marker and therapeutic target. The review also emphasizes the prognostic significance of FAP in predicting tumor progression and patient outcomes. Furthermore, the emerging strategies involving FAPI inhibitor (FAPI) in cancer research and clinical trials for PET/CT diagnosis are discussed. And targeted therapy utilizing FAP including FAPI, chimeric antigen receptor (CAR) T cell therapy, tumor vaccine, antibody-drug conjugates, bispecific T-cell engagers, FAP cleavable prodrugs, and drug delivery system are also introduced.</p><p><strong>Conclusion: </strong>FAP's intricate interactions with tumor cells and the tumor microenvironment make it a promising target for diagnosis and treatment. Promising strategies such as FAPI offer potential avenues for accurate tumor diagnosis, while multiple therapeutic strategies highlight the prospects of FAP targeting treatments which needs further clinical evaluation.</p>","PeriodicalId":49223,"journal":{"name":"Cellular Oncology","volume":" ","pages":"361-381"},"PeriodicalIF":6.6,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41135542","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}

{"title":"Feature-weight based measurement of cancerous transcriptome using cohort-wide and sample-specific information.","authors":"Qilu Wang, Jiaoyang Jessie Song, Feng Zhang","doi":"10.1007/s13402-023-00879-6","DOIUrl":"10.1007/s13402-023-00879-6","url":null,"abstract":"<p><p>Identifying cancerous samples or cells using transcriptomic data is critical for cancer related basic research, early diagnosis, and targeted therapy. However, the high transcriptional heterogeneity of cancers still hinders people from accurately recognizing cancerous transcriptome using bulk, single-cell, or spatial RNA-seq data. Here, we present a novel method named FWP (Feature Weight Pro) that helps measure cancerous transcriptome using transcriptomic data. The workflow of FWP is, first, to calculate feature weights using the training dataset, and then, for each sample in the testing dataset, calculate the feature-weight based final score by combining the cohort-wide and sample-specific information. Those two types of information are utilized through conducting weighted principal component analysis and calculating correlation perturbations. The effectiveness and superiority of FWP over other methods are shown by using bulk, single-cell, and spatial RNA-seq data of multiple cancer types. In addition, the high robustness and efficiency of FWP are also demonstrated by using different numbers of features and cells, respectively. FWP is available at https://github.com/jumphone/fwp .</p>","PeriodicalId":49223,"journal":{"name":"Cellular Oncology","volume":" ","pages":"711-715"},"PeriodicalIF":6.6,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41183946","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}

{"title":"Inhibition of thioredoxin-1 enhances the toxicity of glycolysis inhibitor 2-deoxyglucose by downregulating SLC1A5 expression in colorectal cancer cells.","authors":"Tianbin Tang, Daoquan Fang, Ziwei Ji, Zuyue Zhong, Baojian Zhou, Lechi Ye, Lei Jiang, Xuecheng Sun","doi":"10.1007/s13402-023-00887-6","DOIUrl":"10.1007/s13402-023-00887-6","url":null,"abstract":"<p><strong>Background: </strong>Targeting glycolysis in cancer is an attractive approach for therapeutic intervention. 2-Deoxyglucose (2DG) is a synthetic glucose analog that inhibits glycolysis. However, its efficacy is limited by the systemic toxicity at high doses. Understanding the mechanism of 2DG resistance is important for further use of this drug in cancer treatment.</p><p><strong>Methods: </strong>The expression of thioredoxin-1 (Trx-1) in colorectal cancer (CRC) cells treated with 2DG was detected by Western blotting. The effect of Trx-1 on the cytotoxicity of 2DG in CRC cells was examined in vitro and in vivo. The molecular mechanism involved in Trx-1-mediated activation of the SLC1A5 gene promoter activity was elucidated using in vitro models.</p><p><strong>Results: </strong>Inhibition glycolysis with 2DG increased the expression of Trx-1 in CRC cells. Overexpression of Trx-1 decreased the cytotoxicity of 2DG, whereas knockdown of Trx-1 by shRNA significantly increased the cytotoxicity of 2DG in CRC cells. The Trx-1 inhibitor PX-12 increased the cytotoxicity of 2DG on CRC cells both in vitro and in vivo. In addition, Trx-1 promoted SLC1A5 expression by increasing the promoter activity of the SLC1A5 gene by binding to SP1. We also found that the SLC1A5 expression was upregulated in CRC tissues, and inhibition of SLC1A5 significantly enhanced the inhibitory effect of 2DG on the growth of CRC cells in vitro and in vivo. Overexpression of SLC1A5 reduced the cytotoxicity of 2DG in combination with PX-12 treatment in CRC cells.</p><p><strong>Conclusion: </strong>Our results demonstrate a novel adaptive mechanism of glycolytic inhibition in which Trx-1 increases GSH levels by regulating SLC1A5 to rescue cytotoxicity induced by 2DG in CRC cells. Inhibition of glycolysis in combination with inhibition of Trx-1 or SLC1A5 may be a promising strategy for the treatment of CRC.</p>","PeriodicalId":49223,"journal":{"name":"Cellular Oncology","volume":" ","pages":"607-621"},"PeriodicalIF":6.6,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49693327","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}

{"title":"SUMOylation inhibitors activate anti-tumor immunity by reshaping the immune microenvironment in a preclinical model of hepatocellular carcinoma.","authors":"Zengbin Wang, Banglun Pan, Lili Su, Huahui Yu, Xiaoxuan Wu, Yuxin Yao, Xiaoxia Zhang, Jiacheng Qiu, Nanhong Tang","doi":"10.1007/s13402-023-00880-z","DOIUrl":"10.1007/s13402-023-00880-z","url":null,"abstract":"<p><strong>Purpose: </strong>High levels of heterogeneity and immunosuppression characterize the HCC immune microenvironment (TME). Unfortunately, the majority of hepatocellular carcinoma (HCC) patients do not benefit from immune checkpoint inhibitors (ICIs) therapy. New small molecule therapies for the treatment of HCC are the goal of our research.</p><p><strong>Methods: </strong>SUMOylation inhibitors (TAK-981 and ML-792) were evaluated for the treatment of preclinical mouse HCC models (including subcutaneous and orthotopic HCC models). We profile immune cell subsets from tumor samples after SUMOylation inhibitors treatment using single-cell RNA sequencing (scRNA-seq), mass cytometry (CyTOF), flow cytometry, and multiple immunofluorescences (mIF).</p><p><strong>Results: </strong>We discover that SUMOylation is higher in HCC patient samples compared to normal liver tissue. TAK-981 and ML-792 decrease SUMOylation at nanomolar levels in HCC cells and also successfully reduced the tumor burden. Analysis combining scRNA-seq and CyTOF demonstrate that treatment with SUMOylation inhibitors reduces the exhausted CD8⁺T (T_ex) cells while enhancing the cytotoxic NK cells, M1 macrophages and cytotoxic T lymphocytes (CTL) in preclinical mouse HCC model. Furthermore, SUMOylation inhibitors have the potential to activate innate immune signals from CD8⁺T, NK and macrophages while promoting TNFα and IL-17 secretion. Most notably, SUMOylation inhibitors can directly alter the TME by adjusting the abundance of intestinal microbiota, thereby restoring anti-tumor immunity in HCC models.</p><p><strong>Conclusions: </strong>This preclinical study suggests that SUMO signaling inhibitors may be beneficial for the treatment of HCC.</p>","PeriodicalId":49223,"journal":{"name":"Cellular Oncology","volume":" ","pages":"513-532"},"PeriodicalIF":6.6,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138488873","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}

{"title":"Host-derived growth factors drive ERK phosphorylation and MCL1 expression to promote osteosarcoma cell survival during metastatic lung colonization.","authors":"Camille A McAloney, Rawan Makkawi, Yogesh Budhathoki, Matthew V Cannon, Emily M Franz, Amy C Gross, Maren Cam, Tatyana A Vetter, Rebekka Duhen, Alexander E Davies, Ryan D Roberts","doi":"10.1007/s13402-023-00867-w","DOIUrl":"10.1007/s13402-023-00867-w","url":null,"abstract":"<p><strong>Purpose: </strong>For patients with osteosarcoma, disease-related mortality most often results from lung metastasis-a phenomenon shared with many solid tumors. While established metastatic lesions behave aggressively, very few of the tumor cells that reach the lung will survive. By identifying mechanisms that facilitate survival of disseminated tumor cells, we can develop therapeutic strategies that prevent and treat metastasis.</p><p><strong>Methods: </strong>We analyzed single cell RNA-sequencing (scRNAseq) data from murine metastasis-bearing lungs to interrogate changes in both host and tumor cells during colonization. We used these data to elucidate pathways that become activated in cells that survive dissemination and identify candidate host-derived signals that drive activation. We validated these findings through live cell reporter systems, immunocytochemistry, and fluorescent immunohistochemistry. We then validated the functional relevance of key candidates using pharmacologic inhibition in models of metastatic osteosarcoma.</p><p><strong>Results: </strong>Expression patterns suggest that the MAPK pathway is significantly elevated in early and established metastases. MAPK activity correlates with expression of anti-apoptotic genes, especially MCL1. Niche cells produce growth factors that increase ERK phosphorylation and MCL1 expression in tumor cells. Both early and established metastases are vulnerable to MCL1 inhibition, but not MEK inhibition in vivo. Combining MCL1 inhibition with chemotherapy both prevented colonization and eliminated established metastases in murine models of osteosarcoma.</p><p><strong>Conclusion: </strong>Niche-derived growth factors drive MAPK activity and MCL1 expression in osteosarcoma, promoting metastatic colonization. Although later metastases produce less MCL1, they remain dependent on it. MCL1 is a promising target for clinical trials in both human and canine patients.</p>","PeriodicalId":49223,"journal":{"name":"Cellular Oncology","volume":" ","pages":"259-282"},"PeriodicalIF":6.6,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10899530/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10171853","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}

{"title":"tRNA-derived fragments: mechanism of gene regulation and clinical application in lung cancer.","authors":"Fan Wu, Qianqian Yang, Wei Pan, Wei Meng, Zhongliang Ma, Weiwei Wang","doi":"10.1007/s13402-023-00864-z","DOIUrl":"10.1007/s13402-023-00864-z","url":null,"abstract":"<p><p>Lung cancer, being the most widespread and lethal form of cancer globally, has a high incidence and mortality rate primarily attributed to challenges associated with early detection, extensive metastasis, and frequent recurrence. In the context of lung cancer development, noncoding RNA molecules have a crucial role in governing gene expression and protein synthesis. Specifically, tRNA-derived fragments (tRFs), a subset of noncoding RNAs, exert significant biological influences on cancer progression, encompassing transcription and translation processes as well as epigenetic regulation. This article primarily examines the mechanisms by which tRFs modulate gene expression and contribute to tumorigenesis in lung cancer. Furthermore, we provide a comprehensive overview of the current bioinformatics analysis of tRFs in lung cancer, with the objective of offering a systematic and efficient approach for studying the expression profiling, functional enrichment, and molecular mechanisms of tRFs in this disease. Finally, we discuss the clinical significance and potential avenues for future research on tRFs in lung cancer. This paper presents a comprehensive systematic review of the existing research findings on tRFs in lung cancer, aiming to offer improved biomarkers and drug targets for clinical management of lung cancer.</p>","PeriodicalId":49223,"journal":{"name":"Cellular Oncology","volume":" ","pages":"37-54"},"PeriodicalIF":4.9,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10485407","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}