Cancer Cell International最新文献

{"title":"BCR::ABL1 expression in chronic myeloid leukemia cells in low oxygen is regulated by glutamine via CD36-mediated fatty acid uptake.","authors":"Caterina Mancini, Giulio Menegazzi, Silvia Peppicelli, Giampaolo Versienti, Daniele Guasti, Giuseppe Pieraccini, Elisabetta Rovida, Matteo Lulli, Laura Papucci, Persio Dello Sbarba, Alessio Biagioni","doi":"10.1186/s12935-025-03805-y","DOIUrl":"https://doi.org/10.1186/s12935-025-03805-y","url":null,"abstract":"<p><strong>Background: </strong>Chronic myeloid leukemia (CML) is influenced by microenvironmental nutrients, glucose (Glc), and glutamine (Gln) which regulate cell proliferation, viability, and the expression of the driver oncoprotein (BCR::ABL1).</p><p><strong>Results: </strong>Our study revealed that Glc, while partially supporting alone cell growth in normoxia, is essential in low oxygen conditions, whereas Gln is ineffective. Under low oxygen, Gln reduced oxidative respiratory activity while enhancing glycolysis. In these conditions, fatty acid (FA) metabolism becomes crucial, as evidenced by increased lipid droplets (LD) accumulation when Glc was absent. Gln, in particular, drives CD36-mediated FA uptake, suppressing the BCR::ABL1 oncoprotein and facilitating cell survival. By co-culturing leukemia cells with adipocytes, one of the main bone marrow (BM) cell components, we observed an enhanced FA release, suggesting a link between FA, microenvironmental BM cells, and the maintenance of leukemic stem cells (LSC).</p><p><strong>Methods: </strong>K562 and KCL22 cell lines were subjected to Glc and/or Gln deprivation under hypoxic conditions (96 h at 0.1% O₂). Metabolic profiling was conducted through the Seahorse XFe96 analyzer, and the contribution of L-Glutamine-¹³C₅ to FA de novo synthesis was determined via GC/MS. Intracellular neutral LD were measured using BODIPY 493/503 in confocal microscopy and flow cytometry, with their presence and morphology further examined via transmission electron microscopy. BCR::ABL1 as well as several FA-related markers were evaluated via Western Blotting, whilst CD36 was determined through flow cytometry. LC2 assay was used for measuring leukemia stem cell potential by inhibiting FA uptake via the usage of the Sulfo-N-Succinimidyl Oleate, a CD36 inhibitor. qPCR was exploited to detect markers of FA secretion in CML-adipocytes co-culture together with Nile Red staining to assess free FA in the media.</p><p><strong>Conclusions: </strong>These findings underscore the central role of FA in the regulation of the LSC compartment of CML, highlighting the importance of Gln in facilitating CML cell survival under restrictive metabolic conditions and preparing the cell population for expansion upon the release of these restrictions.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"176"},"PeriodicalIF":5.3,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12080266/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144076178","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":"Bone marrow microenvironment in myelodysplastic neoplasms: insights into pathogenesis, biomarkers, and therapeutic targets.","authors":"Forouzan Bahmani, Maryam Shayanmanesh, Mahdi Safari, Amirarsalan Alaei, Yasaman Pouriafar, Zahra Rasti, Farhad Zaker, Shahrbano Rostami, Fatemeh Damerchiloo, Majid Safa","doi":"10.1186/s12935-025-03793-z","DOIUrl":"https://doi.org/10.1186/s12935-025-03793-z","url":null,"abstract":"<p><p>Myelodysplastic neoplasms (MDS) represent a heterogeneous group of malignant hematopoietic stem and progenitor cell (HSPC) disorders characterized by cytopenia, ineffective hematopoiesis, as well as the potential to progress to acute myeloid leukemia (AML). The pathogenesis of MDS is influenced by intrinsic factors, such as genetic insults, and extrinsic factors, including altered bone marrow microenvironment (BMM) composition and architecture. BMM is reprogrammed in MDS, initially to prevent the development of the disease but eventually to provide a survival advantage to dysplastic cells. Recently, inflammation or age-related inflammation in the bone marrow has been identified as a key pathogenic mechanism for MDS. Inflammatory signals trigger stress hematopoiesis, causing HSPCs to emerge from quiescence and resulting in MDS development. A better understanding of the role of the BMM in the pathogenesis of MDS has opened up new avenues for improving diagnosis, prognosis, and treatment of the disease. This article provides a comprehensive review of the current knowledge regarding the significance of the BMM to MDS pathophysiology and highlights recent advances in developing innovative therapies.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"175"},"PeriodicalIF":5.3,"publicationDate":"2025-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12065391/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144062314","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":"The genomic landscape of esophageal squamous cell carcinoma cell lines.","authors":"Chao Zhang, Chenghao Li, Jian Zhong Su, Kuaile Zhao, Longlong Shao, Jiaying Deng","doi":"10.1186/s12935-025-03686-1","DOIUrl":"https://doi.org/10.1186/s12935-025-03686-1","url":null,"abstract":"<p><strong>Background: </strong>Research on the genomic characteristics of common esophageal squamous cell carcinoma (ESCC) cell lines, including exome mutations and mRNA expression, is limited. This study aims to elucidate the malignancy, invasion capability, classical cancer-related signaling pathways, and immune status of ESCC cell lines, providing a detailed genomic landscape and highlighting the unique features of each cell line.</p><p><strong>Methods: </strong>Whole exome and RNA sequencing were conducted on ESCC cell lines TE-1, ECA-109, KYSE-30, KYSE-150, KYSE-180, KYSE-450, and KYSE-510, with the normal epithelium cell line Het-1a as a comparison. Bioinformatics methods analyzed gene mutation types, mutation frequencies, RNA expression, and classical cancer-related signaling pathways. Specific analyses were also performed on tumor burden, genes related to differentiation, invasion, immunity, and gene enrichment in each cell line.</p><p><strong>Results: </strong>The highest tumor mutation burden (TMB) was 70.4 mutations per megabase (mut/MB) in KYSE-150, while the lowest was 48.7 mut/MB in KYSE-510. Mutations in the Hippo, Notch, PI3K, RTK-Ras, and Wnt signaling pathways were present in all cancer cell lines. Mutations were significantly enriched in signature 3, associated with defective homologous recombination deficiency (HRD). The NRF2 signaling pathway exhibited mutations in KYSE-180, KYSE-450, and TE-1 cell lines. The cell cycle gene mutation frequency was low, occurring only in KYSE-30 and TE-1 cell lines. The expression profiles of KYSE-510 and ECA-109 were similar. The KYSE-150 cell line showed up-regulated invasion genes, while the KYSE-450 cell line had significantly down-regulated poor differentiation-related genes. Immune-related genes were up-regulated in the ECA-109 cell line.</p><p><strong>Conclusion: </strong>The molecular profiles generated in this study provide detailed information on gene mutations and expression in common ESCC cell lines. The KYSE-150 cell line exhibited a prominent invasion capability, while the ECA-109 cell line showed up-regulated immune properties. This genomic landscape offers valuable insights for future research and therapeutic strategies in ESCC.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"174"},"PeriodicalIF":5.3,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12065367/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143982043","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":"Moxibustion regulates KDM4D expression and modulates lipid metabolism to inhibit tumor proliferation in CAC mice.","authors":"Guona Li, Jindan Ma, Luyi Wu, Hanxiao Zhang, Yaying Lin, Hongxiao Xu, Muen Gu, Kunshan Li, Hongsheng Dong, Yan Huang, Huangan Wu","doi":"10.1186/s12935-025-03798-8","DOIUrl":"https://doi.org/10.1186/s12935-025-03798-8","url":null,"abstract":"<p><strong>Background: </strong>Lysine demethylase 4D (KDM4D) and aberrant lipid metabolism are implicated in the development and progression of colitis-associated cancer (CAC). Moxibustion, a therapeutic approach in traditional Chinese medicine, can inhibit intestinal inflammation and improve the intestinal mucosa.</p><p><strong>Methods: </strong>Mice were intraperitoneally injected with AOM, and three cycles of 3-2-2% DSS-free drinking water were administered to establish a CAC mouse model. Moxibustion and KDM4D inhibitor 5-c-8HQ intervention were performed for 30 days after modeling was completed. IHC staining was used to observe the expression of the nuclear-associated antigen Ki67 (Ki67), proliferating cell nuclear antigen (PCNA), and IL-33 in the colon. The expression of colon KDM4D and β-Catenin was observed by immunofluorescence staining and RT‒qPCR. LC‒MS pseudotargeted metabolomic sequencing was used to semiquantitatively detect the expression levels of lipids.</p><p><strong>Results: </strong>Moxibustion inhibited the proliferation of colon tumors in CAC mice, improved histopathology, and reduced the expression of PCNA and Ki67 in the colon. Using kdm4d knockout technology, it was initially confirmed that kdm4d is a key gene affecting CAC tumor proliferation. The inhibition of colon tumor proliferation in CAC mice by moxibustion is associated with the suppression of abnormal activation of the colon KDM4D/β-Catenin signaling pathway. LC-MS-targeted metabolomics revealed abnormal lipid metabolism in the colons of CAC mice. Moxibustion may affect the cholinergic metabolism pathway in the colon of CAC mice and regulate lipids such as sphingomyelin SM (d18:1/26:0) and triacylglycerol TAG58:7 (18:0). After kdm4d knockout, lipid disorders in the colons of CAC mice were partially restored. The kdm4d gene may be involved in the mechanism underlying the effect of moxibustion on lipid metabolism in the CAC colon.</p><p><strong>Conclusions: </strong>Moxibustion inhibited the proliferation of colon tumors in CAC mice, inhibited the activation of the tumor-promoting signaling pathway KDM4D/β-Catenin, and improved lipid metabolism disorders in the colon, thus providing a promising strategy for the clinical adjuvant treatment of colorectal cancer.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"173"},"PeriodicalIF":5.3,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12054041/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143980997","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":"Genomic signatures in plasma circulating tumor DNA reveal treatment response and prognostic insights in mantel cell lymphoma.","authors":"Zhou Ouyang, Ruolan Zeng, Song Wang, Xiaoying Wu, Yajun Li, Yizi He, Caiqin Wang, Chen Xia, Qiuxiang Ou, Hua Bao, Wei Yang, Ling Xiao, Hui Zhou","doi":"10.1186/s12935-025-03789-9","DOIUrl":"https://doi.org/10.1186/s12935-025-03789-9","url":null,"abstract":"<p><strong>Background: </strong>Mantle cell lymphoma (MCL) is an aggressive subtype of B-cell non-Hodgkin's lymphoma. The applicability of circulating tumor DNA (ctDNA) for predicting treatment response and prognosis in MCL remains underexplored.</p><p><strong>Methods: </strong>This study included 34 MCL patients receiving first-line chemoimmunotherapy. We assessed the ability of plasma ctDNA to detect tumor-specific genetic alterations and explored its potential as a noninvasive biomarker for treatment response and prognosis in MCL.</p><p><strong>Results: </strong>Commonly mutated genes in MCL included CCND1 (93.5%), ATM (48.4%), KMT2D (25.8%), and TP53 (25.8%). Subgroup analysis of tissue samples showed that CDKN2A mutations (P = 0.028), along with alterations in BCR and TCR signaling (P = 0.004) and the PI3K pathway (P = 0.008), were enriched in the blastoid subtype. ATM mutations (P = 0.041) were more prevalent in MIPI-low patients, while epigenetic chromatin remodeling pathway alterations (P = 0.028) were more common in MIPI-high patients. Plasma ctDNA demonstrated high sensitivity for detecting structural variants (96.6%), followed by mutations (71.3%) and copy number variants (30.0%). 75% of patients exhibited moderate-to-high concordance in detecting genomic variants between plasma and tissue samples. Pretreatment ctDNA levels exhibited high specificity in predicting clinical efficacy but had a suboptimal sensitivity of 68.2%. Higher ctDNA levels were significantly associated with shorter progression-free survival (PFS; P = 0.002) and overall survival (OS; P = 0.009). Additional ctDNA-based genetic features associated with shorter PFS included TP53 (P = 0.002), TRAF2 (P = 0.023), and SMARCA4 (P = 0.023) mutations, while TP53 (P = 0.006) and TERT (P = 0.031) mutations predicted shorter OS. Persistent positive ctDNA in post-treatment plasma samples indicated molecular relapse and poor prognosis, whereas undetectable ctDNA defined a subset of patients with favorable survival outcomes.</p><p><strong>Conclusions: </strong>This study identified plasma ctDNA as a promising biomarker that noninvasively captures tumor-derived genetic variants associated with treatment response and survival outcomes in MCL, highlighting the clinical value of ctDNA for diagnosis, recurrence prediction, and surveillance monitoring.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"172"},"PeriodicalIF":5.3,"publicationDate":"2025-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12049778/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143983123","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":"Correction: The molecular subtyping and precision medicine in triple-negative breast cancer--- based on Fudan TNBC classification.","authors":"Lijuan Weng, Jianliang Zhou, Shenchao Guo, Nong Xu, Ruishuang Ma","doi":"10.1186/s12935-025-03799-7","DOIUrl":"https://doi.org/10.1186/s12935-025-03799-7","url":null,"abstract":"","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"171"},"PeriodicalIF":5.3,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12044971/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143980517","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":"The emerging functions and clinical implications of circRNAs in acute myeloid leukaemia.","authors":"Shuiqing Liu, Xingyu Wan, Yang Gou, Wuchen Yang, Wei Xu, Yuxuan Du, Xiangui Peng, Xiaoqi Wang, Xi Zhang","doi":"10.1186/s12935-025-03772-4","DOIUrl":"https://doi.org/10.1186/s12935-025-03772-4","url":null,"abstract":"<p><p>Acute myeloid leukaemia (AML) is a prevalent haematologic malignancy characterized by significant heterogeneity. Despite the application of aggressive therapeutic approaches, AML remains associated with poor prognosis. Circular RNAs (circRNAs) constitute a unique class of single-stranded RNAs featuring covalently closed loop structures that are ubiquitous across species. These molecules perform crucial regulatory functions in the pathogenesis of various diseases through diverse mechanisms, including acting as miRNA sponges, interacting with DNA or proteins, and encoding functional proteins/polypeptides. Recently, numerous circRNAs have been confirmed to have aberrant expression patterns in AML patients. In particular, certain circRNAs are closely associated with specific clinicopathological characteristics and thus have great potential as diagnostic/prognostic biomarkers and therapeutic targets in AML. Herein, we systematically summarize the biogenesis, degradation, and functional mechanisms of circRNAs while highlighting their clinical relevance. We also outline a series of online databases and analytical tools available to facilitate circRNA research. Finally, we discuss the current challenges and future research priorities in this evolving field.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"167"},"PeriodicalIF":5.3,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12038945/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143960279","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":"Clinicopathological characterization of Switch/Sucrose-non-fermentable (Swi/Snf) complex (ARID1A, SMARCA2, SMARCA4)-deficient endocervical adenocarcinoma.","authors":"Chao Cao, Zi-Yun Wu, Wei Liao, Li-Jun Wei, Hao-Yu Liang, Xia Yang, Rong-Zhen Luo, Li-Li Liu","doi":"10.1186/s12935-025-03794-y","DOIUrl":"https://doi.org/10.1186/s12935-025-03794-y","url":null,"abstract":"<p><strong>Background: </strong>Subunits of the Switch/Sucrose-non-fermentable (Swi/Snf) complex, such as ARID1A, SMARCA4, SMARCA2, etc., have been implicated in the development of gynecologic cancers. However, their prevalence and clinical implications in endocervical adenocarcinoma (ECA) remain unclear. This study aimed to evaluate the expression of Swi/Snf complex subunits in ECA and characterize the clinicopathological and immune microenvironment features of Swi/Snf-deficient ECA.</p><p><strong>Methods: </strong>We evaluated 604 ECA using representative tissue microarrays, collected clinicopathologic data, reviewed histological features, and performed immunohistochemical staining for several Swi/Snf complex subunits, mismatch repair (MMR), immune cell markers, and immune checkpoint ligands proteins.</p><p><strong>Results: </strong>Among the 604 cases examined, five Swi/Snf subunit expression patterns were identified, including intact expression, deficient expression, 'checkerboard' expression, reduced expression, and heterogeneous expression. Deficiencies of ARID1A (3.97%, 24/604), SMARCA2 (2.32%,14/604), and SMARCA4 (1.49%, 9/604) were observed. Defining Swi/Snf deficiency as loss of any subunit, the overall deficiency rate was 5.96% (36/604). Swi/Snf-deficient ECA tended to advanced FIGO stage (III-IV, P = 0.041), larger tumor size (P < 0.001), deeper stromal invasion (≥ 1/3, P = 0.046), and higher lymph node metastasis rate (P = 0.037). Morphologically, Swi/Snf-deficient ECA displayed frequent poor differentiation (P = 0.001), medullary features (P < 0.001), high nuclear grade (P < 0.001), necrosis (P = 0.001), stromal tumor-infiltrating lymphocytes (sTILs, P < 0.001), peritumoral lymphocyte aggregation (P = 0.001), and tertiary lymphoid structures (TLS, P < 0.001). Immune subset analysis revealed significantly elevated densities of CD3⁺ T cells, CD8⁺ T cells, CD38⁺ plasma cells, CD56⁺ NK cells, CD68⁺ macrophages, and PD-1⁺ T cells in Swi/Snf-deficient ECA (P < 0.05). Swi/Snf-deficient ECA demonstrated higher PD-L1 combined positive score (CPS) positivity (P < 0.001), and was more frequently associated with mismatch repair deficiency (MMRD, P < 0.001). Survival analysis indicated shorter overall survival (median: 53 vs. 64.5 months, P = 0.0307) and disease-free survival (median: 52 vs. 60.5 months, P = 0.0228) in Swi/Snf-deficient ECA patients.</p><p><strong>Conclusions: </strong>Swi/Snf complex deficiency is rare but significantly associated with NHPVA, aggressive pathological features, immunologically activated phenotypes, and MMRD. Swi/Snf status evaluation may inform novel therapeutic strategies for ECA patients.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"170"},"PeriodicalIF":5.3,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12042307/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143966463","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":"Progress of mesenchymal stem cell-derived exosomes in targeted delivery of antitumor drugs.","authors":"Defa Huang, Wenlong Huang, Meijin Liu, Jie Chen, Dewang Xiao, Zongbo Peng, Haoquan He, Haibin Shen, Qing Jin, Linli Chen, Dingyu Rao, Minghong Zhao, Junyun Huang","doi":"10.1186/s12935-025-03795-x","DOIUrl":"https://doi.org/10.1186/s12935-025-03795-x","url":null,"abstract":"<p><p>Mesenchymal stem cells (MSCs) are currently being used in clinical trials for the treatment of a wide range of diseases and have a wide range of applications in the fields of tissue engineering and regeneration. Exosomes are extracellular vesicles containing a variety of components such as proteins, nucleic acids and lipids, which are widely present in biological fluids and have the functions of participating in intercellular information transfer, immune response and tissue repair, and can also be used as carriers to target and deliver tumors to improve therapeutic effects. Mesenchymal stem cell-derived Exosomes (MSC-Exos), which have the advantages of low immunogenicity and high tumor homing ability, have attracted much attention in targeted drug delivery. Here, we review the current knowledge on the involvement of MSC-Exos in tumor progression and their potential as drug delivery systems in targeted therapies. It also discusses the advantages and prospects of MSC-Exos as a drug carrier and the challenges that still need to be overcome.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"169"},"PeriodicalIF":5.3,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12042352/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143961964","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":"Comprehensive pan-cancer analysis identified SLC16A3 as a potential prognostic and diagnostic biomarker.","authors":"Ping Yang, Jiayu Yin, Gongyin Zhang, Xiaofeng Li, Tongtong Chen, Wanying Zhao, Jinhai Tang, Li Lv, Xiupeng Lv","doi":"10.1186/s12935-025-03791-1","DOIUrl":"https://doi.org/10.1186/s12935-025-03791-1","url":null,"abstract":"<p><p>SLC16A3, belonging to the SLC16 gene family, is involved in the transportation of monocarboxylate. SLC16A family members play important roles in tumorigenesis, nonetheless, the specific involvement of SLC16A3 in tumor prognosis and diagnosis in human cancers remains unelucidated. This study dealt with the exploration of SLC16A3 expression in human pan-cancer and its significance regarding disease prognosis. For this investigation, the mRNA expression data of SLC16A3 were acquired from the TCGA and the GTEx datasets. The Kaplan-Meier plots, univariate Cox regression, and the ROC curve were employed for assessing the prognostic and diagnostic significance of SLC16A3 in pan-cancer. Furthermore, the cBioPortal database was used to analyze the SLC16A3 genomic alterations. Moreover, the association of the infiltration of immune cells and immune checkpoint genes with SLC16A3 was analyzed by the TIMER database. Gene Ontology and KEGG pathway analysis were employed to explore the function of SLC16A3 in pan-cancer. The resulting data demonstrated that SLC16A3 mRNA expression was overexpressed in most cancers and its protein expression was also high across diverse cancer types. Moreover, upregulated SLC16A3 expression was linked to poor OS and PFI of certain cancers. Cox regression analysis further indicated that SLC16A3 is a risk factor for patients with PAAD, CESC, LUSC, LUAD, CHOL, LGG, MESO, and OSCC. The ROC curve revealed that SLC16A3 exhibited a high accuracy (AUC > 0.9) in BRCA, CHOL, ESCA, GBM, and KIRC prediction. Moreover, the acquired data indicated that in pan-cancer, the SLC16A3 expression exhibited correlations with immune checkpoint genes and immune cells. These findings collectively suggest that SLC16A3 holds promise as a biomarker for diagnostic and prognostic purposes in pan-cancer.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"168"},"PeriodicalIF":5.3,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12039109/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143980816","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}