Neoplasma最新文献

{"title":"M2-TAM-derived XCL2 suppresses paclitaxel sensitivity in triple-negative breast cancer by transcriptionally activating NEK2.","authors":"Youyuan Deng, Ye He, Hongjun Zhao, Lifen Ye, Jingyong Li, Zhiya Hu, Huaixiao Zhang, Chao Zhang, Qishuo Rao, Yurong Cai, Yiping Xu, Jianguo Wang","doi":"10.4149/neo_2026_260507N143","DOIUrl":"https://doi.org/10.4149/neo_2026_260507N143","url":null,"abstract":"<p><p>Paclitaxel (PTX) resistance is a pivotal factor contributing to the poor prognostic outcome of patients with triple-negative breast cancer (TNBC). M2-type tumor-associated macrophages (M2-TAMs), a key component of the breast tumor microenvironment, foster chemoresistance through the release of multiple cytokines. The chemokine XC motif chemokine ligand 2 (XCL2) is significantly elevated in M2-polarized TAMs, but its role in PTX resistance remains unclear. Human THP-1 monocytes were first differentiated into M0 macrophages (PMA), followed by M2 polarization with IL-4 and IL-13, with polarization efficiency confirmed by flow cytometry. Cell viability and apoptosis were measured using the CCK-8 assay and flow cytometry, respectively. The binding relationship between transcription factor 4 (TCF4) and the never in mitosis gene A-related kinase 2 (NEK2) promoter was investigated by ChIP and dual-luciferase reporter assays. Our results showed that M2-TAM-secreted XCL2 reduced PTX-induced apoptosis and enhanced TNBC cell viability. Mechanistically, XCL2 was associated with XCR1 activation and subsequent β-catenin nuclear translocation, which may enable TCF4 to transcriptionally upregulate NEK2. As expected, TCF4 knockdown in TNBC cells reduced PTX resistance, while this effect was reversed by NEK2 overexpression. In addition, NEK2 knockdown in TNBC cells reversed the promoting effect of M2-CM on PTX resistance in TNBC. In vivo, M2-TAMs were associated with accelerated tumor growth under PTX treatment, whereas XCL2 knockdown restored PTX efficacy. To conclude, M2-TAM-derived XCL2 enhanced PTX resistance in TNBC cells by activating the β-catenin/TCF4/NEK2 pathway. Targeting this signaling may provide novel strategies to overcome PTX resistance in TNBC.</p>","PeriodicalId":19266,"journal":{"name":"Neoplasma","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149195652","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ctDNA retesting to guide anti-EGFR therapy in later-line metastatic colorectal cancer.","authors":"Silvia Mešinová, Marián Streško, Lukáš Šebest, Vanda Repiská, Ľuboš Danišovič, Regína Lohajová Behulová","doi":"10.4149/neo_2026_260622N206","DOIUrl":"https://doi.org/10.4149/neo_2026_260622N206","url":null,"abstract":"<p><p>Circulating tumor DNA (ctDNA) represents a promising tool for dynamic molecular profiling in metastatic colorectal cancer (mCRC), enabling monitoring of clonal tumor evolution and the detection of mechanisms of acquired resistance during treatment. The relevance of ctDNA has increased, particularly in the context of anti-EGFR therapy, where the emergence of RAS gene mutations constitutes a key resistance mechanism. The aim of this study was to evaluate the clinical utility of reassessing mutational status using ctDNA prior to rechallenge with anti-EGFR therapy in later treatment lines in patients with mCRC. A total of 17 patients with confirmed RAS and BRAF wild-type status in tumor tissue before initiation of first-line therapy were included in the analysis. All patients received anti-EGFR monoclonal antibody-based therapy in the first line and subsequently underwent ctDNA analysis from peripheral blood prior to initiation of third-line treatment using the Idylla™ qPCR platform. RAS gene mutations were detected in ctDNA in 4 patients, while 13 patients retained a wild-type status. Patients without detectable mutations achieved longer progression-free survival in the third-line setting compared with patients harboring RAS mutations. Overall survival from the start of third-line therapy was also prolonged in the wild-type ctDNA group. These findings suggest that the absence of resistant RAS clones in ctDNA may predict greater clinical benefit from anti-EGFR rechallenge. Liquid biopsy-based retesting may therefore represent an important tool for treatment individualization in later lines of mCRC therapy. This study also illustrates the translational potential of ctDNA analysis, linking dynamic molecular characterization of tumor evolution with clinically relevant treatment decision-making and the implementation of personalized oncology approaches.</p>","PeriodicalId":19266,"journal":{"name":"Neoplasma","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149195612","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tissue carcinoembryonic antigen as a superior independent prognostic factor for colorectal cancer over serum CEA: a retrospective cohort study.","authors":"Xin Lu, Guixiong Zhang, Yuanqiang Xiao, Lizhu Wang, Xinjian Huang, Yitai Xiao","doi":"10.4149/neo_2026_260503N138","DOIUrl":"https://doi.org/10.4149/neo_2026_260503N138","url":null,"abstract":"<p><p>We explored the relationships between tissue carcinoembryonic antigen (t-CEA) and serum CEA (s-CEA) and further pursued their association with long-term survival among postoperative colorectal cancer (CRC) patients. All patients underwent determination of s-CEA levels and t-CEA expression. Pearson correlation analysis was performed to quantify the interactions between two variables. Kaplan-Meier survival analysis and time-dependent receiver operating characteristic (ROC) analyses were performed. Prognostic factors were subjected to analysis using multivariable Cox regression to form prognostic nomograms. The results showed the positive rate of t-CEA overexpression recorded at 90.96%. No significant correlation was shown between the two variables. CRC patients with high t-CEA expression revealed a significantly poorer overall survival (OS) and progression-free survival (PFS). In unadjusted Kaplan-Meier survival analyses, elevated s-CEA levels were associated with significantly poorer PFS (p = 0.033) but not OS (p = 0.077). Crucially, multivariable Cox proportional hazards regression confirmed that high t-CEA expression, rather than s-CEA, served as a robust independent prognostic factor for both OS (HR = 2.887, p = 0.017) and PFS (HR = 2.500, p = 0.002). Nomograms comprising t-CEA were constructed with superior utility in predicting the survival probability of CRC patients. To conclude, our study demonstrates the superior prognostic value of t-CEA as an independent prognostic factor for CRC compared to s-CEA.</p>","PeriodicalId":19266,"journal":{"name":"Neoplasma","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149112721","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LAMTOR5-AS1 predicts poor prognosis and regulates glioma progression via miR-4653-5p/TCF7 axis.","authors":"Jiayi Li, Jing Li, Lin Yu","doi":"10.4149/neo_2026_260524N169","DOIUrl":"https://doi.org/10.4149/neo_2026_260524N169","url":null,"abstract":"<p><p>Gliomas, the most prevalent primary malignant brain tumors, are characterized by highly invasive growth patterns. Emerging evidence indicates that long non-coding RNAs are essential for regulating key oncogenic pathways. This study focuses on lncRNA LAMTOR5 antisense RNA AS1 (LAMTOR5-AS1, also known as SLC16A4-AS1), seeking to elucidate its regulatory functions in gliomas and assess its potential as a prognostic biomarker. LAMTOR5-AS1 expression in normal brain tissues and glioma samples was assessed using quantitative real-time polymerase chain reaction (qRT-PCR). The Cancer Genome Atlas (TCGA) glioma dataset was mined for COX regression and Kaplan-Meier survival analyses to check LAMTOR5-AS1 correlation with clinical outcomes. The competing endogenous RNA (ceRNA) function of LAMTOR5-AS1 targeting miR-4653-5p was determined using anti-AGO2 immunoprecipitation assays and dual-luciferase reporter assays. The oncogenic properties of LAMTOR5-AS1 in glioma were systematically detected through in vivo and in vitro phenotype experiments. The results revealed that glioma tissues had higher levels of LAMTOR5-AS1 expression, which had a positive correlation with glioma grade and indicated a poor outcome. LAMTOR5-AS1 knocking down inhibits the malignant progression of glioma cells. Mechanistically, it was demonstrated that the LAMTOR5-AS1 regulates TCF7 level via sponging miR-4653-5p, which was correlated with the malignant progression of glioma cells. To conclude, through the miR-4653-5p/TCF7 axis, LAMTOR5-AS1 serves as ceRNA and modulates the progression of glioma.</p>","PeriodicalId":19266,"journal":{"name":"Neoplasma","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149112733","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transcriptomic analysis of vitamin D3 (cholecalciferol)-mediated attenuation of cisplatin sensitivity in gastric cancer cells in vitro.","authors":"Ke Chen, Yu Pan","doi":"10.4149/neo_2026_260310N61","DOIUrl":"https://doi.org/10.4149/neo_2026_260310N61","url":null,"abstract":"<p><p>Cisplatin remains a cornerstone of chemotherapy for gastric cancer, but acquired resistance frequently limits its therapeutic efficacy. Vitamin D3/cholecalciferol (VD3) is widely used as a nutritional supplement; however, its influence on cisplatin responsiveness in gastric cancer cells remains unclear. In this study, gastric cancer cell lines were treated with cisplatin in the presence or absence of VD3, and cell viability, apoptosis, reactive oxygen species (ROS) accumulation, DNA damage-associated signaling, and transcriptomic changes were evaluated. VD3 significantly attenuated cisplatin-induced cytotoxicity in AGS, HGC-27, and MKN-45 cells. Co-treatment with VD3 reduced cisplatin-induced apoptosis, ROS accumulation, PARP cleavage, and γH2AX activation. Transcriptomic analysis showed that VD3 markedly reduced the number of cisplatin-responsive differentially expressed genes and altered gene programs associated with extracellular matrix organization, steroid metabolism, DNA damage response, and ABC transporter-related pathways. These findings suggest that VD3 exposure can attenuate cisplatin-induced cellular responses in gastric cancer cells and modulate transcriptional programs associated with cisplatin treatment. Given that the study was performed under in vitro conditions, further investigations are required to determine the underlying mechanisms and the potential clinical relevance of these observations.</p>","PeriodicalId":19266,"journal":{"name":"Neoplasma","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148963517","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Afatinib combined with oral metronomic vinorelbine as second-line treatment for advanced lung squamous cell carcinoma: a retrospective cohort study.","authors":"Chen Yin, Binfeng Li, Xi Lin, Aoli Zhang, Yi Peng, Jing Tang, Xiaobing Li","doi":"10.4149/neo_2026_260506N141","DOIUrl":"https://doi.org/10.4149/neo_2026_260506N141","url":null,"abstract":"<p><p>The aim of this study was to evaluate the efficacy and safety of afatinib combined with oral metronomic vinorelbine as a second-line treatment for patients with advanced lung squamous cell carcinoma (LSCC). A retrospective analysis was conducted on 38 patients with advanced LSCC who had failed first-line platinum-based doublet chemotherapy combined with immunotherapy between January 2022 and June 2024. All patients received afatinib (30 mg or 40 mg orally once daily) combined with oral metronomic vinorelbine (20 mg or 30 mg orally three times weekly on Monday, Wednesday, and Friday) until disease progression or unacceptable toxicity. The primary endpoints were objective response rate (ORR) and progression-free survival (PFS). Secondary endpoints included overall survival (OS), disease control rate (DCR), and treatment-related adverse events (TRAEs). Based on the data, the ORR was 26.3%, and the DCR was 68.4%. The median PFS was 5.0 months (95% CI: 4.7-5.4), and the median OS was 9.0 months (95% CI: 8.6-10.0). Grade ≥3 TRAEs occurred in 23.7% (9/38) of patients, including diarrhea (5.3%), rash (5.3%), neutropenia (5.3%), stomatitis (2.6%), and fatigue (2.6%). No grade 4-5 TRAEs or treatment-related deaths occurred. To conclude, the combination of afatinib and oral metronomic vinorelbine demonstrates promising antitumor activity and a manageable safety profile as a second-line treatment for advanced LSCC. This combo could represent an option as second-line after failure of chemo+IO.</p>","PeriodicalId":19266,"journal":{"name":"Neoplasma","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148796070","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RNA-binding protein hnRNPD promotes the proliferation of Wilms' tumor cells through activating the p38 MAPK signaling pathway.","authors":"Chunlei Yang, Man Liao, Haibin Bao, Haolun Xu, Jun Wang, Man Zhang, Can Li, Tian Zheng, Gang Li","doi":"10.4149/neo_2026_251230N536","DOIUrl":"https://doi.org/10.4149/neo_2026_251230N536","url":null,"abstract":"<p><p>Wilms' tumor (WT) represents a kidney carcinoma predominantly affecting children aged five years and younger. Heterogeneous nuclear ribonucleoprotein D (hnRNPD), an RNA-binding protein, has been implicated in oncogenic processes across various tumor types, whereas its expression pattern and biological function in WT remain largely unknown. hnRNPD expression within WT tissues was evaluated using publicly available databases, and co-expressed genes were identified through bioinformatic analysis. In vitro, hnRNPD expression in WT cell lines 17.94 and HFWT was modulated via gene silencing or overexpression. We subsequently carried out functional assays to assess cell proliferation and apoptosis. Molecular experiments were conducted to determine p38 mitogen-activated protein kinase (p38 MAPK) pathway activation status within cells with altered hnRNPD expression. Furthermore, SB203580 was utilized to pharmacologically inhibit this pathway to investigate the mechanism of hnRNPD in regulating WT cell proliferation. Data showed that hnRNPD was upregulated in WT tissues and cells. Silencing hnRNPD significantly inhibited WT cell proliferation and promoted apoptosis. Conversely, overexpression of hnRNPD produced the opposing effects. MAPK14, the gene encoding the p38α isoform of p38 MAPK, was identified as a core gene within the hnRNPD co-expression network. Furthermore, the phosphorylation level of p38 MAPK in WT cells was markedly elevated compared to that in normal cells. However, inhibition of the p38 MAPK pathway using SB203580 suppressed WT cell proliferation. Notably, SB203580 effectively counteracted the pro-proliferative effect of hnRNPD overexpression on malignant WT cell growth. In conclusion, hnRNPD is highly expressed in WT and plays a significant role in promoting the malignant proliferation of WT cells. The underlying molecular mechanism involves the regulation of p38 MAPK signaling pathway activation.</p>","PeriodicalId":19266,"journal":{"name":"Neoplasma","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148707376","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CRISPR/Cas9-edited organoids as a platform for tailored research of colorectal cancer.","authors":"Nikoleta Mojzesova, Petra Hladikova, Zuzana Kozovska, Martina Poturnajova, Silvia Tyciakova, Miroslava Matuskova","doi":"10.4149/neo_2026_260529N175","DOIUrl":"https://doi.org/10.4149/neo_2026_260529N175","url":null,"abstract":"<p><p>Colorectal cancer is one of the most commonly diagnosed cancers worldwide. Mortality rates and limited therapeutic options justify the development of reliable preclinical research models, as their translational value remains limited. Simple in vitro models do not recapitulate tumor heterogeneity, while in vivo research faces ethical concerns and interspecies differences. Patient-derived organoids offer a physiologically more relevant platform that retains the genetic, epigenetic, and phenotypic characteristics of the original tumor. Tumor-derived organoids enable precise investigation of novel treatments, functional genomics, and modeling of cancer development. Integration with CRISPR/Cas9 gene editing further enables accurate manipulation of specific genes to study carcinogenesis and therapeutic resistance. This review highlights recent advances in the use of organoids for colorectal cancer research and explores the potential of gene-edited organoids to discover the genetic and molecular mechanisms underlying colorectal cancer development, progression, and treatment resistance.</p>","PeriodicalId":19266,"journal":{"name":"Neoplasma","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148670193","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuroimmune treatment of advanced solid tumors: 3-year survival after angiotensin 1-7, pineal indoles, and cannabinoids.","authors":"Paolo Lissoni, Alejandra Monzon, Savino Marroccoli, Giuseppe Di Fede, Andrea Sassola, Giusy Messina, Ana Cristina Simoes-E-Silva, Irina V Kuznetsova, Denis I Burchakov, Maria Yu Kirillova, Daniel Pedro Cardinali","doi":"10.4149/neo_2026_260610N190","DOIUrl":"https://doi.org/10.4149/neo_2026_260610N190","url":null,"abstract":"<p><p>In a recent study, the exogenous administration of angiotensin 1-7 (Ang 1,7) together with melatonin, 5-methoxytryptamine, and cannabidiol increased 1-year survival in advanced cancer patients, underlining the utility of neuromodulation in oncology. We now report a single-arm interventional study to evaluate the effectiveness of introducing Ang 1-7 in the neuroimmune regime, including pineal indoles and cannabinoids. Two cohorts of patients with advanced solid tumors refractory to standard oncologic treatments and with an estimated life expectancy of less than six months were studied. The full neuroimmune regimen cohort consisted of 100 consecutive patients treated over the last three years with Ang 1-7, pineal indoles, and cannabinoids, while the comparator cohort included 212 consecutive patients treated between 2015 and 2019 with pineal indoles and cannabinoids alone. Gastroprotected capsules of Ang 1-7 coupled with cyclodextrin were administered at 0.5 mg p.o. twice/day. Melatonin (100 mg) and 5-methoxytryptamine (20 mg) were given p.o. at bedtime and in the early afternoon, respectively. Cannabidiol or cannabigerol (in the case of glioblastoma) was given at 20 mg p.o. twice/day. Clinical response, disease control, and overall survival, along with the lymphocyte-to-monocyte ratio, were evaluated. In the full regimen cohort, disease control was achieved in 67 of 100 patients, with objective tumor regression observed in 23%. In the comparator cohort, disease control was obtained in 111 of 212 patients, with objective regression in 8%. Three-year overall survival was significantly higher in the full regimen cohort (37%) compared with the comparator cohort (19%). Both treatments were associated with a significant increase in the lymphocyte-to-monocyte ratio, suggesting an improvement in systemic immune status. The addition of Ang 1-7 to a neuroimmune regimen combining pineal indoles and cannabinoids was associated with improved disease control and long-term survival in patients with end-stage solid tumors lacking effective therapeutic options.</p>","PeriodicalId":19266,"journal":{"name":"Neoplasma","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148670196","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"YTHDF2-regulated hsa_circ_0005882 functions as a sponge for miR-654-3p to suppress nasopharyngeal carcinoma proliferation.","authors":"Xu Wang, Aiyu Ma, Lu Lu, Qiuyu Zhao, Yuzhong Yang, Xuan Meng, Yiping Sun, Shuming Wang, Zhiyi Chen, Yan Zhang, Jinhua Zheng, Xiang Zheng","doi":"10.4149/neo_2026_260223N45","DOIUrl":"10.4149/neo_2026_260223N45","url":null,"abstract":"<p><p>Circular RNAs (circRNAs) are a subclass of non-coding RNAs, playing an important regulatory role in tumor progression. Accumulating evidence has revealed that circRNAs can be regulated by m6A machinery, influencing their expression and biological functions. However, the functions and mechanisms of m6A-mediated circRNAs in nasopharyngeal carcinoma (NPC) remain to be elucidated. In this study, the sequence of hsa_circ_0005882 (circ_0005882) was determined by Sanger sequencing, and its localization in both the cytoplasm and nucleus was confirmed by fluorescence in situ hybridization. Furthermore, m6A RNA immunoprecipitation followed by qPCR (MeRIP-qPCR) and the single-base elongation- and ligation-based qPCR amplification (SELECT) assays revealed that circ_0005882 may harbor m6A modifications. Overexpression of circ_0005882 significantly suppressed NPC cell proliferation. Mechanistically, the m6A reader YTHDF2 binds to circ_0005882 to promote its degradation, thereby reducing circ_0005882 stability. Additionally, circ_0005882 functions as a sponge for miR-654-3p, contributing to the inhibition of NPC proliferation. These findings collectively demonstrate that circ_0005882, which is negatively regulated by YTHDF2, functions as a tumor suppressor by sponging miR-654-3p to inhibit NPC cell proliferation, unveiling a novel regulatory model centered on the YTHDF2/circ_0005882/miR-654-3p axis in NPC pathogenesis.</p>","PeriodicalId":19266,"journal":{"name":"Neoplasma","volume":" ","pages":"269-282"},"PeriodicalIF":2.5,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148422982","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}