LINGJIE XU¹, YIQIN XIA¹, QIN QIN¹, GUIQUN WANG¹, KAI TAO², WEI WEI^1,*

Oncology Research, Vol.33, No.7, pp. 1649-1666, 2025, DOI:10.32604/or.2025.056176 - 26 June 2025

Abstract Background: The centrosome, a crucial cellular structure involved in the mitotic process of eukaryotic cells, plays a significant role in tumor progression by regulating the growth and differentiation of neoplastic cells. This makes the centrosome a promising target for therapeutic strategies in cancer treatment. Methods: Utilizing data from the TCGA database, we identified centrosome-related genes and constructed a prognostic model for 518 lung adenocarcinoma patients. Prognosis-associated genes were initially screened using univariate Cox regression, with overfitting minimized by applying LASSO regression to remove collinearity. Finally, a set of 12 genes was selected through multivariable Cox… More >

Yinghui Ye^1,#, Yulou Luo^2,#, Yutian Sun³, Yujie Zhang¹, Jiaxin Lin⁴, Ziling Yang⁵, Anping Xu^6,*, Bei Xue^1,*

Oncology Research, Vol.33, No.6, pp. 1383-1404, 2025, DOI:10.32604/or.2025.062584 - 29 May 2025

Abstract Objectives: The tumorigenic progression of Lung adenocarcinoma (LUAD), the predominant NSCLC subtype, is predominantly driven by co-occurring mutations in KRAS proto-oncogene (KRAS)/Tumor protein p53 (TP53). However, their impact on tumor microenvironment (TME) heterogeneity, particularly neutrophil dynamics, remains poorly understood. This present study aims to elucidate how KRAS/TP53 mutations reprogram the TME and develop a neutrophil-centric prognostic signature for LUAD. Methods: Leveraging single-cell RNA sequencing data and transcriptome data, neutrophil subpopulations were identified using Seurat and CellChat R packages, with trajectory analysis via Monocle2 R package. High-dimensional weighted gene co-expression network analysis (hdWGCNA), univariate Cox regression,… More >

Oncology Research Editorial Office

Oncology Research, Vol.33, No.5, pp. 1251-1252, 2025, DOI:10.32604/or.2025.065346 - 18 April 2025

Abstract This article has no abstract. More >

GUANGXIAN YOU¹, QIAO YANG², XIN LI², LILI CHEN^2,*

Oncology Research, Vol.33, No.4, pp. 905-917, 2025, DOI:10.32604/or.2024.052089 - 19 March 2025

Abstract Background: Lung cancer remains a major factor causing cancer-associated mortality globally. While there have been advancements in treatment options, advanced lung cancer patients still have poor outcomes. This study aims to investigate the potential role of Transmembrane protein 33 (TMEM33) in the development of lung adenocarcinoma. Methods: We leveraged The Cancer Genome Atlas (TCGA) database to analyze the connection between TMEM33 expression to the prognosis of lung adenocarcinoma (LUAD). Cell proliferation, invasiveness, and sphere formation were analyzed by various experiments. The association of miR-214-3p with TMEM33 was explored using luciferase reporter assay, immunoblotting, and real-time… More >

DAIEN ZHOU^1,#, HAOYANG YUAN^2,#, YIWEI HU³, CHUXU WANG¹, SA GE¹, KOUFENG SHAO⁴, HONGYING WANG¹, XIAOFENG TIAN^1,*, HAIBO HU^1,*

Oncology Research, Vol.33, No.3, pp. 653-663, 2025, DOI:10.32604/or.2024.050182 - 28 February 2025

Abstract Background: Despite the identification of numerous therapeutic targets in lung cancer, achieving significant efficacy has been challenging. TNFRSF21 plays an important role in various cancers. We investigated the function of TNFRSF21 in lung adenocarcinoma (LUAD). Methods: The prognostic value of TNFRSF21 expression in lung cancer was evaluated by the GEPIA and Kaplan-Meier Plotter databases. Lung cancer cell viability was assessed by the CCK8 assay. TNFRSF21 expression patterns in lung cancer tissues and cells were examined using RT-PCR assay. Tumor sphere growth was evaluated through tumor sphere formation assays. MtROS contents in lung cancer cells were… More >

LIANGJIANG XIA¹, GUANGBIN LI², QINGWU ZHOU³, YU FENG^2,*, HAITAO MA^2,*

Oncology Research, Vol.33, No.2, pp. 465-475, 2025, DOI:10.32604/or.2024.050835 - 16 January 2025

Abstract Background: Circular RNAs play an important role in regulating lung adenocarcinoma (LUAD). Bioinformatics analysis identified circ_0015278 as differentially expressed in LUAD. However, the biological mechanism of circ_0015278 in LUAD has not been fully clarified, especially in ferroptosis. Materials and Methods: Bioinformatics analysis was employed to explore the downstream mechanisms of Circ_0015278, subsequently confirmed by luciferase reporter assays. The impact of Circ_0015278 on cell proliferation, migration, invasion, and ferroptosis was investigated through a loss-of-function experiment. A xenotransplantation mouse model elucidated the effect of Circ_0015278 on tumour growth. Results: Circ_0015278 exhibited downregulation in LUAD. It inhibited cell proliferation, More >

LEI WANG¹, XIANJIN XIE^2,*

Oncology Research, Vol.33, No.1, pp. 123-132, 2025, DOI:10.32604/or.2024.048562 - 20 December 2024

Abstract Background: To investigate SCL/TAL 1 interrupting locus (STIL)’s role and prognostic significance in lung adenocarcinoma (LUAD) progression, we examined STIL and E2 promoter binding factor 1 (E2F1) expression and their impacts on LUAD prognosis using Gene Expression Profiling Interactive Analysis (GEPIA). Methods: Functional assays including CCK-8, wound-healing, 5-ethynyl-2-deoxyuridine (EdU), Transwell assays, and flow cytometry, elucidated STIL and E2F1’s effects on cell viability, proliferation, apoptosis, and migration. Gene set enrichment analysis (GSEA) identified potential pathways, while metabolic assays assessed glucose metabolism. Results: Our findings reveal that STIL and E2F1 are overexpressed in LUAD, correlating with adverse outcomes. It enhances More >

GENGYUN SUN^1,*, YIPING ZHENG^1,2, JIANFENG CAI², JIE GAO², LIE DONG², XIANGBIN ZHANG², YINGHUI HUANG^2,*

Oncology Research, Vol.33, No.1, pp. 171-184, 2025, DOI:10.32604/or.2024.047626 - 20 December 2024

Abstract Background: Long noncoding RNA, LINC01106 exhibits high expression in lung adenocarcinoma (LUAD) tumor tissues, but its functional role and regulatory mechanism in LUAD cells remain unclear. Methods: LINC01106 expression was analyzed in LUAD tissues and its functional impact on LUAD cells was assessed. LUAD cells were silenced with sh-LINC01106 and injected into nude mice to investigate tumor growth. The downstream transcription factors and molecular mechanism were determined using the Human transcription factor database (TFDB) database and Gene Expression Profiling Interactive Analysis (GEPIA) database. Additionally, the impact of linc01106 on autophagy was analyzed by determining the… More > Graphic Abstract

Oncology Research Editorial Office

Oncology Research, Vol.32, No.9, pp. 1529-1529, 2024, DOI:10.32604/or.2024.056121 - 23 August 2024

Abstract This article has no abstract. More >

PEILING WU^#, LIFANG ZHAO^#, HONGYAN ZHANG, YUEYAN LOU, DONGFANG CHEN, SHAN XUE, XUEQING LIU^*, HANDONG JIANG^*

Oncology Research, Vol.32, No.9, pp. 1439-1452, 2024, DOI:10.32604/or.2024.047490 - 23 August 2024

Abstract Objectives: The pro-oncogenic effects of NCAPD2 have been extensively studied across various tumor types; however, its precise role within the context of lung adenocarcinoma (LUAD) remains elusive. This study aims to elucidate the biological functions of NCAPD2 in LUAD and unravel the underlying mechanistic pathways. Methods: Utilizing bioinformatics methodologies, we explored the differential expression of NCAPD2 between normal and tumor samples, along with its correlations with clinical-pathological characteristics, survival prognosis, and immune infiltration. Results: In the TCGA-LUAD dataset, tumor samples demonstrated significantly elevated levels of NCAPD2 expression compared to normal samples (p < 0.001). Clinically, higher… More >