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  • Open Access

    ARTICLE

    circACTN4 promotes breast cancer cell cycle progression and oncogenesis via c-MYC induced histone H4 acetylation

    KEFAN LIU1, XIAOSONG WANG1, XIN YANG1, BOWEN SHI1, LEI XING2,*, JUNXIA CHEN1,*

    Oncology Research, Vol.33, No.7, pp. 1709-1722, 2025, DOI:10.32604/or.2025.061721 - 26 June 2025

    Abstract Background: Accumulating studies have shown the important role of circular RNAs (circRNAs) in the oncogenesis and metastasis of various cancers. We previously reported that circACTN4 could bind with FUBP1 to promote tumorigenesis and the development of breast cancer (BC) by increasing the expression of MYC. However, its exact molecular mechanism and biological function have not been fully elucidated. Methods: Here, Circular RNA microarray analysis was conducted in 3 pairs of BC and paracancerous tissues. The expression of circACTN4 in BC cells and tissues was detected via reverse transcription‒quantitative PCR (RT‒qPCR). Cell Counting Kit-8 (CCK-8), 5-ethynyl-2-deoxyuridine… More > Graphic Abstract

    circACTN4 promotes breast cancer cell cycle progression and oncogenesis via c-MYC induced histone H4 acetylation

  • Open Access

    REVIEW

    The Role of Linker Histone Mutation in Oncogenesis: Molecular Mechanism and Structural Impact

    Gege Liu#, Houfang Zhang#, Yunhui Peng*

    BIOCELL, Vol.49, No.4, pp. 519-538, 2025, DOI:10.32604/biocell.2025.061470 - 30 April 2025

    Abstract Nucleosomes play a vital role in chromatin organization and gene regulation, acting as key hubs that interact with various chromatin-associated factors through diverse binding mechanisms. Recent research has highlighted the prevalence of mutations in linker histones across different types of cancer, emphasizing their critical involvement in cancer progression. These cancer-associated mutations in linker histones have been shown to disrupt nucleosome stacking and the formation of higher-order chromatin structures, which in turn significantly affect epigenetic regulatory processes. In this review, we provide a comprehensive analysis of how cancer-associated linker histone mutations alter their physicochemical properties, influencing More >

  • Open Access

    CORRECTION

    Correction: Silencing of the long non-coding RNA LINC00265 triggers autophagy and apoptosis in lung cancer by reducing protein stability of SIN3A oncogene

    XIAOBI HUANG1, CHUNYUAN CHEN2, YONGYANG CHEN1, HONGLIAN ZHOU1, YONGHUA CHEN1, ZHONG HUANG1, YULIU XIE1, BAIYANG LIU1, YUDONG GUO1, ZHIXIONG YANG1, GUANGHUA CHEN3, WENMEI SU1,4

    Oncology Research, Vol.33, No.5, pp. 1249-1250, 2025, DOI:10.32604/or.2024.061822 - 18 April 2025

    Abstract This article has no abstract. More >

  • Open Access

    REVIEW

    Targeting MDM2-p53 interaction for breast cancer therapy

    AMJAD YOUSUF1, NAJEEB ULLAH KHAN2,*

    Oncology Research, Vol.33, No.4, pp. 851-861, 2025, DOI:10.32604/or.2025.058956 - 19 March 2025

    Abstract Breast cancer is a significant global concern, with limited effective treatment options. Therefore, therapies with high efficacy and low complications, unlike the existing chemotherapies, are urgently required. To address this issue, advances have been made in therapies targeting molecular pathways related to the murine double minute 2 proto-oncogene (MDM2)-tumor proteinp53 (TP53) interaction. This review aims to investigate the efficacy of MDM2 inhibition in restoring TP53 activity in breast cancer cells, as evidenced by clinical studies, reviews, and trials. TP53 is a tumor suppressor and MDM2 facilitates proteasomal degradation of TP53. MDM2 and TP53 activity More > Graphic Abstract

    Targeting MDM2-p53 interaction for breast cancer therapy

  • Open Access

    ARTICLE

    TMEM33, an oncogene regulated by miR-214-3p, promotes the progression of lung adenocarcinoma through the Wnt/β-catenin signaling pathway

    GUANGXIAN YOU1, QIAO YANG2, XIN LI2, LILI CHEN2,*

    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 >

  • Open Access

    RETRACTION

    Retraction: miR-144-3p targets FosB proto-oncogene, AP-1 transcription factor subunit (FOSB) to suppress proliferation, migration, and invasion of PANC-1 pancreatic cancer cells

    Oncology Research Editorial Office

    Oncology Research, Vol.33, No.3, pp. 735-735, 2025, DOI:10.32604/or.2024.056907 - 28 February 2025

    Abstract This article has no abstract. More >

  • Open Access

    REVIEW

    Oncogenic and tumor-suppressive roles of Lipocalin 2 (LCN2) in tumor progression

    BAOXING HUANG1,#, ZICHANG JIA1,#, CHENCHEN FU2, MOXIAN CHEN2, ZEZHUO SU3,*, YUNSHENG CHEN1,*

    Oncology Research, Vol.33, No.3, pp. 567-575, 2025, DOI:10.32604/or.2024.051672 - 28 February 2025

    Abstract Lipocalin-2 (LCN2) is a member of the lipocalin superfamily with multiple functions and can participate in the transport of a variety of small lipophilic ligands in vivo. LCN2 is significantly expressed in various tumors and plays an important role in regulating tumor cell proliferation, invasion, and metastasis. The specific actions of LCN2 in tumors may vary depending on the particular type of cancer involved. In this review, we provide an extensive overview of the transcriptional and post-transcriptional regulation of LCN2 in health and disease. Furthermore, we summarize the impact of LCN2 dysregulation in a broad range More >

  • Open Access

    ARTICLE

    DNAJA4, DNAJB11 and DNAJC10 induce cell transformation by inhibiting p53 and oncogene-induced senescence

    HYEON JU LEE1, CHANG SEOP LEE1, SI HOON KIM1, SOOKYUNG KIM1, JEONG MI KIM1, SUN-WHA IM1, YU-JIN JUNG2, SEUNG-PYO HONG3, HYUNJUNG LEE3, JONG-IL KIM3,4,5, JEONG A. HAN1,*

    BIOCELL, Vol.48, No.10, pp. 1455-1464, 2024, DOI:10.32604/biocell.2024.054538 - 02 October 2024

    Abstract Objective: Transformation from normal cells to malignant cells is the basis for tumorigenesis. While this cell transformation is known to result from aberrant activation or inactivation of associated genes, these genes have not yet been fully identified. In addition, DNAJs, proteins with a J domain, are known to be molecular co-chaperones, but their cellular functions remain largely unexplored. In this context, we here identified DNAJA4, DNAJB11, and DNAJC10 as pro-transforming genes and elucidated their action mechanisms. Methods: Senescence-associated (SA)-β-galactosidase staining and western blotting were used to analyze cellular senescence and protein expression. Soft agar assay was used… More >

  • Open Access

    REVIEW

    The role of tazarotene-induced gene 1 in carcinogenesis: is it a tumor suppressor gene or an oncogene?

    CHUN-HUA WANG1,2, LU-KAI WANG3, RONG-YAUN SHYU4, FU-MING TSAI5,*

    BIOCELL, Vol.48, No.9, pp. 1285-1297, 2024, DOI:10.32604/biocell.2024.053746 - 04 September 2024

    Abstract Tazarotene-induced gene 1 (TIG1) is induced by a derivative of vitamin A and is known to regulate many important biological processes and control the development of cancer. TIG1 is widely expressed in various tissues; yet in many cancer tissues, it is not expressed because of the methylation of its promoter. Additionally, the expression of TIG1 in cancer cells inhibits their growth and invasion, suggesting that TIG1 acts as a tumor suppressor gene. However, in some cancers, poor prognosis is associated with TIG1 expression, indicating its protumor growth characteristics, especially in promoting the invasion of inflammatory breast cancer More >

  • Open Access

    ARTICLE

    Silencing of the long non-coding RNA LINC00265 triggers autophagy and apoptosis in lung cancer by reducing protein stability of SIN3A oncogene

    XIAOBI HUANG1,#, CHUNYUAN CHEN2, YONGYANG CHEN1,#, HONGLIAN ZHOU1, YONGHUA CHEN1, ZHONG HUANG1, YULIU XIE1, BAIYANG LIU1, YUDONG GUO1, ZHIXIONG YANG1, GUANGHUA CHEN3,*, WENMEI SU1,4,*

    Oncology Research, Vol.32, No.7, pp. 1185-1195, 2024, DOI:10.32604/or.2023.030771 - 20 June 2024

    Abstract Background: Long non-coding RNAs are important regulators in cancer biology and function either as tumor suppressors or as oncogenes. Their dysregulation has been closely associated with tumorigenesis. LINC00265 is upregulated in lung adenocarcinoma and is a prognostic biomarker of this cancer. However, the mechanism underlying its function in cancer progression remains poorly understood. Methods: Here, the regulatory role of LINC00265 in lung adenocarcinoma was examined using lung cancer cell lines, clinical samples, and xenografts. Results: We found that high levels of LINC00265 expression were associated with shorter overall survival rate of patients, whereas knockdown of LINC00265 inhibited proliferation… More >

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