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  • Open Access

    ARTICLE

    Pik3cb Antagonizes LPS/ATP-Induced Inflammatory Activation in Cardiomyocytes by Inhibiting the PI3K/AKT/NF-κB/NLRP3 Signaling Axis

    Xuekun Shao1,#, Cheng Wang2,#,*, Mengru Zhang2, Yi Wang2, Zhuoya Qiu1, Wen Cai1, Ruiliang Zhu3, Ping Wang2,*

    BIOCELL, Vol.49, No.11, pp. 2181-2194, 2025, DOI:10.32604/biocell.2025.070859 - 24 November 2025

    Abstract Objectives: PI3K plays a pivotal role in the inflammatory response by modulating the production and release of inflammatory factors. Pik3cb is one of the subunits of PI3K, and its specific role in myocardium inflammation remains unelucidated. This study aimed to investigate the role of Pik3cb in the inflammatory response and to elucidate the underlying mechanism. Methods: An inflammation model was established using H9c2 cells treated with LPS and ATP, and Pik3cb expression was evaluated in this model system. Subsequently, an overexpression model was constructed by transfecting cells with a Pik3cb overexpression plasmid, after which the… More > Graphic Abstract

    Pik3cb Antagonizes LPS/ATP-Induced Inflammatory Activation in Cardiomyocytes by Inhibiting the PI3K/AKT/NF-<b>κ</b>B/NLRP3 Signaling Axis

  • Open Access

    REVIEW

    Mechanistic Insights into the Role of Melatonin in Cancer Cell Chemoresistance

    Russel J. Reiter1,*, Ramaswamy Sharma2,*, Walter Manucha3, Walter Balduini4, Doris Loh5, Demetrios A. Spandidos6, Alejandro Romero7, Vasiliki E. Georgakopoulou8, Wei Zhu9

    BIOCELL, Vol.49, No.11, pp. 2033-2067, 2025, DOI:10.32604/biocell.2025.067661 - 24 November 2025

    Abstract The development of cancer cell resistance to conventional treatments continues to be a major obstacle in the successful treatment of tumors of many types. The discovery of a highly efficient direct and indirect free radical scavenger, melatonin, in the mitochondrial matrix may be a factor in determining both the occurrence of cancer cell drug insensitivity as well as radioresistance. This relates to two of the known hallmarks of cancer, i.e., exaggerated free radical generation in the mitochondria and the development of Warburg type metabolism (glycolysis). The hypothesis elaborated in this report assumes that the high… More >

  • Open Access

    ARTICLE

    RAD23B Promotes Colorectal Cancer Metastasis via the Talin1/Integrin/PI3K/AKT/MMP9 Axis

    Jun Li1,#, Yang Chen1,#, Zhijiao Hao2, Zhiyong Zhang3, Jingyi Fan1, Xiao Liu1, Xueli Zhao3, Hongyan Zhang4, Chenpeng Wu3,*

    Oncology Research, Vol.33, No.11, pp. 3523-3541, 2025, DOI:10.32604/or.2025.067535 - 22 October 2025

    Abstract Background: Radiation sensitive 23 homolog B (RAD23B), a DNA repair-related protein, plays a contributory role in the development of multiple malignancies. This study aimed to explore the role of RAD23B in promoting colorectal cancer (CRC) metastasis and to elucidate the underlying molecular mechanisms. Methods: RAD23B was overexpressed in CRC cell lines SW480 and HCT-8, with empty vectors serving as controls. Invasion, cell proliferation, and migration were assessed using CCK-8 and Transwell assays. A xenograft mouse model was used to evaluate metastatic potential in vivo. Immunoprecipitation-mass spectrometry (IP-MS) and transcriptomic analysis by RNA sequencing (RNA-seq) were performed… More >

  • Open Access

    ARTICLE

    TRIM32 Promotes Glycolysis in Keloid Fibroblasts and Progression of Keloid Scars via Regulation of the PI3K/AKT Signaling Pathway

    Yi Zhang1, Hua Jin2,*

    BIOCELL, Vol.49, No.8, pp. 1529-1543, 2025, DOI:10.32604/biocell.2025.066479 - 29 August 2025

    Abstract Objectives: The present study investigated whether Tripartite Motif-Containing Protein 32 (TRIM32) contributes to the aberrant activation of keloid fibroblasts (KFs) via glycolysis. Methods: The expression levels of TRIM32, pyruvate dehydrogenase kinase 1 (PDK1), hexokinase 2 (HK2), and glucose transporter 1 (GLUT1) in normal human skin fibroblasts (NFs) and KFs were analyzed using RT-qPCR analyses and western blotting. Cellular proliferation, invasion, and migration were evaluated using Transwell, wound healing, 5-ethynyl-2-deoxyuridine (EdU), and cell counting kit-8 (CCK-8) assays. The extracellular acidification rate (ECAR) was measured using the XF96 Extracellular Flux Analyzer. Glucose uptake and ATP production were measured using… More >

  • Open Access

    RETRACTION

    Retraction: Knockdown of Rap1b Enhances Apoptosis and Autophagy in Gastric Cancer Cells via the PI3K/Akt/mTOR Pathway

    Oncology Research Editorial Offfce

    Oncology Research, Vol.33, No.8, pp. 2177-2177, 2025, DOI:10.32604/or.2025.070133 - 18 July 2025

    Abstract This article has no abstract. More >

  • Open Access

    REVIEW

    Dysregulated PI3K/AKT signaling in oral squamous cell carcinoma: The tumor microenvironment and epigenetic modifiers as key drivers

    VINOTHKUMAR VEERASAMY1, VEERAVARMAL VEERAN2, SIDDAVARAM NAGINI1,3,*

    Oncology Research, Vol.33, No.8, pp. 1835-1860, 2025, DOI:10.32604/or.2025.064010 - 18 July 2025

    Abstract The phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathway is one of the most frequently dysregulated signaling networks in oral squamous cell carcinoma (OSCC). Although the tumor microenvironment (TME) and epigenetic modifiers are recognized to play a pivotal role in aberrant activation of the PI3K/AKT pathway in OSCC, the available evidence is fragmentary and a comprehensive analysis is warranted. This review evaluates the intricate mechanisms by which various components of the TME facilitate proliferation, apoptosis evasion, invasion, migration, angiogenesis, metastasis, as well as therapy resistance in OSCC through activation of PI3K/AKT signalling. The review has also More >

  • Open Access

    ARTICLE

    ETV1 transcriptional manipulation of KIFC1 regulates the progression of pancreatic cancer

    FANGFANG HU1, ZHIBIN BAI2, YANG WANG1, HAODONG TANG3, JIAHUA ZHOU1,*

    Oncology Research, Vol.33, No.7, pp. 1723-1737, 2025, DOI:10.32604/or.2025.059631 - 26 June 2025

    Abstract Background: Kinesin-14 family protein 1 (KIFC1) is abnormally overexpressed in various cancers, and the transcription factor ETS variant 1 (ETV1) is an oncogenic transcription factor in tumors. The potential binding sites on the KIFC1 promoter by ETV1 were observed; however, no evidence supports that ETV1 targets KIFC1. Aims: This study aimed to investigate the relationship between KIFC1 and ETV1, and their effects and mechanisms in pancreatic cancer. Methods: Pan-cancer analysis of KIFC1 expression was performed in GEPIA2 database. KIFC1 expression levels were determined by immunohistochemistry (IHC) in our pancreatic cancer cohort. The correlation between KIFC1… More >

  • Open Access

    REVIEW

    Evaluating Oncogenic Drivers and Therapeutic Potential of the PI3K/AKT/mTOR Pathway in Hepatocellular Carcinoma: An Overview of Clinical Trials

    Ayda Baghery Saghchy Khorasani1, Mahda Delshad2, Mohammad-Javad Sanaei2,3, Atieh Pourbagheri-Sigaroodi2, Ali Pirsalehi4, Davood Bashash2,*

    BIOCELL, Vol.49, No.4, pp. 539-562, 2025, DOI:10.32604/biocell.2025.059970 - 30 April 2025

    Abstract Hepatocellular carcinoma (HCC) is the most common primary liver tumor and the third leading cause of cancer-related mortality globally. The phosphatidylinositol-3 kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway is critically involved in HCC pathogenesis, stimulating uncontrolled cell proliferation, survival, and tumor progression. The overactivation of this pathway is strongly linked to poor prognosis, making it a crucial target for therapeutic intervention. The oncogenic roles of PI3K/AKT/mTOR components in HCC have been highlighted, noting that class I PI3K deregulation, phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA) upregulation, and mTOR overexpression could be associated… More >

  • Open Access

    RETRACTION

    Retraction: MicroRNA-373 Promotes Growth and Cellular Invasion in Osteosarcoma Cells by Activation of the PI3K/AKT–Rac1–JNK Pathway: The Potential Role in Spinal Osteosarcoma

    Oncology Research Editorial Office

    Oncology Research, Vol.32, No.9, pp. 1535-1535, 2024, DOI:10.32604/or.2024.056124 - 23 August 2024

    Abstract This article has no abstract. More >

  • Open Access

    ARTICLE

    ROR2 promotes invasion and chemoresistance of triple-negative breast cancer cells by activating PI3K/AKT/mTOR signaling

    XIA DA1, HAN GE2, JUNFENG SHI3, CHUNHUA ZHU1, GUOZHU WANG1, YUAN FANG4,*, JIN XU1,*

    Oncology Research, Vol.32, No.7, pp. 1209-1219, 2024, DOI:10.32604/or.2024.045433 - 20 June 2024

    Abstract Objective: This study aimed to investigate the role of receptor tyrosine kinase-like orphan receptor 2 (ROR2) in triple-negative breast cancer (TNBC). Methods: ROR2 expression in primary TNBC and metastatic TNBC tissues was analyzed by immunohistochemical staining and PCR. ROR2 expression in TNBC cell lines was detected by PCR and Western blot analysis. The migration, invasion and chemosensitivity of TNBC cells with overexpression or knockdown of ROR2 were examined. Results: ROR2 expression was high in metastatic TNBC tissues. ROR2 knockdown suppressed the migration, invasion and chemoresistance of TNBC cells. ROR2 overexpression in MDA-MB-435 cells promoted the migration, More >

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