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Search Results (12)
  • Open Access

    ARTICLE

    3-O-Acetyl-11-Keto-β-Boswellic Acid Suppresses Colitis-Associated Colorectal Cancer by Inhibiting the NF-Kb Signaling Pathway and Remodeling Gut Microbiota

    Fang Xu1,2,#, Wan Li1,#, Xiang-Jin Zheng1,2, Yue Hao1,2, Yi-Hui Yang1,2, Hong Yang1,2, Sen Zhang1,2, Wan-Xin Cao1,2, Xiao-Xue Li1,2, Xu Zhang1,2, Guan-Hua Du1,2, Teng-Fei Ji1,*, Jin-Hua Wang1,2,*

    Oncology Research, Vol.33, No.8, pp. 1969-1989, 2025, DOI:10.32604/or.2025.062386 - 18 July 2025

    Abstract Objectives: Colorectal cancer (CRC) is one of the most common cancers all over the world. The progression of CRC is associated with inflammation and disruptions in intestinal flora. 3-O-Acetyl-11-keto-β-boswellic acid (AKBA) has been noted for its potent anti-inflammatory properties. However, the effect of AKBA on colon cancer caused by inflammation and its mechanism are not unclear. The study is to explore the effect of AKBA on CRC and its mechanism. Materials and Methods: Cell proliferation, (5-ethynyl-2-deoxyuridine, EdU)-DNA synthesis assay and colony formation were used to assess the effect of AKBA on the proliferation of CRC cells.… More >

  • Open Access

    ORIGINAL ARTICLE

    NLRP12 reduces proliferation and inflammation of rheumatoid arthritis fibroblast-like synoviocytes by regulating the NF-kB and MAPK pathways

    Xin Zhang1, He Nan1, Jialong Guo1, Jinyu Liu2

    European Cytokine Network, Vol.32, No.2, pp. 15-22, 2021, DOI:10.1684/ecn.2021.0465

    Abstract Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease characterized by abnormal synovial hyperplasia and the release of inflammatory cytokines. NLRP12 is a member of the family nod-like receptor (NLR) families that are activators of inflammation. However, the role of NLRP12 in fibroblast-like synoviocytes (FLSs) is still unclear. In the present study, we have investigated the role of NLRP12 in fibroblast-like synoviocytes (FLSs). The results demonstrated that NLRP12 overexpression inhibited proliferation and promoted cell apoptosis in RA-FLSs. Moreover, NLRP12 overexpression repressed inflammation by downregulation of IL-1β, TNF-α, IL-6, IFN-γ and MCP-1 production and upregulation of More >

  • Open Access

    ARTICLE

    IOX-101 Reverses Drug Resistance Through Suppression of Akt/mTOR/NF-κB Signaling in Cancer Stem Cell-Like, Sphere-Forming NSCLC Cell

    Majed Al Fayi*†, Ahmad Alamri*, Prasanna Rajagopalan*†

    Oncology Research, Vol.28, No.2, pp. 177-189, 2020, DOI:10.3727/096504019X15746768080428

    Abstract Drug discovery research to fight lung cancer is incessantly challenged by drug resistance. In this study, we used drug-resistant lung cancer stem like cells (A549-CS) to compare the efficacy of standard drugs like cisplatin (DDP) and gemcitabine (GEM) with a novel arylidene derivative IOX-101. A549-CS was derived from regular A549 cells by growing in special media. Resistance proteins were detected using Western blotting. Cell proliferations were assessed by MTT assay. Cytokine release was enumerated using enzyme-linked immunosorbent assay. The effect of drugs on apoptosis and cell cycle was studied with flow cytometry protocols. Apoptosis-related proteins,… More >

  • Open Access

    ARTICLE

    Tripartite Motif-Containing 46 Promotes Viability and Inhibits Apoptosis of Osteosarcoma Cells by Activating NF-kB Signaling Through Ubiquitination of PPARα

    Wenwei Jiang*, Xinyu Cai*, Tianyang Xu*, Kaiyuan Liu*, Dong Yang*, Lin Fan*, Guodong Li*, Xiao Yu

    Oncology Research, Vol.28, No.4, pp. 409-421, 2020, DOI:10.3727/096504020X15868639303417

    Abstract Osteosarcoma (OS), the most common bone cancer, causes high morbidity in children and young adults. TRIM46 is a member of the family of tripartite motif (TRIM)-containing proteins that serve as important regulators of tumorigenesis. Here we investigate the possible role of TRIM46 in OS and the underlying molecular mechanism. We report an increase in the expression of TRIM46 in OS and its association with tumor size, Enneking’s stage, and patient prognosis. TRIM46 knockdown inhibits OS cell viability and cell cycle progression and induces apoptosis, while TRIM46 overexpression exerts inverse effects, which are inhibited by peroxisome… More >

  • Open Access

    REVIEW

    Anticancer Activity of Novel NF-kB Inhibitor DHMEQ by Intraperitoneal Administration

    Kazuo Umezawa*, Andrzej Breborowicz, Shamil Gantsev

    Oncology Research, Vol.28, No.5, pp. 541-550, 2020, DOI:10.3727/096504020X15929100013698

    Abstract There have been great advances in the therapy of cancer and leukemia. However, there are still many neoplastic diseases that are difficult to treat. For example, it is often difficult to find effective therapies for aggressive cancer and leukemia. An NF- B inhibitor named dehydroxymethylepoxyquinomicin (DHMEQ) was discovered in 2000. This compound was designed based on the structure of epoxyquinomicin isolated from a microorganism. It was shown to be a specific inhibitor that directly binds to and inactivates NF- B components. Until now, DHMEQ has been used by many scientists in the world to suppress… More >

  • Open Access

    ARTICLE

    TBK1 Inhibitor Exerts Antiproliferative Effect on Glioblastoma Multiforme Cells

    Sarah A. Scuderi*, Marika Lanza*, Giovanna Casili*, Francesca Esposito, Cristina Colarossi, Dario Giuffrida, Paterniti Irene*, Salvatore Cuzzocrea*,* Emanuela Esposito*, Michela Campolo*

    Oncology Research, Vol.28, No.7-8, pp. 779-790, 2020, DOI:10.3727/096504021X16161478258040

    Abstract Glioma are common malignant brain tumors, among which glioblastoma multiforme (GBM) has the worst prognosis. Different studies of GBM revealed that targeting nuclear factor B (NF- B) induced an attenuation tumor proliferation and prolonged cell survival. TBK1 {TANK [TRAF (TNF (tumor-necrosis-factor) receptorassociated factor)-associated NF- B activator]-binding kinase 1} is a serine/threonine protein kinase, and it is a member of the I B kinase (IKK) family involved in NF- B pathway activation. The aim of this study was to investigate the potential effect of BX795, an inhibitor of TBK1, in an in vitro and ex vivo… More >

  • Open Access

    ARTICLE

    miR-449a Suppresses Tumor Growth, Migration, and Invasion in Non-Small Cell Lung Cancer by Targeting a HMGB1-Mediated NF-kB Signaling Pathway

    Dandan Wu*1, Jun Liu†1, Jianliang Chen*, Haiyan He*, Hang Ma*, Xuedong Lv*

    Oncology Research, Vol.27, No.2, pp. 227-235, 2019, DOI:10.3727/096504018X15213089759999

    Abstract MicroRNAs (miRNAs) have been reported to be involved in many human cancers and tumor progression. The dysregulation of miR-449a is found in many types of malignancies and is associated with tumor growth, migration, and invasion. However, its expression and function in non-small cell lung cancer (NSCLC) still remains unclear. In our study, miR-449a was found to be downregulated in both NSCLC tissues and cell lines, and low miR-449a expression was obviously associated with tumor differentiation, TMN stage, and poor overall survival (OS). Moreover, we demonstrated that miR-449a could inhibit tumor proliferation, migration, and invasion in More >

  • Open Access

    ARTICLE

    The Interaction Between lncRNA SNHG1 and miR-140 in Regulating Growth and Tumorigenesis via the TLR4/NF-kB Pathway in Cholangiocarcinoma

    Zhen Li*1, Xin Li*1, Xiao Du, Henghui Zhang, Zhengyang Wu*, Kewei Ren*, Xinwei Han*

    Oncology Research, Vol.27, No.6, pp. 663-672, 2019, DOI:10.3727/096504018X15420741307616

    Abstract Cholangiocarcinoma (CCA) is the second most common primary hepatobiliary carcinoma. The long noncoding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) has been reported to contribute to the progression of multiple cancers. Nonetheless, the functions and hidden mechanism of SNHG1 remain unclear in CCA. In this study, the SNHG1 levels were boosted in CCA cell lines, and knockdown of SNHG1 repressed CCA cell proliferation and invasion in vitro. The data also demonstrated that miR-140 could act as a target of SNHG1 in CCA and inhibited CCA cell proliferation and invasion, whereas the inhibition effects More >

  • Open Access

    ARTICLE

    NLRP3 Promotes Glioma Cell Proliferation and Invasion via the Interleukin-1b/NF-kB p65 Signals

    Liping Xue*1, Bin Lu†1, Bibo Gao, Yangyang Shi, Jingqi Xu, Rui Yang, Bo Xu, Peng Ding

    Oncology Research, Vol.27, No.5, pp. 557-564, 2019, DOI:10.3727/096504018X15264647024196

    Abstract Because of the characteristics of high invasiveness, relapse, and poor prognosis, the management of malignant gliomas has always been a great challenge. Nod-like receptor (NLR) family pyrin domain containing 3 (NLRP3) is a crucial component of the NLRP3 inflammasome, a multiprotein complex that can trigger caspase 1/interleukin-1 (IL-1)-mediated inflammatory response once activated and participates in the pathogeny of diverse inflammatory diseases as well as cancers. We examined the function of NLRP3 in the development of glioma. Glioma cells were treated with NLRP3 interference or overexpression vectors, recombinant IL-1 , IL-1 antibody, and NF- B inhibitor.… More >

  • Open Access

    ARTICLE

    Inhibition of NF-kB Activity Enhances Sensitivity to Anticancer Drugs in Cholangiocarcinoma Cells

    Wunchana Seubwai*†‡, Kulthida Vaeteewoottacharn‡§, Ratthaphol Kraiklang, Kazuo Umezawa#, Seiji Okada**, Sopit Wongkham‡§

    Oncology Research, Vol.23, No.1-2, pp. 21-28, 2015, DOI:10.3727/096504015X14424348426071

    Abstract Cholangiocarcinoma (CCA) is a dismal cancer. At present, there is no effective chemotherapeutic regimen for CCA. This may be due to the marked resistance of CCA to chemotherapy drugs, for which a mechanism remains unknown. Nuclear factor-kB (NF-kB) is constitutively activated in a variety of cancer cells, including CCA. It has been shown to play roles in growth, metastasis, and chemoresistance of cancer. In the present study, we examined whether NF-kB is involved in the chemoresistance of CCA and whether dehydroxymethylepoxyquinomicin (DHMEQ), an effective NF-kB inhibitor, can overcome the drug resistance of CCA. Two CCA… More >

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