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  • Open Access

    ARTICLE

    MPPa-PDT induced apoptosis and autophagy through JNK and p38 MAPK signaling pathways in A549 cells

    PINGHUA TU, SHANSHAN WANG, KELAN DENG, XINJUN LI, ZHANLING WU*

    BIOCELL, Vol.48, No.11, pp. 1603-1612, 2024, DOI:10.32604/biocell.2024.054364 - 07 November 2024

    Abstract Objectives: The antitumor effects of pyropheophorbide-α methyl ester-mediated photodynamic therapy (MPPa-PDT) were observed in several cancers. The objective of this investigation was to examine the antineoplastic efficacy of MPPa-PDT acting on lung carcinoma A549 cells and further elaborate mechanisms. Methods: The viability of A549 cells was examined with cell counting kit-8 after MPPa-PDT disposal. Hoechst 33342 staining, monodansylcadaverine (MDC) staining, and transmission electron microscopy were employed to observe apoptotic bodies and autophagic vesicles. Flow cytometry with Annexin V/propidium iodide (PI) labeling objectively assessed cell death. The expression of associated proteins, including Caspase-3, Beclin-1, LC-3II, and More > Graphic Abstract

    MPPa-PDT induced apoptosis and autophagy through JNK and p38 MAPK signaling pathways in A549 cells

  • Open Access

    RETRACTION

    Retraction: miR-3188 Regulates Cell Proliferation, Apoptosis, and Migration in Breast Cancer by Targeting TUSC5 and Regulating the p38 MAPK Signaling Pathway

    Oncology Research Editorial Office

    Oncology Research, Vol.32, No.9, pp. 1523-1523, 2024, DOI:10.32604/or.2024.056118 - 23 August 2024

    Abstract This article has no abstract. More >

  • Open Access

    ARTICLE

    Absent in melanoma 2 attenuates proliferation and migration and promotes apoptosis of human colorectal cancer cells by activating P38MAPK signaling pathway

    ZHI ZHANG1,#, XIAOSONG LI1,2,#, YING ZHANG1,2,#, HAO ZHU1,2, ZHENGUO QIAO3, YANG LU4, XIUWEI MI4, HUIHUA CAO5, GENHAI SHEN1,*, SONGBING HE4,*

    Oncology Research, Vol.32, No.2, pp. 353-360, 2024, DOI:10.32604/or.2023.042986 - 28 December 2023

    Abstract Colorectal cancer (CRC) stands among the top prevalent cancers worldwide and holds a prominent position as a major contributor to cancer-related mortality globally. Absent in melanoma 2 (AIM2), a constituent of the interferon-inducible hematopoietic interferon-inducible nuclear antigens with 200 amino acid repeats protein family, contributes to both cancer progression and inflammasome activation. Despite this understanding, the precise biological functions and molecular mechanisms governed by AIM2 in CRC remain elusive. Consequently, this study endeavors to assess AIM2’s expression levels, explore its potential antitumor effects, elucidate associated cancer-related processes, and decipher the underlying signaling pathways in CRC. More > Graphic Abstract

    Absent in melanoma 2 attenuates proliferation and migration and promotes apoptosis of human colorectal cancer cells by activating P38MAPK signaling pathway

  • Open Access

    ARTICLE

    FBXW7 regulates epithelial barrier impairment in human bronchial epithelial cells in vitro by targeting apoptosis signal-regulating kinase1 via the p38 pathway

    JINGRONG SONG#, JUAN KANG#, WEI LV, YAN DONG, XIAOYING ZHANG*

    BIOCELL, Vol.45, No.3, pp. 723-731, 2021, DOI:10.32604/biocell.2021.014453 - 03 March 2021

    Abstract Bronchial asthma is a common chronic inflammatory disease characterized by airway hyperresponsiveness (AHR), inflammatory cell infiltration, and airway remodeling. F-box/WD repeat-containing protein 7 (FBXW7), an E3 ubiquitin ligase, is required for various endothelial functions, such as cell migration, inflammation, and endothelial integrity. This study aimed to investigate the role of FBXW7 in lipopolysaccharide (LPS)-induced epithelial barrier impairment in bronchial epithelial cells in vitro. By using lentivirus-based technology, FBXW7 was overexpressed or silenced (24 h) in human bronchial epithelial (16HBE) cells, which were treated with LPS or not (24 h). Immunoprecipitation (IP) detection and Western blot… More >

  • Open Access

    ARTICLE

    Silencing of long non-coding RNA CCHE1 inhibits the ovarian cancer SKOV3 cell invasion and migration and inactivates the p38-MAPK signaling pathway

    HONGWEI CHEN#, XUAN SONG#, HEMEI LI*

    BIOCELL, Vol.44, No.3, pp. 345-351, 2020, DOI:10.32604/biocell.2020.08944 - 22 September 2020

    Abstract Ovarian cancer (OC) is a major cause of cancer-related deaths among gynaecological malignancies. Emerging studies suggest that the long non-coding RNA (lncRNA) may be the potential biomarker for the diagnosis and prognosis of the cancer. The current study was carried out to investigate the role of lncRNA CCHE1 silencing in OC cell invasion and migration. Expression of lncRNA CCHE1 in normal ovarian cell Hose and OC cell lines HO 8910, A2780 and SKOV3 was detected. LncRNA were transfected with siRNA, and then the proliferation of cells was detected by using MTT assay. Cell invasion and… More >

  • Open Access

    ARTICLE

    Triptolide Inhibits Proliferation and Migration of Human Neuroblastoma SH-SY5Y Cells by Upregulating MicroRNA-181a

    Jian Jiang*, Xuewen Song, Jing Yang*, Ke Lei*, Yongan Ni*, Fei Zhou, Lirong Sun*

    Oncology Research, Vol.26, No.8, pp. 1235-1243, 2018, DOI:10.3727/096504018X15179661552702

    Abstract Neuroblastoma is the primary cause of cancer-related death for children 1 to 5 years of age. New therapeutic strategies and medicines are urgently needed. This study aimed to investigate the effects of triptolide (TPL), the major active component purified from Tripterygium wilfordii Hook F, on neuroblastoma SH-SY5Y cell proliferation, migration, and apoptosis, as well as underlying potential mechanisms. We found that TPL inhibited SH-SY5Y cell viability, proliferation, and migration, but induced cell apoptosis. The expression of matrix metalloproteinase-2 (MMP-2) and MMP-9 after TPL treatment in SH-SY5Y cells was decreased. The expression of microRNA-181a (miR-181a) was upregulated More >

  • Open Access

    ARTICLE

    miR-3188 Regulates Cell Proliferation, Apoptosis, and Migration in Breast Cancer by Targeting TUSC5 and Regulating the p38 MAPK Signaling Pathway

    Xiaowen Chen*1, Jianli Chen†1

    Oncology Research, Vol.26, No.3, pp. 363-372, 2018, DOI:10.3727/096504017X14953948675421

    Abstract This study intended to investigate the effects of miR-3188 on breast cancer and to reveal the possible molecular mechanisms. miR-3188 was upregulated and TUSC5 was downregulated in breast cancer tissues and MCF-7 cells compared to normal tissue and MCF-10 cells. After MCF-7 cells were transfected with miR-3188 inhibitor, cell proliferation and migration were inhibited, whereas apoptosis was promoted. Luciferase reporter assay suggested that TUSC5 was a target gene of miR-3188. In addition, miR-3188 overexpression increased the p-p38 expression, while miR-3188 suppression decreased the p-p38 expression significantly. miR-3188 regulated breast cancer progression via the p38 MAPK More >

  • Open Access

    ARTICLE

    Inhibitors of PI3K/ERK1/2/p38 MAPK Show Preferential Activity Against Endocrine-Resistant Breast Cancer Cells

    Maitham A. Khajah, Princy M. Mathew, Yunus A. Luqmani

    Oncology Research, Vol.25, No.8, pp. 1283-1295, 2017, DOI:10.3727/096504017X14883245308282

    Abstract Current mainstream pharmacological options for the treatment of endocrine-resistant breast cancer have limitations in terms of their side effect profile and lack of discrimination between normal and cancer cells. In the current study, we assessed the responses of normal breast epithelial cells MCF10A, estrogen receptorpositive (ER+ ) MCF-7, and ER-silenced pII breast cancer cells to inhibitors (either individually or in combination) of downstream signaling molecules. The expression/activity of ERK1/2, p38 MAPK, and Akt was determined by Western blotting. Cell proliferation, motility, and invasion were determined using MTT, wound healing, and Matrigel assays, respectively. Morphological changes… More >

  • Open Access

    ARTICLE

    Three Combined Treatments, a Novel HDAC Inhibitor OBP-801/YM753, 5-Fluorouracil, and Paclitaxel, Induce G2 Phase Arrest Through the p38 Pathway in Human Ovarian Cancer Cells

    Makoto Akiyama*†, Yoshihiro Sowa*, Tomoyuki Taniguchi*, Motoki Watanabe*, Shingo Yogosawa, Jo Kitawaki,Toshiyuki Sakai*

    Oncology Research, Vol.25, No.8, pp. 1245-1252, 2017, DOI:10.3727/096504017X14850164661097

    Abstract Ovarian cancer is the most lethal disease among gynecological malignancies. More effective therapy is required to counter high recurrence rates and chemotherapy resistance. We investigated the efficacy and molecular mechanisms of three combined treatments (TCTs)—a novel histone deacetylase (HDAC) inhibitor OBP-801/YM753, 5-fluorouracil (5-FU), and paclitaxel (PTX)—in human ovarian cancer SKOV-3 and OVCAR-3 cells. The inhibition of cell growth was stronger with TCTs than with each single agent and with two combined treatments. The TCTs significantly induce G2 phase arrest in both cell lines. We then analyzed the molecular mechanisms and found that the TCTs increased the More >

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