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  • Open Access

    ARTICLE

    UBE2T mediates the stemness properties of breast cancer cells through the mTOR signaling pathway

    JIAWEI YIN1, YONGSHENG WANG2,3, GUANGWEI WEI4, MINGXIN WEN3,*

    BIOCELL, Vol.48, No.6, pp. 959-970, 2024, DOI:10.32604/biocell.2024.049349

    Abstract Objectives: This study aimed to reveal the role and possible mechanism of the ubiquitin-conjugating enzyme 2T (UBE2T) in the biological activities of breast cancer stem cells (BCSCs). Methods: The specific protein and gene expression were quantified by Western blotting and quantitative real-time polymerase chain reaction, the proportion of BCSCs was examined by flow cytometry, and the self-renewal and proliferation of BCSCs were verified by serial sphere formation and soft agar. Results: Increasing expression of UBE2T was drastically found in breast cancer than that in adjacent tissues. Furthermore, UBE2T overexpression significantly increased the proportion of BCSCs in More >

  • Open Access

    ARTICLE

    RNA Interference of IQ Motif Containing GTPase-Activating Protein 3 (IQGAP3) Inhibits Cell Proliferation and Invasion in Breast Carcinoma Cells

    Gaowu Hu*, Ye Xu*, Wenquan Chen*, Jiandong Wang, Chunying Zhao†1, Ming Wang*1

    Oncology Research, Vol.24, No.6, pp. 455-461, 2016, DOI:10.3727/096504016X14685034103635

    Abstract Breast cancer is a highly prevalent disease affecting women. The association of IQ motif containing GTPaseactivating protein 3 (IQGAP3) and breast cancer is poorly defined. Here we reported that IQGAP3 is a key regulator of cell proliferation and metastasis during breast cancer progression. The expression of IQGAP3 was significantly increased in breast tissues compared to nontumor tissues at both protein and mRNA levels. Furthermore, IQGAP3 had a high expression level in ZR-75-30 and BT474 compared to other breast cancer cell lines. Depletion of IQGAP3 through RNA interference in ZR-75-30 and BT474 significantly inhibited cell proliferation. More >

  • Open Access

    ARTICLE

    Knockdown of REV7 Inhibits Breast Cancer Cell Migration and Invasion

    Liu Feng*†, Wang Wei*, Zhang Heng, Han Yantao, Wang Chunbo

    Oncology Research, Vol.24, No.5, pp. 315-325, 2016, DOI:10.3727/096504016X14666990347590

    Abstract REV7 (also known as MAD2L2) is a multifunctional protein involved in DNA damage tolerance, cell cycle regulation, gene expression, and carcinogenesis. Although its expression is reportedly associated with poor prognosis in several kinds of human cancers, the significance of REV7 expression in breast malignancies is unclear. In this study, REV7 was found to be increased in breast cancer. We found that knockdown of REV7 inhibited the migration, invasion, and epithelial–mesenchymal transition (EMT) of breast cancer cells. Meanwhile, overexpression of REV7 promoted the migration, invasion, and EMT of breast cancer cells. As shown by Western blot, More >

  • Open Access

    ARTICLE

    Overexpression of miR-509 Increases Apoptosis and Inhibits Invasion via Suppression of Tumor Necrosis Factor-α in Triple-Negative Breast Cancer Hs578T Cells

    Guoqiang Zhang*1, Zengyan Liu†1, Yong Han*, Xiaohong Wang*, Zhenlin Yang*

    Oncology Research, Vol.24, No.4, pp. 233-238, 2016, DOI:10.3727/096504016X14648701447977

    Abstract Triple-negative breast cancer (TNBC) is associated with high recurrence rates of metastasis and death. miR-509 has been reported to be a tumor suppressor in many cancers, but its effect in TNBC has not yet been identified. In this article, we explored the effects of miR-509 on the malignant phenotype of TNBC cells, including proliferation, apoptosis, migration, and invasion. We transiently transfected TNBC cells, Hs578T, with miR-509 mimic. Upon transfection, the expression of miR-509 was upregulated about 50-fold compared with cells transfected with scramble mimic. Overexpression of miR-509 inhibited cell proliferation, induced cell apoptosis, and suppressed More >

  • Open Access

    ARTICLE

    Clinical Value of Capecitabine-Based Combination Adjuvant Chemotherapy in Early Breast Cancer: A Meta-Analysis of Randomized Controlled Trials

    Guanling Chen1, Zhaoze Guo1, Minfeng Liu, Guangyu Yao, Jianyu Dong, Jingyun Guo, Changsheng Ye

    Oncology Research, Vol.25, No.9, pp. 1567-1578, 2017, DOI:10.3727/096504017X14897173032733

    Abstract Capecitabine has consistently demonstrated high efficacy and acceptable tolerability in salvage chemotherapy for advanced breast cancer. However, there remains no consensus on its role in adjuvant chemotherapy for early breast cancer (EBC). To estimate the value of capecitabine-based combination adjuvant treatment in EBC, eight randomized controlled trials with 14,072 participants were analyzed. The efficacy and safety outcomes included disease-free survival (DFS), overall survival (OS), relapse, breast cancer-specific survival (BCSS), and grades 3–5 adverse events. Capecitabine-based combination adjuvant chemotherapy demonstrated a 16% increase in BCSS (HR = 0.84, 95% CI = 0.71–0.98, p = 0.03) in the… More >

  • Open Access

    ARTICLE

    Function of miR-152 as a Tumor Suppressor in Human Breast Cancer by Targeting PIK3CA

    Shuke Ge*, Dan Wang, Qinglong Kong, Wei Gao*, Jiayi Sun*

    Oncology Research, Vol.25, No.8, pp. 1363-1371, 2017, DOI:10.3727/096504017X14878536973557

    Abstract miR-152, as a tumor suppressor, has been reported to be downregulated in a number of cancer cell lines and tumor tissues, including breast cancer. This study aimed to investigate the role of miR-152 in human breast cancer and its underlying mechanisms. Human breast cancer cell line HCC1806 was transfected with hsa-miR- 152-3p mimic, inhibitor, or scrambled negative controls. The efficiency of miR-152-3p transfection was evaluated by quantitative real-time PCR, and the effects on cell viability and apoptosis as well as on the PI3K/AKT signaling pathway were investigated by MTT assay, flow cytometry, and Western blot… 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

    Polymorphic Variations Associated With Doxorubicin-Induced Cardiotoxicity in Breast Cancer Patients

    Valentina K. Todorova*, Issam Makhoul, Ishwori Dhakal, Jeanne Wei§, Annjanette Stone, Weleetka Carter, Aaron Owen*, V. Suzanne Klimberg*

    Oncology Research, Vol.25, No.8, pp. 1223-1229, 2017, DOI:10.3727/096504017X14876245096439

    Abstract Doxorubicin (DOX) is a commonly used antineoplastic agent for the treatment of various malignancies, and its use is associated with unpredictable cardiotoxicity. Susceptibility to DOX cardiotoxicity is largely patient dependent, suggesting genetic predisposition. We have previously found that individual sensitivity to DOX cardiotoxicity was associated with differential expression of genes implicated in inflammatory response and immune trafficking, which was consistent with the increasing number of reports highlighting the important role of human leukocyte antigen (HLA) complex polymorphism in hypersensitivity to drug toxicity. This pilot study aimed to investigate DNA from patients treated with DOX-based chemotherapy… More >

  • Open Access

    ARTICLE

    Overexpression of Forkhead Box L1 (FOXL1) Inhibits the Proliferation and Invasion of Breast Cancer Cells

    Jiateng Zhong*†, Haijun Wang*, Jian Yu, Jinghang Zhang, Hui Wang†§

    Oncology Research, Vol.25, No.6, pp. 959-965, 2017, DOI:10.3727/096504016X14803482769179

    Abstract Forkhead box L1 (FOXL1) is a member of the Forkhead box (FOX) superfamily and was reported to be dysregulated in various types of cancers. However, its expression pattern and underlying cellular function in breast cancer remain largely unexplored. Thus, the aim of this study was to detect FOXL1 expression in breast cancer and to analyze its role in the progression of breast cancer. Our results demonstrated that FOXL1 expression at both the mRNA and protein levels was downregulated in breast cancer tissues and cell lines. Ectopic FOXL1 suppressed breast cancer cell proliferation, migration, and invasion More >

  • Open Access

    ARTICLE

    Downregulation of MicroRNA-449 Promotes Migration and Invasion of Breast Cancer Cells by Targeting Tumor Protein D52 (TPD52)

    Zhiling Zhang, Jiawei Wang, Runfang Gao, Xuan Yang, Yafen Zhang, Jie Li, Jing Zhang, Xingjuan Zhao, Chunfang Xi, Xiaoting Lu

    Oncology Research, Vol.25, No.5, pp. 753-761, 2017, DOI:10.3727/096504016X14772342320617

    Abstract Our study aimed to investigate whether microRNA-449 (miR-449) plays a key role in regulating the migration and invasion of breast cancer cells via targeting tumor protein D52 (TPD52). The results of the qRT-PCR and Western blotting showed that, in comparison with normal breast tissues and cells, miR-449 was significantly downregulated in breast cancer tissues and cells, while TPD52 was markedly upregulated. After transfection with an miR-449 inhibitor, suppression of miR-449 significantly promoted cell migration and invasion. Also, when miR-449 was overexpressed by transfection with miR-449 mimics, E-cadherin expression significantly increased, and the expression of N-cadherin More >

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