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  • Open Access

    ARTICLE

    Trametinib boosts palbociclib’s efficacy in breast cancer via autophagy inhibition

    ANGUO WU1,#, JIAO YAN2,3,#, TING SU2,4, CHI FENG1, XIN LONG5,6, YIRU PAN1, RUPEI YE2, TIAN XIA2, HANAN LONG2, JIANMING WU1,*, XIULI XIAO2,*

    Oncology Research, Vol.32, No.7, pp. 1197-1207, 2024, DOI:10.32604/or.2024.046139

    Abstract Breast cancer, a predominant global health issue, requires ongoing exploration of new therapeutic strategies. Palbociclib (PAL), a well-known cyclin-dependent kinase (CDK) inhibitor, plays a critical role in breast cancer treatment. While its efficacy is recognized, the interplay between PAL and cellular autophagy, particularly in the context of the RAF/MEK/ERK signaling pathway, remains insufficiently explored. This study investigates PAL’s inhibitory effects on breast cancer using both in vitro (MCF7 and MDA-MB-468 cells) and in vivo (tumor-bearing nude mice) models. Aimed at elucidating the impact of PAL on autophagic processes and exploring the potential of combining it with trametinib… More > Graphic Abstract

    Trametinib boosts palbociclib’s efficacy in breast cancer via autophagy inhibition

  • 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

    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 >

  • 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 >

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