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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

    Silencing of the long non-coding RNA LINC00265 triggers autophagy and apoptosis in lung cancer by reducing protein stability of SIN3A oncogene

    XIAOBI HUANG1,#, CHUNYUAN CHEN2, YONGYANG CHEN1,#, HONGLIAN ZHOU1, YONGHUA CHEN1, ZHONG HUANG1, YULIU XIE1, BAIYANG LIU1, YUDONG GUO1, ZHIXIONG YANG1, GUANGHUA CHEN3,*, WENMEI SU1,4,*

    Oncology Research, Vol.32, No.7, pp. 1185-1195, 2024, DOI:10.32604/or.2023.030771

    Abstract Background: Long non-coding RNAs are important regulators in cancer biology and function either as tumor suppressors or as oncogenes. Their dysregulation has been closely associated with tumorigenesis. LINC00265 is upregulated in lung adenocarcinoma and is a prognostic biomarker of this cancer. However, the mechanism underlying its function in cancer progression remains poorly understood. Methods: Here, the regulatory role of LINC00265 in lung adenocarcinoma was examined using lung cancer cell lines, clinical samples, and xenografts. Results: We found that high levels of LINC00265 expression were associated with shorter overall survival rate of patients, whereas knockdown of LINC00265 inhibited proliferation… More >

  • Open Access

    ARTICLE

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

    Yazhou Li*†, Yang Liu, Feiyu Shi, Liang Cheng, Junjun She

    Oncology Research, Vol.24, No.5, pp. 287-293, 2016, DOI:10.3727/096504016X14648701447779

    Abstract Gastric cancer (GC) is the fourth most common malignancy and the second leading cause of cancer mortality around the world. However, the regulatory mechanisms of GC tumorigenesis and cancer cell motility are completely unknown. We investigated the role of a RAS-related protein (Rap1b) in the progression of GC. Our results showed that the expression of Rap1b is aberrantly upregulated in GC tissue samples and human GC cell lines, and the high expression of Rap1b indicated a positive correlation with poor prognosis in patients with GC. Inhibition of endogenous Rap1b dramatically reduced the cell cycle progression… More >

  • Open Access

    ARTICLE

    Gastrin Enhances Autophagy and Promotes Gastric Carcinoma Proliferation via Inducing AMPKα

    Zhuang Kun*†, Guo Hanqing*, Tang Hailing*, Yan Yuan*, Zhang Jun, Zhang Lingxia*, Han Kun*, Zhang Xin*

    Oncology Research, Vol.25, No.8, pp. 1399-1407, 2017, DOI:10.3727/096504016X14823648620870

    Abstract Gastric cancer (GC) is one of the most frequent epithelial malignancies worldwide. The gastrointestinal (GI) peptide gastrin is an important regulator of the secretion and release of gastric acid from stomach parietal cells, and it also plays a vital role in the development and progression of GC. The aim of the current study was to investigate the role and underlying mechanism of gastrin and autophagy in regulating GC tumorigenesis. Gastrin-17 amide (G-17) was applied in the GC cell lines SGC7901 and MGC-803. The results showed that G-17 maintained the high viability of SGC7901 and MGC-803.… More >

  • Open Access

    ARTICLE

    Inhibition of Beclin-1-Mediated Autophagy by MicroRNA-17-5p Enhanced the Radiosensitivity of Glioma Cells

    Weichen Hou*, Lei Song, Yang Zhao*, Qun Liu*, Shuyan Zhang

    Oncology Research, Vol.25, No.1, pp. 43-53, 2017, DOI:10.3727/096504016X14719078133285

    Abstract The role of miRNAs in the radiosensitivity of glioma cells and the underlying mechanism is still far from clear. In the present study, we detected six downregulated and seven upregulated miRNAs in the serum after radiotherapy compared with paired serum samples before radiotherapy via miRNA panel PCR. Among these, miR-17-5p was highly reduced (fold change = −4.21). Further, we validated the levels of miR-17-5p in all serum samples with qRT-PCR. In addition, statistical analysis suggested that a reduced miR-17-5P level was positively associated with advanced clinical stage of glioma, incidence of relapse, and tumor differentiation. More >

  • Open Access

    ARTICLE

    Ailanthone Promotes Human Vestibular Schwannoma Cell Apoptosis and Autophagy by Downregulation of miR-21

    Peizhen Yang*, Dezhong Sun*, Fei Jiang

    Oncology Research, Vol.26, No.6, pp. 941-948, 2018, DOI:10.3727/096504018X15149775533331

    Abstract Ailanthone (AIL) is a quassinoid isolated from the traditional Chinese medicinal herb Ailanthus altissima. The antitumor activities of AIL have been reported in several cancers. The purpose of the present study was to explore the effect of AIL on vestibular schwannomas (VSs). Various concentrations of AIL (0–1 µM) were used to treat human primary VS cells, and then cell viability, proliferation, apoptosis, and autophagy were assessed. Expression of miR-21 in VS cells was altered by miRNA transfection. The functional actions of AIL on miR-21 dysregulated cells were also assessed. AIL significantly reduced the viability of VS… More >

  • Open Access

    ARTICLE

    Emodin Induces Apoptosis of Colon Cancer Cells via Induction of Autophagy in a ROS-Dependent Manner

    Yuanyuan Wang*1, Qin Luo*1, Xianlu He†1, He Wei*, Ting Wang*, Jichun Shao, Xinni Jiang*

    Oncology Research, Vol.26, No.6, pp. 889-899, 2018, DOI:10.3727/096504017X15009419625178

    Abstract Recent studies revealed that emodin extracted from Chinese herbs exhibits an anticancer effect on different cancer types, including colon cancer. However, the mechanism is not well understood. In our study, we confirmed that emodin treatment inhibited cell viability and induced apoptosis in colon cancer cells. Further experiments found that emodin was also able to induce autophagy, which is indispensible for apoptosis induced by emodin. More interestingly, emodin treatment also results in mitochondrial dysfunction and ROS accumulation in colon cancer cells. Finally, we stressed that ROS accumulation is essential for autophagy and apoptosis induced by emodin. More >

  • Open Access

    ARTICLE

    Long Noncoding RNA (lncRNA) HOTAIR Affects Tumorigenesis and Metastasis of Non-Small Cell Lung Cancer by Upregulating miR-613

    Caiyu Jiang, Yan Yang, Yang Yang, Lu Guo, Jiang Huang, Xingren Liu, Chi Wu, Jun Zou

    Oncology Research, Vol.26, No.5, pp. 725-734, 2018, DOI:10.3727/096504017X15119467381615

    Abstract Non-small cell lung cancer (NSCLC) is one of the most deadly cancers with poor prognosis. Recent findings suggested that the lncRNA HOTAIR played an important role in tumorigenesis and metastasis. In the present study, HOTAIR was highly expressed in NSCLC tumor tissues and cell lines (H1299, H23, H292, and A549). Downregulation of HOTAIR suppressed cell proliferation and invasion, while it promoted apoptosis of NSCLC cells. The targeting relationship between HOTAIR and miR-613 was first revealed by bioinformatics prediction. miR-613 was found to be lowly expressed in NSCLC tumor tissues and cell lines. Knockdown of HOTAIR… More >

  • Open Access

    ARTICLE

    ClC5 Decreases the Sensitivity of Multiple Myeloma Cells to Bortezomib via Promoting Prosurvival Autophagy

    Huimin Zhang*†, Yuhui Pang, Chuanbao Ma, Jianying Li, Huaquan Wang*, Zonghong Shao*

    Oncology Research, Vol.26, No.3, pp. 421-429, 2018, DOI:10.3727/096504017X15049221237147

    Abstract Resistance to bortezomib (BZ) is the major problem that largely limits its clinical application in multiple myeloma treatment. In the current study, we investigated whether ClC5, a member of the chloride channel family, is involved in this process. The MTT assay showed that BZ treatment decreased cell viability in three multiple myeloma cell lines (ARH77, U266, and SKO-007), with IC50 values of 2.83, 4.37, and 1.91 nM, respectively. Moreover, BZ increased the conversion of LC3B-I to LC3B-II and expressions of beclin-1 and ATG5, concomitantly with a decreased p62 expression. Pharmacological inhibition of autophagy with 3-MA… More >

  • Open Access

    ARTICLE

    2-Deoxy-d-glucose Suppresses the In Vivo Antitumor Efficacy of Erlotinib in Head and Neck Squamous Cell Carcinoma Cells

    Arya Sobhakumari*1, Kevin P. Orcutt†‡1, Laurie Love-Homan§, Christopher E. Kowalski†‡, Arlene D. Parsons, C. Michael Knudson†‡§¶, Andrean L. Simons*†‡§¶

    Oncology Research, Vol.24, No.1, pp. 55-64, 2016, DOI:10.3727/096504016X14586627440192

    Abstract Poor tumor response to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) is a significant challenge for effective treatment of head and neck squamous cell carcinoma (HNSCC). Therefore, strategies that may increase tumor response to EGFR TKIs are warranted in order to improve HNSCC patient treatment and overall survival. HNSCC tumors are highly glycolytic, and increased EGFR signaling has been found to promote glucose metabolism through various mechanisms. We have previously shown that inhibition of glycolysis with 2-deoxy-d-glucose (2DG) significantly enhanced the antitumor effects of cisplatin and radiation, which are commonly used to treat… More >

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