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  • 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

    Astragaloside IV Enhances Cisplatin Chemosensitivity in Human Colorectal Cancer via Regulating NOTCH3

    Tao Xie*, Yao Li, Shi-Lei Li*, Hai-Feng Luo

    Oncology Research, Vol.24, No.6, pp. 447-453, 2016, DOI:10.3727/096504016X14685034103590

    Abstract Although astragaloside IV exhibits anti-inflammation, immunoregulatory, and anticancer properties, the chemosensitization effects of astragaloside IV in colorectal cancer have never been reported. Our study tested whether astragaloside could increase cisplatin sensitivity in colorectal cancer. CCK-8 assay was used to measure the cell viability of colorectal cancer cells. Quantitative real-time PCR and Western blot were performed to determine the mRNA and protein expression, respectively. Our data revealed that astragaloside IV administration significantly suppressed the cell growth of colorectal cancer cells, whereas no obvious cytotoxicity of astragaloside IV was observed in nonmalignant colonic cells. In addition, combined… More >

  • Open Access

    ARTICLE

    Knockdown of SPOCK1 Inhibits the Proliferation and Invasion in Colorectal Cancer Cells by Suppressing the PI3K/Akt Pathway

    Ping Zhao*, Hai-Tao Guan, Zhi-Jun Dai, Yu-Guang Ma, Xiao-Xu Liu, Xi-Jing Wang

    Oncology Research, Vol.24, No.6, pp. 437-445, 2016, DOI:10.3727/096504016X14685034103554

    Abstract Sparc/osteonectin, cwcv, and kazal-like domains proteoglycan (testican) 1 (SPOCK1), known as testican-1, were found to be involved in the development and progression of tumors. However, in colorectal cancer (CRC), the expression pattern of SPOCK1 and its functional role remain poorly investigated. In the present study, we explored the role of SPOCK1 in CRC. Our results demonstrated that SPOCK1 is overexpressed in CRC cell lines. SPOCK1 silencing significantly inhibited the proliferation in vitro and the tumor growth in vivo. Furthermore, SPOCK1 silencing significantly attenuated the migration/invasion by reversing the EMT process in CRC cells. Finally, knockdown More >

  • Open Access

    ARTICLE

    MicroRNA-1284 Inhibits Cell Viability and Induces Apoptosis of Ovarian Cancer Cell Line OVCAR3

    Changqing Pan, Dan Wang, Yao Zhang, Wenliang Yu

    Oncology Research, Vol.24, No.6, pp. 429-435, 2016, DOI:10.3727/096504016X14685034103518

    Abstract Ovarian cancer is a malignancy with high mortality among women. Multiple reports show that microRNAs (miRs) act as regulators in ovarian cancer inhibition, while the role of miR-1284 in ovarian cancer is still unknown. This study aimed to investigate the effects of miR-1284 on ovarian cancer cells. Human ovarian cancer cell line OVCAR3 was cultured and transfected with miR-1284 mimics, inhibitors, or control. Viability and apoptosis of transfected cells were then determined by MTT assay, BrdU assay, and flow cytometry. Expression changes of p27, p21, and PI3K/Akt pathway-related proteins were measured by Western blot. Results More >

  • Open Access

    RETRACTION

    [ARTICLE WITHDRAWN] MicroRNA-223 Promotes Tumor Progression in Lung Cancer A549 Cells via Activation of the NF-κB Signaling Pathway

    Huang Li, Li Fang, Deng Pengbo, Hu Chengping

    Oncology Research, Vol.24, No.6, pp. 405-413, 2016, DOI:10.3727/096504016X14685034103437

    Abstract THIS ARTICLE WAS WITHDRAWN BY THE PUBLISHER IN NOVEMBER 2020 More >

  • Open Access

    ARTICLE

    miR-489 Suppresses Proliferation and Invasion of Human Bladder Cancer Cells

    Jing Li, Weixing Qu, Yazhou Jiang, Yi Sun, Yongyi Cheng, Tiejun Zou, Shuangkuan Du

    Oncology Research, Vol.24, No.6, pp. 391-398, 2016, DOI:10.3727/096504016X14666990347518

    Abstract MicroRNAs (miRNAs) have been shown to be involved in bladder cancer progression. miR-489 (also known as miR-489-3p) was recently reported to be a tumor suppressor in several cancers. However, its exact role and mechanism in the progression of bladder cancer are largely unknown. In this study, we explore the role of miR-489 in the proliferation and invasion of human bladder cancer cells. The miR-489 expression levels were detected in bladder cancer and normal adjacent tissues, as well as in human normal bladder epithelial cells and bladder cancer cell lines. The results showed that miR-489… More >

  • Open Access

    ARTICLE

    Suppressive Role of MicroRNA-148a in Cell Proliferation and Invasion in Ovarian Cancer Through Targeting Transforming Growth Factor-β-Induced 2

    Min Zhao*, Zhiying Su, Shiyang Zhang, Liangjin Zhuang§, Yudi Xie*, Xiaodong Li*

    Oncology Research, Vol.24, No.5, pp. 353-360, 2016, DOI:10.3727/096504016X14685034103275

    Abstract Ovarian cancer (OC) is one of the most common gynecological malignancies. MicroRNAs (miRs) play a crucial role in the development and progression of OC, but the underlying mechanism remains largely unclear. Our study investigated the regulatory role of miR-148a in OC cell proliferation and invasion. We found that miR- 148a was significantly downregulated in OC tissues compared to their matched adjacent nontumor tissues. In addition, its expression was also reduced in OC cell lines (SKOV3, ES-2, OVCAR, and A2780) compared to normal ovarian epithelial cells. Overexpression of miR-148a caused a significant decrease in OC cell… More >

  • Open Access

    RETRACTION

    [ARTICLE WITHDRAWN] MicroRNA-16-1 Inhibits Tumor Cell Proliferation and Induces Apoptosis in A549 Non-Small Cell Lung Carcinoma Cells

    Wang Weihua, Chen Jie, Dai Jinhua, Zhang Burong, Wang Feng, Sun Yizhe

    Oncology Research, Vol.24, No.5, pp. 345-351, 2016, DOI:10.3727/096504016X14685034103194

    Abstract THIS ARTICLE WAS WITHDRAWN BY THE PUBLISHER IN NOVEMBER 2020 More >

  • Open Access

    ARTICLE

    Knockdown of Long Noncoding RNA uc.338 by siRNA Inhibits Cellular Migration and Invasion in Human Lung Cancer Cells

    Xuexin Gao*, Xuezhen Gao, Chao Li*, Yukun Zhang*, Lei Gao

    Oncology Research, Vol.24, No.5, pp. 337-343, 2016, DOI:10.3727/096504016X14666990347671

    Abstract Lung cancer remains a critical health concern worldwide. Long noncoding RNAs with ultraconserved elements have recently been implicated in human tumorigenesis. The present study investigated the role of ultraconserved element 338 (uc.338) in the regulation of cell proliferation and metastasis in human lung cancer. Our data showed that the expression of uc.338 in lung cancer was remarkably increased in vivo and in vitro. Depletion of uc.338 with specific siRNA interference retarded the cell proliferative rate in lung cancer cell lines NCI-H929 and H1688. Furthermore, knockdown of uc.338 caused cell cycle arrest in the G0/G1 phase in More >

  • Open Access

    ARTICLE

    Ritonavir Interacts With Belinostat to Cause Endoplasmic Reticulum Stress and Histone Acetylation in Renal Cancer Cells

    Makoto Isono, Akinori Sato, Kazuki Okubo, Takako Asano, Tomohiko Asano

    Oncology Research, Vol.24, No.5, pp. 327-335, 2016, DOI:10.3727/096504016X14666990347635

    Abstract The histone deacetylase (HDAC) inhibitor belinostat increases the amount of unfolded proteins in cells by promoting the acetylation of heat shock protein 90 (HSP90), thereby disrupting its chaperone function. The human immunodeficiency virus protease inhibitor ritonavir, on the other hand, not only increases unfolded proteins by suppressing HSP90 but also acts as a proteasome inhibitor. We thought that belinostat and ritonavir together would induce endoplasmic reticulum (ER) stress and kill renal cancer cells effectively. The combination of belinostat and ritonavir induced drastic apoptosis and inhibited the growth of renal cancer cells synergistically. Mechanistically, the combination More >

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