Home / Advanced Search

  • Title/Keywords

  • Author/Affliations

  • Journal

  • Article Type

  • Start Year

  • End Year

Update SearchingClear
  • Articles
  • Online
Search Results (62)
  • Open Access

    ARTICLE

    Neural Wiskott-Aldrich syndrome protein (N-WASP) promotes distant metastasis in pancreatic ductal adenocarcinoma via activation of LOXL2

    HYUNG SUN KIM1,#, YUN SUN LEE2,#, SEUNG MYUNG DONG3, HYO JUNG KIM1, DA EUN LEE2, HYEON WOONG KANG2, MYEONG JIN KIM2, JOON SEONG PARK1,*

    Oncology Research, Vol.32, No.4, pp. 615-624, 2024, DOI:10.32604/or.2024.044029 - 20 March 2024

    Abstract Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive solid malignancies. A specific mechanism of its metastasis has not been established. In this study, we investigated whether Neural Wiskott-Aldrich syndrome protein (N-WASP) plays a role in distant metastasis of PDAC. We found that N-WASP is markedly expressed in clinical patients with PDAC. Clinical analysis showed a notably more distant metastatic pattern in the N-WASP-high group compared to the N-WASP-low group. N-WASP was noted to be a novel mediator of epithelial-mesenchymal transition (EMT) via gene expression profile studies. Knockdown of N-WASP in pancreatic cancer cells… More > Graphic Abstract

    Neural Wiskott-Aldrich syndrome protein (N-WASP) promotes distant metastasis in pancreatic ductal adenocarcinoma via activation of LOXL2

  • Open Access

    ARTICLE

    STAT3 Polymorphism Associates With mTOR Inhibitor-Induced Interstitial Lung Disease in Patients With Renal Cell Carcinoma

    Kazuhiro Yamamoto*, Takeshi Ioroi*, Kazuaki Shinomiya, Ayaka Yoshida*, Kenichi Harada, Masato Fujisawa, Tomohiro Omura*, Yasuaki Ikemi§, Shunsaku Nakagawa§, Atsushi Yonezawa§, Osamu Ogawa, Kazuo Matsubara§, Takuya Iwamoto#, Kohei Nishikawa**, Sayaka Hayashi††, Daichi Tohara††, Yoji Murakami‡‡, Takanobu Motoshima‡‡, Hirofumi Jono††, Ikuko Yano

    Oncology Research, Vol.29, No.1, pp. 11-23, 2021, DOI:10.3727/096504022X16418911579334

    Abstract We evaluated the association of signal transducer and activator of transcription 3 (STAT3) polymorphisms with the incidence of mammalian target of rapamycin (mTOR) inhibitor-induced interstitial lung disease (ILD) in patients with renal cell carcinoma (RCC). We also used lung-derived cell lines to investigate the mechanisms of this association. Japanese patients with metastatic RCC who were treated with mTOR inhibitors were genotyped for the STAT3 polymorphism, rs4796793 (−1697C/G). We evaluated the association of the STAT3 genotype with the incidence of ILD and therapeutic outcome. In the 57 patients included in the primary analysis, the ILD rate… More >

  • Open Access

    ARTICLE

    The lncRNA FEZF1-AS1 Promotes the Progression of Colorectal Cancer Through Regulating OTX1 and Targeting miR-30a-5p

    Jing Li*†, Lian-mei Zhao, Cong Zhang, Meng Li§, Bo Gao, Xu-hua Hu, Jian Cao, Gui-ying Wang

    Oncology Research, Vol.28, No.1, pp. 51-63, 2020, DOI:10.3727/096504019X15619783964700

    Abstract Long noncoding RNAs (lncRNAs) participate in and regulate the biological process of colorectal cancer (CRC) progression. Our previous research identified differentially expressed lncRNAs in 10 CRC tissues and 10 matched nontumor tissues by next-generation sequencing (NGS). In this study, we identified an lncRNA, FEZF1 antisense RNA 1 (FEZF1-AS1), and further explored its function and mechanism in CRC. We verified that FEZF1-AS1 is highly expressed in CRC tissues and cell lines. Through functional experiments, we found that reduced levels of FEZF1-AS1 significantly suppressed CRC cell migration, invasion, and proliferation and inhibited tumor growth in vivo. Mechanistically,… More >

  • Open Access

    ARTICLE

    MicroRNA-6884-5p Regulates the Proliferation, Invasion, and EMT of Gastric Cancer Cells by Directly Targeting S100A16

    Huifang Lv, Honglin Hou, Huijun Lei, Caiyun Nie, Beibei Chen, Liangyu Bie, Lili Han, Xiaobing Chen

    Oncology Research, Vol.28, No.3, pp. 225-236, 2020, DOI:10.3727/096504019X15753718797664

    Abstract S100 binding protein A16 (S100A16) expression levels are closely associated with microRNA (miRNA) processing. Higher levels of S100A16 are reported during the progression of many cancers. Our study mainly explored the interaction between S100A16 and miR-6884-5p in gastric cancer (GC). Quantitative real-time polymerase chain reaction (qRT-PCR) was used to determine the level of S100A16 and miR-6884-5p in GC tissues and cell lines. The si-S100A16, pcDNA-S100A16, miR-6884-5p mimic or inhibitor was transfected into GC cells, and the effects of S100A16 and miR-6884-5p on the proliferation, invasion, and epithelial–mesenchymal transition (EMT) were explored by qRT-PCR and Western… More >

  • Open Access

    ARTICLE

    The AKT/GSK3β-Mediated Slug Expression Contributes to Oxaliplatin Resistance in Colorectal Cancer via Upregulation of ERCC1

    Wei Wei*1, Xiao-Dong Ma†1, Guan-Min Jiang, Bin Shi§, Wen Zhong, Chun-Lei Sun§, Liang Zhao*, Yan-Jiao Hou*, Hao Wang*

    Oncology Research, Vol.28, No.4, pp. 423-438, 2020, DOI:10.3727/096504020X15877284857868

    Abstract Although oxaliplatin serves as one of the first-line drugs prescribed for treating colorectal cancer (CRC), the therapeutic effect is disappointing due to drug resistance. So far, the molecular mechanisms mediating oxaliplatin resistance remain unclear. In this study, we found the chemoresistance in oxaliplatin-resistant HCT116 cells (HCT116/OXA) was mediated by the upregulation of ERCC1 expression. In addition, the acquisition of resistance induced epithelial–mesenchymal transition (EMT) as well as the Slug overexpression. On the contrary, Slug silencing reversed the EMT phenotype, decreased ERCC1 expression, and ameliorated drug resistance. Further mechanistical studies revealed the enhanced Slug expression resulted More >

  • Open Access

    CORRECTION

    TRAF4 Regulates Migration, Invasion, and Epithelial–Mesenchymal Transition via PI3K/AKT Signaling in Hepatocellular Carcinoma

    Kairui Liu*, Xiaolin Wu*, Xian Zang, Zejian Huang*, Zeyu Lin, Wenliang Tan*, Xiang Wu*, Wenrou Hu*, Baoqi Li*, Lei Zhang*

    Oncology Research, Vol.28, No.5, pp. 559-560, 2020, DOI:10.3727/096504020X16032056440102

    Abstract Overexpression of the tumor necrosis factor receptor-associated factor 4 (TRAF4) has been detected in many cancer types and is considered to foster tumor progression. However, the role of TRAF4 in hepatocellular carcinoma (HCC) remains elusive. In this study, we found that TRAF4 was highly expressed in HCC cell lines and HCC tissues compared with normal liver cell lines and adjacent noncancerous tissues. TRAF4 overexpression in HCC tissues was correlated with tumor quantity and vascular invasion. In vitro studies showed that TRAF4 was associated with HCC cell migration and invasion. An in vivo study verified that More >

  • Open Access

    CORRECTION

    Knockdown of Long Noncoding RNA CCAT2 Inhibits Cellular Proliferation, Invasion, and Epithelial–Mesenchymal Transition in Glioma Cells

    Jing Zeng*1, Tianping Du†1, Yafeng Song, Yan Gao, Fuyan Li, Ruimin Wu, Yijia Chen, Wei Li, Hong Zhou, Yi Yang, Zhijun Pei

    Oncology Research, Vol.28, No.5, pp. 551-552, 2020, DOI:10.3727/096504020X16032056440085

    Abstract Long noncoding RNA (lncRNA) colon cancer-associated transcript 2 (CCAT2) has been demonstrated to play an important role in diverse tumorigenesis. However, the biological function of lncRNAs in glioma is still unknown. In this study, we found that lncRNA CCAT2 was overexpressed in glioma tissues and cell lines and associated with tumor grade and size. Furthermore, patients with high levels of lncRNA CCAT2 had poorer survival than those with lower levels of lncRNA CCAT2. Knocking down lncRNA CCAT2 expression significantly suppressed the glioma cell growth, migration, and invasion, as well as induced early apoptosis of glioma More >

  • Open Access

    ARTICLE

    miR-186 Represses Proliferation, Migration, Invasion, and EMT of Hepatocellular Carcinoma via Directly Targeting CDK6

    Junfeng Lu*, Zhongsong Zhao, Yanhong Ma

    Oncology Research, Vol.28, No.5, pp. 509-518, 2020, DOI:10.3727/096504020X15954139263808

    Abstract The present study aimed to investigate the effect of miR-186 on proliferation, migration, invasion, and epithelial–mesenchymal transition (EMT) of hepatocellular carcinoma (HCC). In this work, miR-186 was downregulated in HCC tissues and cells, and low miR-186 level helped predict the occurrence of vascular invasion and poor prognosis in patients with HCC. miR-186 overexpression inhibited cell proliferation and tumor growth in nude mice, repressed migration and invasion abilities, and enhanced apoptosis in HCC cells. miR-186 also retarded progression of EMT. miR-186 directly bound to the 3 -untranslated regions of cyclin-dependent kinase 6 (CDK6) to inhibit its More >

  • Open Access

    CORRECTION

    Emodin Inhibits Colon Cancer Cell Invasion and Migration by Suppressing Epithelial–Mesenchymal Transition via the Wnt/β-Catenin Pathway

    Juan Gu*, Chang-fu Cui, Li Yang, Ling Wang*, Xue-hua Jiang*

    Oncology Research, Vol.28, No.6, pp. 681-682, 2020, DOI:10.3727/096504021X16137463165424

    Abstract Colon cancer (CC) is the third most common cancer worldwide. Emodin is an anthraquinone-active substance that has the ability to affect tumor progression. Our study aims to explore the effects and the relevant mechanism of emodin on the invasion and migration of CC in vitro and in vivo. In our study, we found that emodin inhibited the invasion and migration abilities of RKO cells and decreased the expression of matrix metalloproteinase-7 (MMP-7), MMP-9, and vascular endothelial growth factor (VEGF) in a dose-dependent manner. Further research suggested that emodin inhibited EMT by increasing the mRNA level… More >

  • Open Access

    ARTICLE

    MicroRNA-548m Suppresses Cell Migration and Invasion by Targeting Aryl Hydrocarbon Receptor in Breast Cancer Cells

    WM Farhan Syafiq B. WM Nor*†, Ivy Chung‡§, Nur Akmarina B. M. Said

    Oncology Research, Vol.28, No.6, pp. 615-629, 2020, DOI:10.3727/096504020X16037933185170

    Abstract Breast cancer is the most commonly diagnosed cancer among women and one of the leading causes of cancer mortality worldwide, in which the most severe form happens when it metastasizes to other regions of the body. Metastasis is responsible for most treatment failures in advanced breast cancer. Epithelial–mesenchymal transition (EMT) plays a significant role in promoting metastatic processes in breast cancer. MicroRNAs (miRNAs) are highly conserved endogenous short noncoding RNAs that play a role in regulating a broad range of biological processes, including cancer initiation and development, by functioning as tumor promoters or tumor suppressors.… More >

Displaying 1-10 on page 1 of 62. Per Page