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  • 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

    Long Noncoding RNA PlncRNA-1 Promotes Colorectal Cancer Cell Progression by Regulating the PI3K/Akt Signaling Pathway

    Wei Song*, Jia-Zhuan Mei, Mingzhi Zhang

    Oncology Research, Vol.28, No.9, pp. 971-972, 2020, DOI:10.3727/096504022X16414984936791

    Abstract Accumulating evidence has indicated that long noncoding RNA (lncRNA) PlncRNA-1 plays an important regulatory role in cancers. However, the expression and biological functions of PlncRNA-1 in colorectal cancer (CRC) are still unclear. In the present study, we determined the expression of PlncRNA-1 in CRC and explored the function of PlncRNA-1 on CRC cell progression. The results showed that PlncRNA-1 was significantly increased in CRC tissues and cell lines; high PlncRNA-1 expression was associated with depth of invasion, lymph node metastasis, and TNM stage of CRC patients. Kaplan–Meier curve analysis showed that patients with high PlncRNA-1 More >

  • Open Access

    CORRECTION

    MicroRNA-133a Inhibits Proliferation of Gastric Cancer Cells by Downregulating ERBB2 Expression

    Chang Li*, Xiaoping Li, Shuohui Gao*, Chang Li, Lianjun Ma§

    Oncology Research, Vol.28, No.7-8, pp. 819-822, 2020, DOI:10.3727/096504021X16240202940003

    Abstract Gastric cancer is the fourth most common type of cancer and the second highest leading cause of cancer-related deaths worldwide. It has already been established that miR-133a is involved in gastric cancer. In this study, we investigated the molecular mechanisms by which miR-133a inhibits the proliferation of gastric cancer cells. We analyzed the proliferative capacity of human gastric cancer cells SNU-1 using an MTT assay. Cell apoptosis was determined using flow cytometry. The expression levels of ERBB2, p-ERK1/2, and p-AKT in SNU-1 cells were determined using Western blot analysis. To confirm that ERBB2 is a… More >

  • Open Access

    ARTICLE

    Curcumol Inhibits Lung Adenocarcinoma Growth and Metastasis via Inactivation of PI3K/AKT and Wnt/β-Catenin Pathway

    Sheng Li*1, Guoren Zhou*1, Wei Liu, Jinjun Ye, Fangliang Yuan, Zhi Zhang

    Oncology Research, Vol.28, No.7-8, pp. 685-700, 2020, DOI:10.3727/096504020X15917007265498

    Abstract Curcumol (Cur), isolated from the Traditional Chinese Medical plant Rhizoma Curcumae, is the bioactive component of sesquiterpene reported to possess antitumor activity. However, its bioactivity and mechanisms against lung adenocarcinoma are still unclear. We investigated its effect on lung adenocarcinoma and elucidated its underlying molecular mechanisms. In vitro, Cur effectively suppressed proliferation, migration, and invasion of lung adenocarcinoma cells A549 and H460, which were associated with the altered expressions of signaling molecules, including p-AKT, p-PI3K, p-LRP5/6, AXIN, APC, GSK3 and p- -catenin, matrix metalloproteinase (MMP)-2, and MMP-9. Furthermore, Cur significantly induced cell apoptosis of A549… More >

  • Open Access

    ARTICLE

    VASH2 Promotes Cell Proliferation and Resistance to Doxorubicin in Non-Small Cell Lung Cancer via AKT Signaling

    Xiangbin Tan*1, Zefei Liao†1, Shuangyou Zou*, Liangyun Ma, Aimin Wang*

    Oncology Research, Vol.28, No.1, pp. 3-11, 2020, DOI:10.3727/096504019X15509383469698

    Abstract Vasohibin2 (VASH2), a proangiogenic factor, has been demonstrated to play an oncogenic role in some common human cancers. However, the detailed function of VASH2 in non-small cell lung cancer (NSCLC) has not previously been studied. In this study, we found that VASH2 was significantly upregulated in NSCLC tissues and cell lines, and its increased expression was associated with NSCLC progression and poor prognosis of patients. Knockdown of VASH2 markedly inhibited cell proliferation and P-glycoprotein expression in NSCLC cells. Overexpression of VASH2 enhanced cell proliferation, P-glycoprotein expression, as well as doxorubicin resistance in NSCLC cells. Moreover,… More >

  • Open Access

    ARTICLE

    Human umbilical cord blood mesenchymal stem cells conditioned media inhibits hypoxia-induced apoptosis in H9c2 cells by activation of the survival protein Akt

    XUHE GONG1, GUANGPU FAN2, HUI LIU1, SIJIA WANG3, RONGCHONG HUANG1,*

    BIOCELL, Vol.44, No.3, pp. 329-336, 2020, DOI:10.32604/biocell.2020.09639 - 22 September 2020

    Abstract This work aimed to study the beneficial role of human umbilical cord blood-derived mesenchymal stem cellconditioned medium (MSC-CM) in hypoxia-induced apoptosis in H9c2 cardiomyoblasts, in which the serine/heroine kinases (Akt) pathway would be involved. For this, CM was collected by culturing MSCs in serum-free DMEM medium for 24 h, and paracrine factors were analyzed by protein chip. H9c2 cells were divided into the following groups: control group, hypoxia group, MSC-CM intervention group (CM group), MSC-CM + Akt phosphorylation inhibitor (LY294002) group (LY group). Apoptosis of the H9c2 cells was tested with chromatin dye Hoechst 33342… More >

  • Open Access

    ARTICLE

    Liquiritigenin Inhibits Colorectal Cancer Proliferation, Invasion, and Epithelial-to-Mesenchymal Transition by Decreasing Expression of Runt-Related Transcription Factor 2

    Fan-Chun Meng, Jun-Kai Lin

    Oncology Research, Vol.27, No.2, pp. 139-146, 2019, DOI:10.3727/096504018X15185747911701

    Abstract Inhibition of tumor metastasis is one of the most important purposes in colorectal cancer (CRC) treatment. This study aimed to explore the effects of liquiritigenin, a flavonoid extracted from the roots of Glycyrrhiza uralensis Fisch, on HCT116 cell proliferation, invasion, and epithelial-to-mesenchymal transition (EMT). We found that liquiritigenin significantly inhibited HCT116 cell proliferation, invasion, and the EMT process, but had no influence on cell apoptosis. Moreover, liquiritigenin remarkably reduced the expression of runt-related transcription factor 2 (Runx2) in HCT116 cells. Overexpression of Runx2 obviously reversed the liquiritigenininduced invasion and EMT inhibition. Furthermore, liquiritigenin inactivated the More >

  • Open Access

    ARTICLE

    Profilin 2 Promotes Proliferation and Metastasis of Head and Neck Cancer Cells by Regulating PI3K/AKT/b-Catenin Signaling Pathway

    Kecheng Zhou*†1, Jie Chen*†1, Jiayu Wu*†1, Yangxinzi Xu, Qiaoyun Wu*†, Jingjing Yue*†, Yu Song§, Shengcun Li*†, Peng Zhou, Wenzhan Tu*†, Guanhu Yang*†, Songhe Jiang*†

    Oncology Research, Vol.27, No.9, pp. 1079-1088, 2019, DOI:10.3727/096504019X15579146061957

    Abstract Profilin 2 (PFN2) was found to be mainly expressed in neurons and involved in the development of the brain. In recent years, emerging evidence indicated that PFN2 is also significantly upregulated in various cancers including head and neck cancer (HNSC) and influences cancer cell proliferation, migration, and invasion. However, the role of PFN2 in HNSC development and progression remains unclear. The aim of our study was to investigate the role of PFN2 in the development of HNSC and its possible molecular mechanisms. Bioinformatics showed that increased expression of PFN2 in tumors correlated highly with poor… More >

  • Open Access

    ARTICLE

    CRISPR/Cas9-Mediated Gene Knockout of ARID1A Promotes Primary Progesterone Resistance by Downregulating Progesterone Receptor B in Endometrial Cancer Cells

    Haizhen Wang*, Zhenghua Tang*, Ting Li*, Menglu Liu*, Yong Li, Baoling Xing*

    Oncology Research, Vol.27, No.9, pp. 1051-1060, 2019, DOI:10.3727/096504019X15561873320465

    Abstract Medroxyprogesterone (MPA) is used for the conservative treatment of endometrial cancer. Unfortunately, progesterone resistance seriously affects its therapeutic effect. The purpose of the current study was to investigate the influence of deletion of AT-rich interactive domain 1A (ARID1A) in progesterone resistance in Ishikawa cells. Ablation of ARID1A was conducted through the CRISPR/Cas9 technology. Acquired progesterone-resistant Ishikawa (Ishikawa-PR) cells were generated by chronic exposure of Ishikawa cells to MPA. The sensitivity of the parental Ishikawa, Ishikawa-PR, and ARID1A-deficient cells to MPA and/or LY294002 was determined using the Cell Counting Kit-8 (CCK-8) assay and flow cytometry analysis.… More >

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