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  • Open Access


    Chemokine-like factor 1 (CKLF1) is expressed in myocardial ischemia injury in vivo and in vitro


    BIOCELL, Vol.48, No.6, pp. 981-990, 2024, DOI:10.32604/biocell.2024.050011

    Abstract Introduction: Chemokine-like factor 1 (CKLF1) is a chemokine that is overexpressed in several diseases. Our previous findings revealed a significant increase in CKLF1 expression in the ischemic brain, suggesting its potential as a therapeutic target for ischemic stroke. Methods: In this study, we examined the expression dynamics of CKLF1 in both in vivo and in vitro models of ischemic cardiac injury. Myocardial infarction (MI) was induced in vivo by ligation of the left anterior descending artery (LAD) of the rat heart. The levels of CKLF1, Creatine Kinase MB Isoenzyme (CK-MB), and Lactate dehydrogenase (LDH) in the serum were… More > Graphic Abstract

    Chemokine-like factor 1 (CKLF1) is expressed in myocardial ischemia injury <i>in vivo</i> and <i>in vitro</i>

  • Open Access


    OPA3 overexpression modulates lipid droplet production and sensitizes colorectal cancer cells to bevacizumab treatment


    BIOCELL, Vol.48, No.6, pp. 971-980, 2024, DOI:10.32604/biocell.2024.049466

    Abstract Background: Colorectal cancer (CRC) represents a substantial risk to public health. Bevacizumab, the first US FDA-approved antiangiogenic drug (AAD) for human CRC treatment, faces resistance in patients. The role of lipid metabolism, particularly through OPA3-regulated lipid droplet production, in overcoming this resistance is under investigation. Methods: The protein expression pattern of OPA3 in CRC primary/normal tissues was evaluated by bioinformatics analysis. OPA3-overexpressed SW-480 and HCT-116 cell lines were established, and bevacizumab resistance and OPA3 effects on cell malignancy were examined. OPA3 protein/mRNA expression and lipid droplet-related genes were measured with Western blot and qRT-PCR. OPA3… More > Graphic Abstract

    OPA3 overexpression modulates lipid droplet production and sensitizes colorectal cancer cells to bevacizumab treatment

  • Open Access


    Potential Role of CD133 Expression in the Susceptibility of Human Liver Cancer Stem-Like Cells to TRAIL

    Su-Hoon Lee, Suh-Kyung Hyun, Hak-Bong Kim, Chi-Dug Kang, Sun-Hee Kim

    Oncology Research, Vol.24, No.6, pp. 495-509, 2016, DOI:10.3727/096504016X14685034103950

    Abstract Hepatocellular carcinoma (HCC) is one of the most common malignancies, with a poor prognosis and high recurrence rate. In the present study, we identified CD133, one of the markers of cancer stem cells, as a novel molecular target of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). In four human HCC cell lines established from primary HCC tumors, we found that CD133-high human liver cancer stem-like cells (CD133hi) derived from the SNU-475 cell line were highly susceptible to TRAIL compared to other HCC cell lines with a small population of CD133. CD133hi SNU-475 cells showed upregulation of TRAIL… More >

  • Open Access


    TIPE2 Overexpression Suppresses the Proliferation, Migration, and Invasion in Prostate Cancer Cells by Inhibiting PI3K/Akt Signaling Pathway

    Qiang Lu, Zhe Liu, Zhuo Li, Jia Chen, Zhi Liao, Wan-rui Wu, Yuan-wei Li

    Oncology Research, Vol.24, No.5, pp. 305-313, 2016, DOI:10.3727/096504016X14666990347437

    Abstract Tumor necrosis factor-a (TNF-a)-induced protein 8-like 2 (TNFAIP8L2, TIPE2) is involved in the invasion and metastasis of human tumors. However, the functional role of TIPE2 in prostate cancer remains unclear. In the present study, we explored the role of TIPE2 in prostate cancer and cancer progression including the molecular mechanism that drives TIPE2-mediated oncogenesis. Our results showed that TIPE2 was lowly expressed in human prostate cancer tissues and cell lines. In addition, restored TIPE2 obviously inhibits proliferation in prostate cancer cells. TIPE2 overexpression also suppresses the epithelial–mesenchymal transition (EMT) process and migration/invasion in prostate cancer More >

  • Open Access


    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


    Knockdown of Upregulated Gene 11 (URG11) Inhibits Proliferation, Invasion, and b-Catenin Expression in Non-Small Cell Lung Cancer Cells

    Zhe-liang Liu*, Jiao Wu, Lin-xian Wang, Jin-feng Yang, Gao-ming Xiao*, Hui-ping Sun, Yue-jun Chen*

    Oncology Research, Vol.24, No.3, pp. 197-204, 2016, DOI:10.3727/096504016X14648701447850

    Abstract Upregulated gene 11 (URG11), a new gene upregulated by hepatitis B virus X protein, was found to be involved in the development and progression of several tumors. However, the role of URG11 in human non-small cell lung cancer (NSCLC) has not yet been determined. Therefore, the aim of the present study was to explore the role of URG11 in human NSCLC. Our results found that URG11 was highly expressed in human NSCLC tissues compared with matched normal lung tissues, and higher levels were found in NSCLC cell lines in comparison to the normal lung cell More >

  • Open Access


    Knockdown of PFTK1 Expression by RNAi Inhibits the Proliferation and Invasion of Human Non-Small Lung Adenocarcinoma Cells

    Mei-han Liu*, Shao-min Shi, Kai Li, En-qi Chen*

    Oncology Research, Vol.24, No.3, pp. 181-187, 2016, DOI:10.3727/096504016X14635761799038

    Abstract PFTK1 (PFTAIRE protein kinase 1), also named CDK14 (cyclin-dependent kinase 14), is a member of the cell division cycle 2 (CDC2)-related protein kinase family. It is highly expressed in several malignant tumors. However, the role of PFTK1 in the progression of non-small cell lung cancer (NSCLC) is still elusive. In this study, we aimed to explore the expression and function of PFTK1 in NSCLC cells. Our results showed that PFTK1 was significantly upregulated in human NSCLC cell lines. Silencing the expression of PFTK1 inhibited the proliferation of NSCLC cells. In addition, silencing the expression of More >

  • Open Access


    Inhibition of MMP-2 Expression Enhances the Antitumor Effect of Sorafenib in Hepatocellular Carcinoma by Suppressing the PI3K/AKT/mTOR Pathway

    Wenliang Tan*†1, Sicong Zhu*†1, Jun Cao*†, Lei Zhang*†, Wenda Li*†, Kairui Liu*†, Jinyi Zhong, Changzhen Shang*†, Yajin Chen*†

    Oncology Research, Vol.25, No.9, pp. 1543-1553, 2017, DOI:10.3727/096504017X14886444100783

    Abstract Sorafenib has been globally approved as the standard treatment for patients with advanced hepatocellular carcinoma (HCC). However, the response rate of HCC patients to sorafenib is limited because of tumor recurrence and metastasis. Therefore, seeking combined therapeutic strategies with sorafenib is necessary to improve the antitumor efficiency. Here we demonstrated that expression of MMP-2 is positively correlated with the migration ability of HCC cells. Cells with a higher MMP-2 expression (SK-HEP-1 cells) were less sensitive to sorafenib than those with lower MMP-2 expression (HepG2 cells). Cotreatment of cells with SB-3CT and sorafenib more strongly inhibited… More >

  • Open Access


    Overexpression of T-box Transcription Factor 5 (TBX5) Inhibits Proliferation and Invasion in Non-Small Cell Lung Carcinoma Cells

    Ruoting Ma*†, Yu Yang*, Qiuyun Tu, Ke Hu

    Oncology Research, Vol.25, No.9, pp. 1495-1504, 2017, DOI:10.3727/096504017X14883287513729

    Abstract T-box transcription factor 5 (TBX5), a member of the conserved T-box transcription factor family that functions in organogenesis and embryogenesis, has recently been identified as a critical player in cancer development. The aim of this study was to determine the role of TBX5 in non-small cell lung carcinoma (NSCLC). Immunohistochemistry was used to detect the correlation between levels of TBX5 and clinicopathological features of NSCLC patients in tissue microarray. Expression of TBX5 in NSCLC tissues and cell lines was evaluated by quantitative PCR and Western blot. The role of TBX5 in regulating proliferation, colony formation,… More >

  • Open Access


    Overexpression of MicroRNA-216a Suppresses Proliferation, Migration, and Invasion of Glioma Cells by Targeting Leucine-Rich Repeat-Containing G Protein-Coupled Receptor 5

    Junfeng Zhang*1, Kun Xu†1, Lili Shi*, Li Zhang*, Zhaohua Zhao*, Hao Xu*, Fei Liang*, Hongbo Li*, Yan Zhao*, Xi Xu*, Yingfang Tian

    Oncology Research, Vol.25, No.8, pp. 1317-1327, 2017, DOI:10.3727/096504017X14874323871217

    Abstract Increasing studies have suggested that microRNAs (miRNAs) are involved in the development of gliomas. MicroRNA-216a has been reported to be a tumor-associated miRNA in many types of cancer, either as an oncogene or as a tumor suppressor. However, little is known about the function of miR-216a in gliomas. The present study was designed to explore the potential role of miR-216a in gliomas. We found that miR-216a was significantly decreased in glioma tissues and cell lines. Overexpression of miR-216a significantly suppressed the proliferation, migration, and invasion of glioma cells. Leucine-rich repeat-containing G protein-coupled receptor 5 (LGR5) More >

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