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  • Open Access

    ARTICLE

    Tmem39b promotes tumor progression and sorafenib resistance by inhibiting ferroptosis in hepatocellular carcinoma

    MING ZHUANG, XUE ZHANG, LU LI, LIMING WEN, JIAMIN QIN*

    Oncology Research, Vol.32, No.8, pp. 1347-1357, 2024, DOI:10.32604/or.2024.046170

    Abstract Hepatocellular carcinoma (HCC) poses a significant threat to human health. Resistance to sorafenib in the chemotherapy of HCC is a common and significant issue that profoundly impacts clinical treatment. While several members of the transmembrane (TMEM) protein family have been implicated in the occurrence and progression of HCC, the association between TMEM39b and HCC remains unexplored. This study revealed a significant overexpression of TMEM39b in HCC, which correlated with a poor prognosis. Subsequent investigation revealed that RAS-selective lethal 3 (RSL3) induced pronounced ferroptosis in HCC, and knocking down the expression of TMEM39b significantly decreased its More >

  • Open Access

    ARTICLE

    miR-557 suppresses hepatocellular carcinoma cell proliferation and migration via downregulating CBX4

    XULONG SUN1,#, WENTAO DING2,#, CHAO JIANG3, ZHIAN FANG4,*

    BIOCELL, Vol.48, No.7, pp. 1071-1079, 2024, DOI:10.32604/biocell.2024.050519

    Abstract Introduction: Hepatocellular carcinoma (HCC), a prevalent malignancy, poses significant challenges with high tumor heterogeneity and poor prognosis. MicroRNAs (miRNAs) play a pivotal role in hepatocarcinogenesis. Although abnormalities in microRNA-557 (miR-557) expression have been implicated in various cancer types, its role in HCC remains unclear. Therefore, there is a need to explore the function of microRNA-557 in HCC. Methods: Candidate miRNAs were identified through screening in GSE108724 and GSE20077. Real-time PCR was employed to analyze the expression level of miR-557 in hepatoma cell lines and tissues. Cell viability and migration assays were applied to assess the… More > Graphic Abstract

    miR-557 suppresses hepatocellular carcinoma cell proliferation and migration via downregulating CBX4

  • Open Access

    ARTICLE

    Sciadopitysin exerts anticancer effects on HepG2 hepatocellular carcinoma cells by regulating reactive oxygen species-mediated signaling pathways

    YAN-NAN LI1,#, YUN-HONG XIU2,#, YAN-JUN TANG3, JING-LONG CAO1, WEN-SHUANG HOU1, AN-QI WANG1, TIAN-ZHU LI4,*, CHENG-HAO JIN1,3,5,*

    BIOCELL, Vol.48, No.7, pp. 1055-1069, 2024, DOI:10.32604/biocell.2024.050515

    Abstract Objectives: Sciadopitysin (SP) is a flavonoid in Ginkgo biloba that exhibits various pharmacological activities. This study aimed to investigate its antitumor effects and the underlying molecular mechanism of SP in hepatocellular carcinoma (HCC) cells. Methods: Network pharmacology was used for target prediction analysis. Cell Counting Kit-8 (CCK-8) assay was used to test the cell viability. Flow cytometry was used to test the cell cycle distribution, apoptosis status, and reactive oxygen species (ROS) levels. Transwell and wound-healing assay was used to test the migration effect of SP on HepG2 cells. Western Blot assay was used to… More > Graphic Abstract

    Sciadopitysin exerts anticancer effects on HepG2 hepatocellular carcinoma cells by regulating reactive oxygen species-mediated signaling pathways

  • Open Access

    REVIEW

    Research progress on natural products against hepatocellular carcinoma

    LINGLI ZHANG1,2,#, YAN LI1,#, JINGXIN MAO1,*

    BIOCELL, Vol.48, No.6, pp. 905-922, 2024, DOI:10.32604/biocell.2024.050396

    Abstract Hepatocellular carcinoma (HCC) remains a prevalent and challenging malignancy globally, characterized by its numerous causal factors and generally unfavorable prognosis. In the relentless pursuit of effective treatment modalities, natural products have emerged as a promising and relatively non-toxic alternative, garnering significant interest. The integration of natural products with contemporary medical research has yielded encouraging therapeutic outcomes in the management of HCC. This review offers a comprehensive overview of the causal factors underlying HCC, and the diverse treatment options available, and highlights the advancements made by natural products in anti-HCC research. Particularly, we provide an outline More >

  • Open Access

    ARTICLE

    Knockdown of SLC34A2 Inhibits Hepatocellular Carcinoma Cell Proliferation and Invasion

    Yanhua Li*1, Xia Chen†1, Hong Lu*

    Oncology Research, Vol.24, No.6, pp. 511-519, 2016, DOI:10.3727/096504016X14719078133483

    Abstract The gene solute carrier family 34 (sodium phosphate), member 2 (SLC34A2), is a member of the SLC34 family. Increasing evidence suggests that SLC34A2 is involved in the development of many human carcinomas. However, its role in hepatocellular carcinoma (HCC) is still unclear. Therefore, in this study we investigated the role of SLC34A2 in HCC and explored the underlying mechanism. We found that the expression of SLC34A2 is upregulated in HCC cell lines. Knockdown of SLC34A2 obviously inhibited HCC cell proliferation, migration/invasion, and the epithelial–mesenchymal transition (EMT) phenotype. Furthermore, knockdown of SLC34A2 significantly inhibited the expression More >

  • Open Access

    ARTICLE

    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

    ARTICLE

    Knockdown of Histone Methyltransferase hSETD1A Inhibits Progression, Migration, and Invasion in Human Hepatocellular Carcinoma

    Xin-sheng Cheng*†, Shi-bo Sun*, Feng Zhong*, Kun He*, Jie Zhou*

    Oncology Research, Vol.24, No.4, pp. 239-245, 2016, DOI:10.3727/096504016X14648701448011

    Abstract Our aim was to study the expression of human SET domain containing protein 1A (hSETD1A) in hepatocellular carcinoma patients and its relationship with human hepatocellular carcinoma cell function. A total of 30 patients with hepatocellular carcinoma were enrolled in this study. The expression of hSETD1A was detected by real-time polymerase chain reaction (PCR) and Western blotting. The immortalized normal human liver cell line including SMMC-7721 was subjected to real-time PCR for hSETD1A mRNA. Furthermore, hSETD1A-small hairpin RNA (shRNA) was used to knock down hSETD1A expression in SMMC-7721 cells. Cell proliferation, cell apoptosis, and cell migration More >

  • Open Access

    ARTICLE

    Inhibition of ERK1/2 Signaling Impairs the Promoting Effects of TGF-β1 on Hepatocellular Carcinoma Cell Invasion and Epithelial–Mesenchymal Transition

    Ling Liu, Nianfeng Li, Qi Zhang, Jixiang Zhou, Ling Lin, Xinxin He

    Oncology Research, Vol.25, No.9, pp. 1607-1616, 2017, DOI:10.3727/096504017X14938093512742

    Abstract Transforming growth factor-b (TGF-β) and ERK signaling have been implicated in various human cancers including hepatocellular carcinoma, but the underlying mechanism remains largely unclear. In this study, we aimed to explore the role of ERK1/2 in the regulation of TGF-β’s promoting and suppressive activities in HCC cells. Our data showed that treatment with TGF-β1 enhanced invasion and epithelial–mesenchymal transition (EMT) in HCC HepG2 cells, accompanied with increased MMP9 production and activation of Smad2/3 and ERK1/2, but inhibited tumor cell proliferation. These effects were eliminated by treatment with SB431542, a TGF-β inhibitor. Afterward, treatment with the… More >

  • Open Access

    ARTICLE

    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

    ARTICLE

    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.25, No.8, pp. 1329-1340, 2017, DOI:10.3727/096504017X14876227286564

    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 >

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