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 >

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 (CD133^hi) derived from the SNU-475 cell line were highly susceptible to TRAIL compared to other HCC cell lines with a small population of CD133. CD133^hi SNU-475 cells showed upregulation of TRAIL… More >

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 >

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 >

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 >

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 >

Hui Li^*, Zhigang Xiang^*, Yan Liu^*, Bin Xu^*, Jianzhou Tang^†

Oncology Research, Vol.25, No.8, pp. 1269-1282, 2017, DOI:10.3727/096504017X14850151453092

Abstract MicroRNAs (miRs), a class of small noncoding RNAs, are key gene regulators through inducing translational repression or degradation of their target genes. However, the regulatory mechanism of miR-133b underlying hepatocellular carcinoma (HCC) growth and metastasis remains largely unclear. Here we found that miR-133b was significantly downregulated in HCC tissues and cell lines. Moreover, low miR-133b levels were significantly associated with the malignant progression of HCC. LASP1, upregulated in HCC tissues and cell lines, was then identified as a novel target of miR-133b in HCC HepG2 and Hep3B cells. Moreover, the increased expression of LASP1 was… More >

Tinghui Jiang^*, Mengfan Li^†, Qiuyin Li^‡, Zhiqiang Guo^§, Xianjun Sun^‡, Xufeng Zhang^§, Yan Liu^‡, Wenyi Yao^‡, Ping Xiao^*

Oncology Research, Vol.25, No.7, pp. 1117-1127, 2017, DOI:10.3727/096504016X14821952695683

Abstract Some microRNAs (miRs) have been demonstrated to play promoting or tumor-suppressing roles in the development and progression of hepatocellular carcinoma (HCC). However, the regulatory mechanism of miR-98-5p in HCC still remains largely unclear. In the present study, our data showed that miR-98-5p was significantly downregulated in 84 cases of HCC tissues compared to the matched adjacent nontumor tissues. In addition, downregulation of miR-98-5p was associated with tumor size, portal vein tumor embolus, node metastasis, and clinical stage in HCC. HCC patients with low expression of miR-98-5p showed a shorter survival time compared with those with… More >

Nan Zhu¹, Mahui Si¹, Ning Yang, Yingying Jing, Yong Fu, Xijun Zhao, Zhipeng Lin, Guangshun Yang

Oncology Research, Vol.25, No.6, pp. 1001-1008, 2017, DOI:10.3727/096504016X14796039599926

Abstract Ras-association domain family 6 (RASSF6), a member of the RASSF family, is frequently downregulated in various types of cancer. However, the roles of RASSF6 in human hepatocellular carcinoma (HCC) are still unclear. In this study, we investigated the biological functions and related molecular mechanisms in HCC. Our results found that RASSF6 is expressed in low amounts in HCC tissues and cell lines. Overexpression of RASSF6 obviously inhibited the proliferation, invasion, and EMT process in HCC cells. Furthermore, overexpression of RASFF6 greatly downregulated the protein levels of phosphorylated focal adhesion kinase (FAK), MMP-2, and MMP-9 in More >

Xin Jin^*, Shenghua Tian^†, Pingping Li^‡

Oncology Research, Vol.25, No.6, pp. 939-946, 2017, DOI:10.3727/096504016X14809827856524

Abstract Hepatocellular carcinoma (HCC) is one of the most common malignant diseases in the world. Mutations, overexpression, and improper recruitment of HATs can lead to tumorigenesis. HAT1 is the first histone acetyltransferase identified and is related with developing HCC, but the mechanism is still unclear. Interestingly, we found that HAT1 was upregulated in HCC patient specimens and showed that its upregulation facilitates HCC cell growth in vitro and in vivo. Moreover, we demonstrated that HAT1 promoted glycolysis in HCC cells and knockdown of HAT1 sensitized HCC cells to apoptotic death induced by cisplatin. Our results suggest More >