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 >

Xue-fei Jin, Hai Li, Shi Zong, Hong-yan Li

Oncology Research, Vol.24, No.6, pp. 477-485, 2016, DOI:10.3727/096504016X14685034103716

Abstract Collagen triple helix repeat containing-1 (CTHRC1), a secreted glycoprotein, is frequently upregulated in human cancers. However, the functional role of CTHRC1 in renal cell carcinoma (RCC) remains unclear. Thus, the aim of this study was to explore the role of CTHRC1 in RCC. Our results demonstrated that CTHRC1 was upregulated in RCC tissues and cell lines. Knockdown of CTHRC1 significantly inhibits the proliferation in RCCs. Furthermore, knockdown of CTHRC1 significantly inhibited the epithelial-to-mesenchymal transition (EMT) process in RCCs, as well as suppressed RCC cell migration and invasion. Mechanistically, knockdown of CTHRC1 inhibited the expression of More >

Gaowu Hu^*, Ye Xu^*, Wenquan Chen^*, Jiandong Wang^†, Chunying Zhao^†1, Ming Wang^*1

Oncology Research, Vol.24, No.6, pp. 455-461, 2016, DOI:10.3727/096504016X14685034103635

Abstract Breast cancer is a highly prevalent disease affecting women. The association of IQ motif containing GTPaseactivating protein 3 (IQGAP3) and breast cancer is poorly defined. Here we reported that IQGAP3 is a key regulator of cell proliferation and metastasis during breast cancer progression. The expression of IQGAP3 was significantly increased in breast tissues compared to nontumor tissues at both protein and mRNA levels. Furthermore, IQGAP3 had a high expression level in ZR-75-30 and BT474 compared to other breast cancer cell lines. Depletion of IQGAP3 through RNA interference in ZR-75-30 and BT474 significantly inhibited cell proliferation. More >

Ping Zhao^*, Hai-Tao Guan^†, Zhi-Jun Dai^†, Yu-Guang Ma^†, Xiao-Xu Liu^†, Xi-Jing Wang^†

Oncology Research, Vol.24, No.6, pp. 437-445, 2016, DOI:10.3727/096504016X14685034103554

Abstract Sparc/osteonectin, cwcv, and kazal-like domains proteoglycan (testican) 1 (SPOCK1), known as testican-1, were found to be involved in the development and progression of tumors. However, in colorectal cancer (CRC), the expression pattern of SPOCK1 and its functional role remain poorly investigated. In the present study, we explored the role of SPOCK1 in CRC. Our results demonstrated that SPOCK1 is overexpressed in CRC cell lines. SPOCK1 silencing significantly inhibited the proliferation in vitro and the tumor growth in vivo. Furthermore, SPOCK1 silencing significantly attenuated the migration/invasion by reversing the EMT process in CRC cells. Finally, knockdown More >

Feng Jiang^*1, Yan Shi^†1, Hong Lu^†, Guojun Li^*

Oncology Research, Vol.24, No.5, pp. 381-389, 2016, DOI:10.3727/096504016X14685034103392

Abstract Armadillo repeat-containing protein 8 (ARMC8) plays an important role in regulating cell migration, proliferation, tissue maintenance, signal transduction, and tumorigenesis. However, the expression pattern and role of ARMC8 in osteosarcoma are still unclear. In this study, our aims were to examine the effects of ARMC8 on osteosarcoma and to explore its underlying mechanism. Our results demonstrated that ARMC8 was overexpressed in osteosarcoma cell lines. Knockdown of ARMC8 significantly inhibited osteosarcoma cell proliferation in vitro and markedly inhibited xenograft tumor growth in vivo. ARMC8 silencing also suppressed the epithelial– mesenchymal transition (EMT) phenotype, as well as More >

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 >

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 >

Jiankang Zhu, Chongzhong Liu, Fengyue Liu, Yadong Wang, Min Zhu

Oncology Research, Vol.24, No.3, pp. 137-144, 2016, DOI:10.3727/096504016X14611963142218

Abstract PFTK1 is a member of the cyclin-dependent kinase (CDK) family and is upregulated in many types of tumors. However, its expression and role in colon cancer remain unclear. In this study, we aimed to investigate the expression and function of PFTK1 in colon cancer. Our results showed that PFTK1 was highly expressed in colon cancer cell lines. The in vitro experiments demonstrated that knockdown of PFTK1 inhibited the proliferation, migration, and invasion of colon cancer cells as well as the epithelial-to-mesenchymal transition (EMT) progress. Furthermore, knockdown of PFTK1 suppressed the expression of Shh as well More >

Ping He^*, Hong-xia Zhang^†, Chang-yu Sun^*, Chun-yong Chen^‡, He-qing Jiang^*

Oncology Research, Vol.24, No.1, pp. 25-32, 2016, DOI:10.3727/096504016X14575597858609

Abstract The SASH1 (SAM- and SH3-domain containing 1) gene, a member of the SLY (SH3 domain containing expressed in lymphocytes) family of signal adapter proteins, has been implicated in tumorigenesis of many types of cancers. However, the role and mechanism of SASH1 in the invasion and metastasis of hepatocarcinoma are largely unknown. In this study, we investigated the role and mechanism of SASH1 in the invasion and metastasis of hepatocarcinoma. Our results showed that SASH1 was lowly expressed in hepatocarcinoma cell lines. The in vitro experiments showed that overexpression of SASH1 inhibited the proliferation and migration/invasion More >

Wei Zong^*, Chen Yu^†, Ping Wang^*, Lei Dong^‡

Oncology Research, Vol.24, No.1, pp. 17-23, 2016, DOI:10.3727/096504016X14570992647203

Abstract The epithelial–mesenchymal transition (EMT) is considered to be one of the critical steps in gastric cancer cell invasion and metastasis. SAM- and SH3-domain containing 1 (SASH1), a member of the SLY family of signal adapter proteins, is a candidate for tumor suppression in several cancers. However, the biological role of SASH1 in gastric cancer remains largely unknown. Therefore, the purpose of this study was to investigate the impact of SASH1 on the biological behavior of gastric cancer cells treated with transforming growth factor (TGF)-β1. In the current study, we provide evidence that SASH1 was lowly More >