Wang Weihua, Chen Jie, Dai Jinhua, Zhang Burong, Wang Feng, Sun Yizhe

Oncology Research, Vol.24, No.5, pp. 345-351, 2016, DOI:10.3727/096504016X14685034103194

Abstract THIS ARTICLE WAS WITHDRAWN BY THE PUBLISHER IN NOVEMBER 2020 More >

Yaqiong Tian^*1, Zengli Zhang^†1, Liyun Miao^*, Zhimin Yang^‡, Jie Yang^*, Yinhua Wang^§, Danwen Qian^¶, Hourong Cai^*, Yongsheng Wang^*

Oncology Research, Vol.24, No.5, pp. 295-303, 2016, DOI:10.3727/096504016X14648701447814

Abstract Recently, epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) have revolutionized nonsmall cell lung cancer (NSCLC) treatment. However, resistance remains a major obstacle. Anexelekto (AXL) is a member of receptor tyrosine kinases (RTKs) and shares the same downstream signaling pathways with EGFR, such as PI3K/AKT and MAPK/ERK. AXL overexpression in resistant tumors has been implicated in many previous studies in vitro and in vivo. In this study, we further examined whether expression of AXL and its downstream targets increased in gefitinib-resistant PC9 cells (PC9GR). In addition, we hypothesize that knocking down AXL in PC9GR and… More >

Xuguang Wang^*, Zhe Chen^†

Oncology Research, Vol.24, No.4, pp. 271-277, 2016, DOI:10.3727/096504016X14666990347473

Abstract Cullin 4B (CUL4B), a scaffold protein that assembles CRL4B ubiquitin ligase complexes, was found to be overexpressed in many types of tumors. However, the expression pattern and role of CUL4B in non-small cell lung cancer (NSCLC) remain largely unknown. Therefore, in the present study, we investigated the role of CUL4B in NSCLC, and the underlying mechanism was also explored. Our results showed that CUL4B was highly expressed in NSCLC cell lines. Silencing CUL4B obviously inhibited proliferation and migration/invasion of NSCLC cells, and it also suppressed the epithelial–mesenchymal transition (EMT) progress in NSCLC cells. Furthermore, knockdown More >

Shengchao Zhang, Jun Yuan, Ruheng Zheng

Oncology Research, Vol.24, No.4, pp. 263-269, 2016, DOI:10.3727/096504016X14666990347392

Abstract Recently, deubiquitinating enzymes (DUBs) are emerging as new regulators in cancer progression. However, understanding of the involvement of DUBs in non-small cell lung cancer (NSCLC) is just beginning. In this study, we investigated the expression and biological function of ubiquitin-specific peptidase 17 (USP17) in NSCLC progression in vitro and in vivo. We found that the expression of USP17 was higher than in a normal control. We further efficiently depleted USP17 expression in two different NSCLC cells, A549 and H1299. The anchorage-independent growth ability of these cells, estimated by soft agar colony formation assay, was significantly More >

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 >

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 >

Baohong Yang^*1, Aiying Qin^†1, Kongyuan Zhang^‡, Haipeng Ren^*, Shuzhen Liu^*, Xiaolei Liu^§, Xiangpo Pan^¶, Guohua Yu^*

Oncology Research, Vol.25, No.9, pp. 1601-1606, 2017, DOI:10.3727/096504017X14928634401178

Abstract Epithelial growth factor receptor (EGFR) mutations are present in 10%–26% of non-small cell lung cancer (NSCLC) tumors and are associated with the response to tyrosine kinase inhibitors (TKIs). This study aimed to detect and quantify the presence of circulating tumor cells (CTCs) in EGFR-mutant NSCLC patients and investigate their possible role in providing prognostic information. Enrolled patients received erlotinib (150 mg) or gefitinib (250 mg) orally once daily as the first-line treatment. Serial blood samples were taken at baseline (CTC-d0) and on day 28 (CTC-d28) following the initiation of erlotinib/gefitinib for detection of CTCs using… More >

Yingbo Xue, Tingting Ni, Ying Jiang, Yong Li

Oncology Research, Vol.25, No.8, pp. 1305-1316, 2017, DOI:10.3727/096504017X14850182723737

Abstract Growth arrest-specific transcript 5 (GAS5) has been demonstrated to correlate with clinicopathological characteristics and serve as a tumor suppressor in non-small cell lung cancer (NSCLC). However, the underlying mechanism of the competing endogenous RNA (ceRNA) regulatory network involving GAS5 in NSCLC remains to be elucidated. In this study, qRT-PCR results showed that GAS5 was downregulated and miR-135b was upregulated in NSCLC tissues and cells. The expressions of GAS5 and miR-135b changed inversely in response to irradiation. Gain-of-function experiments revealed that GAS5 overexpression and miR-135b downregulation significantly suppressed tumorigenesis by repressing cell proliferation and invasion, and More >

Yan Zhen^*1, Jia Liu^*†1, Yujie Huang^*†1, Yajun Wang^*, Wen Li^*†, Jun Wu^*†

Oncology Research, Vol.25, No.7, pp. 1109-1116, 2017, DOI:10.3727/096504016X14800889609439

Abstract Although increasing evidence indicates that the deregulation of microRNAs (miRNAs) contributes to tumorigenesis and invasion, little is known about the role of miR-133b in human non-small cell lung cancer (NSCLC). In the present study, we revealed that the introduction of miR-133b dramatically suppressed NSCLC cell growth, migration, and invasion in vitro. On the contrary, miR-133b inhibitors promoted cell growth, migration, and invasion in vitro. Further studies revealed that matrix metallopeptidase 9 (MMP9) is a direct target gene of miR-133b. Silencing MMP9 inhibited cell growth, migration, and invasion of NSCLC cells, which was consistent with the More >

Yongcheng Mei^*, Jinchun Si^†, Yun Wang^‡, Zhuangshi Huang^§, Haiwen Zhu^*, Shijun Feng^*, Xuezhi Wu^*, Liwen Wu^*

Oncology Research, Vol.25, No.6, pp. 1027-1037, 2017, DOI:10.3727/096504016X14822800040451

Abstract Previous studies reported that elevated expression of long noncoding RNA (lncRNA) GAS5 led to the arrest of non-small cell lung cancer (NSCLC) cell growth and a promotion of apoptosis both in vitro and in vivo. However, its underlying molecular mechanism in NSCLC is still unclear. In the present study, we noted that GAS5 was downregulated in NSCLC tissues and cells and was negatively correlated with miR-23a expression. Luciferase reporter assay and qRT-PCR analysis demonstrated that GAS5 directly interacted with miR-23a and reversely regulated its expression. miR-23a overexpression markedly promoted NSCLC cell proliferation and invasion, while More >