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 >

Yuefeng Ma^*, Jie Feng^†, Xin Xing^‡, Bin Zhou^*, Shaomin Li^*, Wei Zhang^*, Jiantao Jiang^*, Jin Zhang^*, Zhe Qiao^*, Liangzhang Sun^*, Zhenchuan Ma^*, Ranran Kong^*

Oncology Research, Vol.24, No.1, pp. 9-15, 2016, DOI:10.3727/096504016X14570992647168

Abstract The ribosomal protein (RP)–p53 pathway has been shown to play a key role in apoptosis and senescence of cancer cells. miR-1908 is a newly found miRNA that was reported to have prognostic potential in melanoma. However, its role and mechanism in the progression of non-small cell lung cancer (NSCLC) are largely unknown. In this study, we found that expression of miR-1908 was significantly downregulated in human NSCLC cell lines, including SK-MES-1, A549, and NCI-H460. Then the role of miR-1908 in NSCLC cell proliferation was explored. The miR-1908 mimic was transfected into NSCLC cell lines, and… More >

Yifan Zhao^*†1, Longxiao Wang^*1, Qianyi Huang^*‡, Youqin Jiang^*, Jingdong Wang^*, Liyuan Zhang^‡§, Ye Tian^‡§, Hongying Yang^*§

Oncology Research, Vol.24, No.1, pp. 1-7, 2016, DOI:10.3727/096504016X14570992647087

Abstract Although medically inoperable patients with stage I non-small cell lung cancer cells (NSCLC) are often treated with stereotactic body radiation therapy, its efficacy can be compromised due to poor radiosensitivity of cancer cells. Inhibition of transforming growth factor-β1 (TGF-β1) using LY364947 and LY2109761 has been demonstrated to radiosensitize cancer cells such as breast cancer, glioblastoma, and lung cancer. Our previous results have demonstrated that another potent and selective inhibitor of TGF-β1 receptor kinases, SB431542, could radiosensitize H460 cells both in vitro and in vivo. In the present study, we investigated whether SB431542 could radiosensitize other… More >

Yan Zhen^*1, Dongming Li^*†1, Wen Li^*, Weimin Yao^*†1, Aibing Wu^‡, Jing Huang^‡, Hongli Gu^*†, Yujie Huang^*†, Yajun Wang^*, Jun Wu^*†, Min Chen^*†, Dong Wu^*†, Quanchao Lyu^*, Weiyi Fang^§, Bin Wu^*†

Oncology Research, Vol.23, No.1-2, pp. 61-68, 2015, DOI:10.3727/096504015X14478843952861

Abstract It is largely recognized that PDCD4 is frequently lost in tumors of various origins, including lung cancer, and its loss contributes to tumor progression. However, its role and molecular mechanism remain largely unexplored in non-small cell lung cancer (NSCLC). In this study, downregulated PDCD4 mRNA expression was found in NSCLC tissues compared to their corresponding paracarcinoma tissues and distal paracarcinoma tissues. Induced expression of PDCD4 inhibited cell growth and proliferation and cell cycle transition in vitro. Conversely, knocking down PDCD4 expression promoted cell growth and proliferation. Mechanistically, PDCD4 inactivated PI3K/Akt signaling and its downstream cell More >

Fei Liu^*1, Bihua Lin^*1, Xin Liu^*, Wenzhang Zhang^*, Erying Zhang^*, Liang Hu^*, Yuefan Ma^*, Xiangyong Li^*, Xudong Tang^*†

Oncology Research, Vol.23, No.3, pp. 109-118, 2015, DOI:10.3727/096504015X14496932933610

Abstract Extracellular signal-regulated kinase (ERK)1/2 signaling pathway plays a critical role in regulating tumor angiogenesis. Our previous studies have demonstrated that HPV-16 oncoproteins enhanced hypoxia-inducible factor-1α (HIF-1α) protein accumulation and vascular endothelial growth factor (VEGF) and interleukin-8 (IL-8) expression in non-small cell lung cancer (NSCLC) cells, thus contributing to angiogenesis. In this study, we further investigated the role of ERK1/2 signaling pathway in HPV-16 oncoprotein-induced HIF-1α, VEGF, and IL-8 expression and in vitro angiogenesis in NSCLC cells. Our results showed that HPV-16 E6 and HPV-16 E7 oncoproteins promoted the activation of ERK1/2 signaling pathway in A549 More >