Li Wan¹, Lin Zhang¹, Kai Fan, Zai-Xing Cheng, Quan-Chao Sun, Jian-Jun Wang

Oncology Research, Vol.24, No.3, pp. 161-170, 2016, DOI:10.3727/096504016X14618564639178

Abstract As a newly identified oncogenic long noncoding RNA (lncRNA), prostate cancer-associated transcript 6 (PCAT6) promoted cellular proliferation and colony formation of prostate cancer. However, the biological function of PCAT6 in lung cancer is still largely unknown. In this study, we found that PCAT6 is significantly increased in cancer tissues compared to normal tissues and positively correlates with metastasis of lung cancer in patients. We then examined PCAT6 expression in lung cancer cell lines and identified that PCAT6 expression was significantly elevated in lung cancer cells compared to normal human bronchial epithelial (NHBE) cells, especially in… More >

Yangjing Chen, Ruimin Zhao, Qian Zhao, Yuan Shao, Shaoqiang Zhang

Oncology Research, Vol.24, No.3, pp. 153-160, 2016, DOI:10.3727/096504016X14612603423476

Abstract Hematopoietic pre-B-cell leukemia transcription factor (PBX)-interacting protein (HPIP/PBXIP1) is a corepressor for the transcription factor PBX. Previous studies showed that HPIP is frequently overexpressed in many tumors. However, the role of HPIP in head-and-neck squamous cell carcinoma (HNSCC) has not yet been determined. Thus, we decided to investigate the effects and mechanisms of HPIP in HNSCC. Our results demonstrated that HPIP is highly expressed in human HNSCC cell lines and provides the first evidence that knockdown of HPIP obviously inhibits proliferation and migration/invasion in HNSCC cells in vitro, as well as inhibits tumor growth in More >

Kang Zhu^*, Ying He^†, Cui Xia^*, Jing Yan^*, Jin Hou^*, Demin Kong^*, Yeye Yang^*, Guoxi Zheng^*

Oncology Research, Vol.24, No.3, pp. 145-151, 2016, DOI:10.3727/096504016X14611963142290

Abstract Nasopharyngeal carcinoma (NPC) is a highly metastatic cancer, frequently occurring in Southeast Asia and Southern China. Several microRNAs (miRNAs) have been shown to have an inhibitive effect on NPC, while the effect of miR-15a on NPC remains unclear. Thus, our study aimed to investigate the potential effect of miR-15a on NPC cell proliferation, apoptosis, and possible functional mechanism. Human NPC CNE1 cells were transfected with miR-15a mimics, miR-15a inhibitors, or a control. Afterward, cell viability and apoptosis were assayed by using CCK-8, BrdU assay, and flow cytometry. Moreover, Western blot was used to detect the… 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 >

Yue-shen Wang^*1, Jing Tian^†1, Yong Han^†, Shu-mei Han^†, Sheng-bin Shi^†

Oncology Research, Vol.24, No.2, pp. 129-135, 2016, DOI:10.3727/096504016X14618564639213

Abstract We evaluated the efficacy and feasibility of the combination of gemcitabine plus vinorelbine in patients with platinum-based chemotherapy-refractory esophageal cancer. We enrolled 35 patients who received gemcitabine plus vinorelbine as second-line treatment after platinum-based chemotherapy failure between May 2009 and April 2012. Dosage: gemcitabine 1,000 mg/m² plus vinorelbine 25 mg/m² ; all drugs were administered on days 1 and 8 of a 21-day cycle, and this was continued until failure or unacceptable toxicity. A total of 125 cycles of treatment were administered, and all patients received at least two cycles of treatment (two to five cycles;… More >

Jiahao Su^*, Meiqin Cai^*, Wensheng Li^*, Bo Hou^†, Haiyong He^†, Cong Ling^†,Tengchao Huang^†, Huijiao Liu^†, Ying Guo^*

Oncology Research, Vol.24, No.2, pp. 117-128, 2016, DOI:10.3727/096504016X14612603423511

Abstract Glioblastoma (GBM) is the most common primary malignant brain tumor that nearly always results in a bad prognosis. Temozolomide plus radiotherapy (TEM+RAD) is the most common treatment for newly diagnosed GBM. With the development of molecularly targeted drugs, several clinical trials were reported; however, the efficacy of the treatment remains controversial. So we attempted to measure the dose of the molecularly targeted drug that could improve the prognosis of those patients. The appropriate electronic databases (PubMed, MEDLINE, EMBASE, and the Cochrane Library) were searched for relevant studies. A meta-analysis was performed after determining which studies… More >

Gangcan Li, Yanping Song, Yunjie Zhang, Hao Wang, Jia Xie

Oncology Research, Vol.24, No.2, pp. 109-116, 2016, DOI:10.3727/096504016X14611963142254

Abstract Acute myeloid leukemia (AML) is the most lethal hematological malignancy, and the occurrence of chemoresistance prevents the achievement of complete remission following the standard therapy. MicroRNAs have been extensively investigated as critical regulators of hematopoiesis and leukemogenesis, and they represent a promising strategy for AML therapy. In this study, we identified miR-34b as a novel regulator in myeloid proliferation and apoptosis of leukemic cells. We found that miR-34b was developmentally upregulated in plasma and myeloid cells of healthy subjects, while it was significantly reduced in blood samples of patients with AML and AML cell lines.… More >

Dongling Zou^*, Qi Zhou^†, Dong Wang^†, Lili Guan^*, Li Yuan^*†, Shaolin Li^*

Oncology Research, Vol.24, No.2, pp. 99-108, 2016, DOI:10.3727/096504016X14611963142173

Abstract It has been demonstrated that microRNAs (miRNAs) act as oncogenes or tumor suppressors in a variety of cancers. Our previous work suggested that miR-10a/b functioned as a tumor suppressor in gastric cancer, and miR-10b was also reported to be significantly downregulated in advanced stage cervical cancer tissues. However, the aberrant expression of miR-10b in cervical cancer and its possible role in cervical carcinogenesis was largely unknown. In this study, we investigated the expression of miR-10b in cervical cancer tissues, carcinoma in situ tissues, mild dysplasia, moderate dysplasia, severe dysplasia tissues, and normal controls. We found More >

Ye Lou^*1, Lei Liu^†1, Lihui Zhan^‡, Xuewei Wang^§, Hua Fan^¶

Oncology Research, Vol.24, No.2, pp. 89-97, 2016, DOI:10.3727/096504016X14597766487753

Abstract Acute lymphoblastic leukemia (ALL) is the most common childhood malignancy and causes a high rate of mortality in affected adults. Many subtypes of ALL exist with disruptions in distinct genetic pathways, including those regulated by miRNAs. Here we identify miR-187-5p as being highly upregulated in B-cell ALL and a driver of cellular proliferation and suppressor of apoptosis. We show that miR-187-5p directly targets the 3'-UTR of DKK2 to mediate these effects. We further determine that inhibition of DKK2 by miR-187-5p in Nalm-6 B cells leads to inappropriate activation of Wnt/β-catenin signaling. Together, these findings reveal More >

Shenggang Liu^*, Hongzhong Yang^†, Ying Chen^‡, Baimei He^§, Qiong Chen^§

Oncology Research, Vol.24, No.2, pp. 81-87, 2016, DOI:10.3727/096504016X14597766487717

Abstract In order to improve therapeutic efficacy, it is a current emergency to better know the mechanisms underlying cisplatin resistance in lung cancer cells. In this study, we aim to investigate the role of Krüppel-like factor 4 (KLF4) in cisplatin-resistant lung cancer cells. We developed cisplatin-resistant lung cancer cell line A549/ DDP, and then a battery of experiments was used to analyze the effects of KLF4 in cisplatin resistance of lung cancer. We found that KLF4 was significantly downregulated in cisplatin-resistant A549 cells and forced KLF4 expression inhibited cell growth and induced apoptosis. Further, we found More >