Chao Jiang^*, Xueyan Liu^†, Meng Wang^*, Guoyue Lv^*, Guangyi Wang^*

Oncology Research, Vol.27, No.9, pp. 1025-1034, 2019, DOI:10.3727/096504018X15456687424096

Abstract miR-802 has been reported to be dysregulated in multiple tumors and contribute to tumor progression. However, its role in HCC was still largely unknown. The aim of this study is to investigate the function and mechanism of miR-802 in HCC progression. The results showed that miR-802 was upregulated in the peripheral blood and tumor tissue of HCC patients, and high levels of blood miR-802 predicted poor prognosis. miR-802 had no effect on the proliferation and migration of HCC cell lines. Interestingly, the levels of CD8/CD28 and regulated in development and DNA damage response 1 (REDD1) More >

Lihui Wang, Qi Li, Zhuo Ye, Baoping Qiao

Oncology Research, Vol.27, No.9, pp. 1007-1014, 2019, DOI:10.3727/096504018X15231148037228

Abstract Renal carcinoma greatly threatens human health, but the involved molecular mechanisms are far from complete understanding. As a master oncogene driving the initiation of many other cancers, ZBTB7 has not been established to be associated with renal cancer. Our data revealed that ZBTB7 is highly expressed in renal carcinoma specimens and cell lines, compared with normal cells. The silencing of ZBTB7 suppressed the proliferation and invasion of renal cancer cells. ZBTB7 overexpression rendered normal cells with higher proliferation rates and invasiveness. An animal study further confirmed the role of ZBTB7 in the growth of renal More >

Linglan Gu, Yi Shi, Weimin Xu, Yangyang Ji

Oncology Research, Vol.27, No.8, pp. 923-933, 2019, DOI:10.3727/096504019X15518706875814

Abstract In previous investigations, we reported that peroxisome proliferator-activated receptor / (PPAR / ) activation by GW501516 inhibits proliferation and promotes apoptosis in the undifferentiated C666-1 nasopharyngeal carcinoma (NPC) cells by modulating caspase-dependent apoptotic pathway. In the present study, the mechanism by which GW501516 induces apoptosis was explored from the perspective of microRNA (miRNA) expression. Among the assayed miRNAs that were involved in regulating the expression of antiapoptotic protein Bcl-2, miR-206 was increased significantly and specifically by GW501516 in C666-1 cells at both the in vitro level and at the in vivo xenograft samples. The induction… More >

Yue Cai^*†‡, Chizhi Zhang^*†‡, Lei Zhan^*†, Liangbin Cheng^*†, Dingbo Lu^*†, Xiaodong Wang^*†, Hanlin Xu^§, Shuxue Wang^¶, Deng Wu^*†, Lianguo Ruan^#

Oncology Research, Vol.27, No.8, pp. 889-899, 2019, DOI:10.3727/096504018X15482423944678

Abstract The thorns of Gleditsia sinensis have been historically used in Chinese medicine and are considered one of the fundamental therapeutic herbs. Its anticancer effects are currently being explored. Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer and still requires the development of new drugs with higher efficiency. By using a rat HCC model implanted with cancerous Walker-256 cells, the therapeutic effects of G. sinensis extract (GSE) were assessed, as well as its regulatory effects on miRNAs. GSE significantly restored liver morphology and dramatically induced cell apoptosis in HCC rats. In addition, miR-21/181b/183 was More >

Qing Wei¹, Rui Zhu¹, Junying Zhu, Rongping Zhao, Min Li

Oncology Research, Vol.27, No.7, pp. 827-834, 2019, DOI:10.3727/096504018X15462920753012

Abstract Emerging evidence suggests that 17β-estradiol (E2) and estrogen receptor (ER) signaling are protective against hepatocellular carcinoma (HCC). In our previous study, we showed that E2 suppressed the carcinogenesis and progression of HCC by targeting NLRP3 inflammasome activation, whereas the molecular mechanism by which the NLRP3 inflammasome initiated cancer cell death was not elucidated. The present study aimed to investigate the effect of NLRP3 inflammasome activation on cell death pathways and autophagy of HCC cells. First, we observed an increasing mortality in E2-treated HCC cells, and then apoptotic and pyroptotic cell death were both detected. The… More >

Zhenghua Fei^*1, Zhenxiang Deng^†1, Lingyang Zhou^‡, Kejie Li^*, Xiaofang Xia^*, Raoying Xie^*

Oncology Research, Vol.27, No.7, pp. 801-807, 2019, DOI:10.3727/096504018X15446984186056

Abstract Nasopharyngeal cancer (NPC) is a malignant epithelial carcinoma of the head and neck. Cancer therapy targeting programmed cell death protein-1 (PD-1) or programmed death ligand-1 (PD-L1) is revolutionary. However, the tumorigenic mechanism of PD-L1 is not yet clear in NPC. Here we demonstrated an oncogenic role of PD-L1 via activating PI3K/AKT in NPC cells. PD-L1 overexpression was frequently detected in NPC biopsies and cell lines by qRT-PCR. PD-L1 overexpression and knockdown demonstrated that PD-L1 promoted NPC cell invasion and metastasis in vitro and in vivo. Mechanistically, PD-L1 prominently activated the epithelial–mesenchymal transition (EMT) process in More >

Youwei Zhang^*, Bi Chen^†, Yongsheng Wang^‡, Qi Zhao^‡, Weijun Wu^§, Peiying Zhang^*, Liyun Miao^‡, Sanyuan Sun^*

Oncology Research, Vol.27, No.7, pp. 751-761, 2019, DOI:10.3727/096504018X15372657298381

Abstract Acquired resistance remains a key challenge in epidermal growth factor receptor (EGFR)–tyrosine kinase inhibitors (TKIs) therapy in lung adenocarcinoma (LUAD). Recent studies have shown that Notch signaling is associated with drug resistance. However, its role and possible mechanisms in EGFR-TKI resistance are not yet clear. In our study, we found that among four members of NOTCH1–4, only NOTCH3 was upregulated in LUAD tissues and TKI-resistant cell line (HCC827GR6). Knockdown of NOTCH3 by siRNA significantly inhibited proliferative ability, and decreased colony and sphere formation in HCC827GR6 cells. Then miR-150 was identified as a posttranscriptional regulator of… More >

Yankun Zhang^*, Wei Qian^*, Feng Feng^†, Qian Cao^*, Yanqi Li^*, Ying Hou^*, Luyang Zhang^*, Jufeng Fan^*

Oncology Research, Vol.27, No.3, pp. 371-377, 2019, DOI:10.3727/096504018X15178740729367

Abstract This study aimed to investigate the effect and underlying mechanism of lncRNA CASC2 in malignant melanoma (MM). Expression of CASC2 in MM tissues and cells was detected. A375 cells were transfected with pc-CASC2, si-CASC2, miR-18a-5p inhibitor, or corresponding controls, and then cell proliferation, migration, and invasion were detected using MTT assay, colony formation assay, and Transwell analysis, respectively. The relationship of miR-18a-5p and CASC2 or RUNX1 was detected by luciferase reporter assay. The levels of CASC2 and RUNX1 were significantly reduced in MM tissues compared with normal skin tissues or cells, while the miR-18a-5p level… More >

Xiyan Sun^*1, Chao Zhang^†1, Yang Cao^†, Erbiao Liu^*

Oncology Research, Vol.27, No.3, pp. 317-323, 2019, DOI:10.3727/096504018X15228863026239

Abstract miR-150 has been demonstrated to inhibit tumor progression in various human cancers, including colorectal cancer, ovarian cancer, and thyroid cancer. However, the role of miR-150 in melanoma remains to be determined. In this study, we found that miR-150 was underexpressed in melanoma tissues and cell lines. Through transfection of miR-150 mimics, we found that miR-150 significantly inhibited the proliferation, migration, and invasion of melanoma cells. In mechanism, we found that MYB was a target of miR-150 in melanoma cells. Overexpression of miR-150 significantly inhibited mRNA and protein levels of MYB in melanoma cells. Moreover, there More >

Xinshan Cao^*, Ling Xu^†, Quanyuan Liu^*, Lijuan Yang^‡, Na Li^§, Xiaoxiao Li^*

Oncology Research, Vol.27, No.3, pp. 301-309, 2019, DOI:10.3727/096504018X15213058045841

Abstract Our study aimed to investigate the roles and possible regulatory mechanism of miR-1277 in the development of hepatocellular carcinoma (HCC). HCC patients were identified from patients who were diagnosed with focal liver lesions using magnetic resonance imaging (MRI). The expression levels of miR-1277 in the serum of HCC patients and HepG2 cells were measured. Then miR-1277 mimic, miR-1277 inhibitor, or scramble RNA was transfected into HepG2 cells. The effects of miR-1277 overexpression and suppression on HepG2 cell proliferation, migration, and invasion were then investigated. Additionally, the expression levels of epithelial– mesenchymal transition (EMT)-related markers, including… More >