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 >

Tao Liang, Xiao-Yong Hu, Yong-Hui Li, Bin-Qiang Tian, Zuo-Wei Li, Qiang Fu

Oncology Research, Vol.24, No.5, pp. 371-380, 2016, DOI:10.3727/096504016X14685034103356

Abstract MicroRNA-21 (miRNA-21), a kind of short, noncoding RNAs, functioned as a tumor marker and was upregulated in renal cell carcinoma (RCC). However, the underlying mechanisms of miRNA-21 in RCC were uncertain. Therefore, the effects and mechanisms of miRNA-21 on the proliferation, differentiation, and apoptosis of cultured human RCC cells were further investigated in this study. After slicing miRNA-21 in RCC cells, the viability, mRNA expression of C/EBPα and PPARγ, caspase 3 activity, and protein expression of mTOR, STAT3, and pSTAT3 were determined. It was found that knockdown of miRNA-21 downregulated the optical density (OD) value More >

Zhenhua Zhao¹, Hui Liu¹, Junqing Hou, Tieqiang Li, Xinyi Du, Xiaolei Zhao, Wenchao Xu, Weibo Xu, Junkai Chang

Oncology Research, Vol.25, No.5, pp. 773-779, 2017, DOI:10.3727/096504016X14774889687280

Abstract Tumor protein D52 (TPD52) is a member of the TPD52-like protein family and plays different roles in various types of malignancies. However, its role in renal cell carcinoma (RCC) is still unclear. In this study, we investigated the role of TPD52 in RCC. The mechanism of TPD52 in RCC was also investigated. Our data demonstrated that the expression levels of TPD52 in both mRNA and protein were significantly decreased in RCC cells. Overexpression of TPD52 inhibited proliferation, migration, and invasion with decreased epithelial–mesenchymal transition (EMT) phenotype in RCC cells, as well as attenuated tumor growth More >

Xingtao Han^*†, Jinjian Yang^*, Zhankui Jia^*, Pengtao Wei^†, Han Zhang^†, Wenwei Lv^†, Jiantao Sun^†, Qingxiang Huo^†

Oncology Research, Vol.25, No.3, pp. 389-395, 2017, DOI:10.3727/096504016X14743324568129

Abstract The pre-mRNA splicing regulator serine–arginine protein kinase 1 (SRPK1), a member of the SR kinase family, plays an essential role in cancer development and various pathophysiological processes. However, its expression pattern and functions in renal cell carcinoma (RCC) remain unknown. Therefore, the aim of this study was to assess the role of SRPK1 in RCC. Our data showed that SRPK1 was significantly upregulated in human RCC tissues and cell lines. SRPK1 interference significantly inhibited the proliferation of RCC cells and inhibited tumor growth in vivo. In addition, SRPK1 interference also suppressed migration and invasion in More >

Chun-ming Yang^*, Shan Ji^†, Yan Li^‡, Li-ye Fu^‡, Tao Jiang^‡, Fan-dong Meng^‡

Oncology Research, Vol.25, No.2, pp. 195-205, 2017, DOI:10.3727/096504016X14732772150424

Abstract Renal cell carcinoma (RCC) represents one of the most resistant tumors to radiation and chemotherapy. Current therapies for RCC patients are inefficient due to the lack of diagnostic and therapeutic markers. The expression of novel tumor-associated kinases has the potential to dramatically shape tumor cell behavior. Identifying tumor-associated kinases can lend insight into patterns of tumor growth and characteristics. In the present study, we investigated the receptor tyrosine kinase-like orphan receptor 2 (Ror2), a new tumor-associated kinase, in RCC primary tumors and cell lines. Knockdown of Ror2 expression in RCC cells with specific shRNA significantly More >

Xiangfei He, Fuguang Sun, Fengfu Guo, Kai Wang, Yisheng Gao, Yanfei Feng, Bin Song, Wenzhi Li, Yang Li

Oncology Research, Vol.25, No.2, pp. 157-166, 2017, DOI:10.3727/096504016X14719078133203

Abstract Renal cell carcinoma (RCC) is one of the most common kidney cancers worldwide. Although great progressions have been made in the past decades, its morbidity and lethality remain increasing. Long noncoding RNAs (lncRNAs) are demonstrated to play significant roles in the tumorigenesis. This study aimed to investigate the detailed roles of lncRNA FTX in RCC cell proliferation and metastasis. Our results showed that the transcript levels of FTX in both clinical RCC tissues and the cultured RCC cells were significantly upregulated and associated with multiple clinical parameters of RCC patients, including familial status, tumor sizes, More >

Jianping Xu, Liguo Sun, Wei Sun, Jianhai Tian, Huaiyuan Guo

Oncology Research, Vol.26, No.7, pp. 997-1003, 2018, DOI:10.3727/096504017X15140544654946

Abstract To investigate the effect of Kim-1 on 786-0 cells in vivo and in vitro, several experiments such as quantitative real-time PCR, Western blot, MTT, colony formation, and flow cytometry were performed to evaluate the biological behavior of 786-0 cells treated with Kim-1 siRNA. Furthermore, the tumor xenograft model was applied to BALB/c nude mice to assess the effect of Kim-1 silencing. Lentivirus-mediated RNAi effectively silenced Kim-1 in 786-0 cells. Kim-1 knockdown significantly inhibited the proliferation and colony formation ability of 786-0 cells (p < 0.01). The cell cycle of 786-0 cells was arrested in the G₀/G₁ phase (p < More >

Amanda Ikegami^*, Luiz Felipe S. Teixeira^*, Marina S. Braga^†, Matheus Henrique Dos S. Dias^‡, Eduardo C. Lopes^‡, Maria Helena Bellini^*

Oncology Research, Vol.26, No.5, pp. 743-751, 2018, DOI:10.3727/096504017X15120379906339

Abstract Renal cell carcinoma (RCC) accounts for approximately 2%–3% of human malignancies and is the most aggressive among urologic tumors. Biological heterogeneity, drug resistance, and chemotherapy side effects are the biggest obstacles to the effective treatment of RCC. The NF-kB transcription factor is one of several molecules identified to be responsible for the aggressive phenotype of this tumor. In the past decade, several studies have demonstrated the activation of NF-kB in RCC, and many have implicated NF-kB1 (p50) as an important molecule in tumor progression and metastasis. In the present study, a lentivirus was used to… More >

Haitao Song^*, Yanwei Rao^†, Gang Zhang^*, Xiangbo Kong^*

Oncology Research, Vol.26, No.3, pp. 457-466, 2018, DOI:10.3727/096504017X15035025554553

Abstract MicroRNAs (miRNAs) are emerging as pivotal regulators in the development and progression of various cancers, including renal cell carcinoma (RCC). MicroRNA-384 (miR-384) has been found to be an important cancer-related miRNA in several types of cancers. However, the role of miR-384 in RCC remains unclear. In this study, we aimed to investigate the potential function of miR-384 in regulating tumorigenesis in RCC. Here we found that miR-384 was significantly downregulated in RCC tissues and cell lines. Overexpression of miR-384 significantly inhibited the growth and invasion of RCC cells, whereas inhibition of miR-384 had the opposite More >

Dan Jiao^*, Man Wu^†, Lei Ji^‡, Feng Liu^§, Yingying Liu^§

Oncology Research, Vol.26, No.2, pp. 249-259, 2018, DOI:10.3727/096504017X14953948675430

Abstract Recent evidence suggests that dysregulation of microRNAs is associated with the development of multiple malignancies. miR-186 has been reported as a critical cancer regulator in several types of cancers. However, its functional significance and molecular mechanism underlying renal cell carcinoma (RCC) remain unknown. In this study, our results showed that miR-186 expression was dramatically downregulated in RCC tissues and cell lines compared to that in adjacent normal tissues and cell lines. Overexpression of miR-186 significantly inhibited cell growth, colony formation, and cell invasion; caused cell cycle arrest at the G₀/G₁ phase; and induced cell apoptosis as… More >