scholarly journals Treatment of etoposide combined with 15-deoxy-Δ12,14-prostaglandin J2 exerted synergistic antitumor effects against renal cell carcinoma via peroxisome proliferator-activated receptor-γ-independent pathways

2013 ◽  
Vol 2 (2) ◽  
pp. 292-296 ◽  
Author(s):  
YASUHIRO YAMAMOTO ◽  
HIROMI KOMA ◽  
HIROKI HIRAMATSU ◽  
MISA ABE ◽  
KAZUNORI MURAKAMI ◽  
...  
2001 ◽  
Vol 287 (3) ◽  
pp. 727-732 ◽  
Author(s):  
Ken-ichiro Inoue ◽  
Yutaka Kawahito ◽  
Yasunori Tsubouchi ◽  
Masataka Kohno ◽  
Rikio Yoshimura ◽  
...  

2006 ◽  
Vol 13 (3) ◽  
pp. 265-270 ◽  
Author(s):  
JINYANG YUAN ◽  
ATSUSHI TAKAHASHI ◽  
NAOYA MASUMORI ◽  
NAOKI ITOH ◽  
TAIJI TSUKAMOTO

Urology ◽  
2005 ◽  
Vol 65 (3) ◽  
pp. 594-599 ◽  
Author(s):  
Jinyang Yuan ◽  
Atsushi Takahashi ◽  
Naoya Masumori ◽  
Kohsuke Uchida ◽  
Shin-Ichi Hisasue ◽  
...  

Author(s):  
Haitao Song ◽  
Yanwei Rao ◽  
Gang Zhang ◽  
Xiangbo Kong

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 effects. Bioinformatic analysis and luciferase reporter assay showed that miR-384 directly targeted the 3′-untranslated region of astrocyte elevated gene 1 (AEG-1). Further data showed that miR-384 could negatively regulate the expression of AEG-1 in RCC cells. Importantly, miR-384 expression was inversely correlated with AEG-1 expression in clinical RCC specimens. Moreover, miR-384 regulates the activation of Wnt signaling. Overexpression of AEG-1 significantly reversed the antitumor effects of miR-384. Overall, these findings suggest that miR-384 suppresses the growth and invasion of RCC cells via downregulation of AEG-1, providing a potential therapeutic target for the treatment of RCC.


Cells ◽  
2019 ◽  
Vol 8 (11) ◽  
pp. 1469 ◽  
Author(s):  
Chung-Sheng Shi ◽  
Kuan-Lin Kuo ◽  
Mei-Sin Chen ◽  
Po-Ming Chow ◽  
Shing-Hwa Liu ◽  
...  

Cancer cells rely on aberrant transcription for growth and survival. Cyclin-dependent kinases (CDKs) play critical roles in regulating gene transcription by modulating the activity of RNA polymerase II (RNAPII). THZ1, a selective covalent inhibitor of CDK7, has antitumor effects in several human cancers. In this study, we investigated the role and therapeutic potential of CDK7 in regulating the angiogenic activity of endothelial cells and human renal cell carcinoma (RCC). Our results revealed that vascular endothelial growth factor (VEGF), a critical activator of angiogenesis, upregulated the expression of CDK7 and RNAPII, and the phosphorylation of RNAPII at serine 5 and 7 in human umbilical vein endothelial cells (HUVECs), indicating the transcriptional activity of CDK7 may be involved in VEGF-activated angiogenic activity of endothelium. Furthermore, through suppressing CDK7 activity, THZ1 suppressed VEGF-activated proliferation and migration, as well as enhanced apoptosis of HUVECs. Moreover, THZ1 inhibited VEGF-activated capillary tube formation and CDK7 knockdown consistently diminished tube formation in HUVECs. Additionally, THZ1 reduced VEGF expression in human RCC cells (786-O and Caki-2), and THZ1 treatment inhibited tumor growth, vascularity, and angiogenic marker (CD31) expression in RCC xenografts. Our results demonstrated that CDK7-mediated transcription was involved in the angiogenic activity of endothelium and human RCC. THZ1 suppressed VEGF-mediated VEGFR2 downstream activation of angiogenesis, providing a new perspective for antitumor therapy in RCC patients.


2019 ◽  
Vol 68 (3) ◽  
pp. 776-781
Author(s):  
Yu-Ching Chou ◽  
Chih-Hung Lin ◽  
Chih-Shung Wong ◽  
Wan-Yun Chou ◽  
Jin-Yin Chang ◽  
...  

Statins are a therapeutic drug with reducing plasma cholesterol levels and have been linked with potential antitumor effects. However, epidemiological studies on statin use and renal cell carcinoma (RCC) risk have been inconsistent. This cohort study aimed to examine this association in an Asian population. We identified patients who filled initial prescriptions for statins in the inpatient and ambulatory care order files from Taiwan’s National Health Insurance Research Database between January 1, 1998 and December 31, 2005 as the statin users cohort (n=14,067). The comparison cohort comprised of patients who had not taken any statin in the previous years prior to January 1, 1998 or had used statins for less than 28 cumulative defined daily doses between January 1, 1998 and December 31, 2005 (n=56 268). The outcome of interest was pathologically verified RCC occurred between January 1, 1999 and December 31, 2013. The Fine-Gray competing risk model was fitted to estimate HRs accompanying 95% CI. Patients with the use of statins had a significantly lower risk of RCC as compared with the non-users cohort, yielding an adjusted HR of 0.64 (95% CI, 0.38 to 0.87). Moreover, we found a significant inverse association between cumulative statin use and the risk of RCC. Further, the inverse association between statin use and risk of RCC was evident in both sexes. This population-based cohort study provides longitudinal evidence that the use of statins was associated with a reduced risk of RCC.


Sign in / Sign up

Export Citation Format

Share Document