CXCL5, the upregulated chemokine in patients with uterine cervix cancer, in vivo and in vitro contributes to oncogenic potential of Hela uterine cervix cancer cells

2018 ◽  
Vol 107 ◽  
pp. 1496-1504 ◽  
Author(s):  
Xiaona Feng ◽  
Danfeng Zhang ◽  
Xinyi Li ◽  
Shuxia Ma ◽  
Chunbin Zhang ◽  
...  
2004 ◽  
Vol 93 (1) ◽  
pp. 182-188 ◽  
Author(s):  
Emmanuel Contassot ◽  
Mirna Tenan ◽  
Valérie Schnüriger ◽  
Marie-Françoise Pelte ◽  
Pierre-Yves Dietrich

2020 ◽  
Author(s):  
XiaXia Man ◽  
XiaoLin Yang ◽  
ZhenTong Wei ◽  
YuYing Tan ◽  
WanYing Li ◽  
...  

Abstract Background It has previously accepted that several types of human cancer constitutively express CXCL1, which may implicated in various aspects of tumors. Here, we sought to assess the expression and of CXCL1 in human uterine cervix cancer (UCC) and its potential role and mechanism in UCC. Methods CXCL1 protein expression in a uterine cervical tissue microarray was assessed by immunohistochemistry. The roles of CXCL1 on HeLa UCC cells were detected by CCK-8, transwell and apoptosis assays. Western blotting and ERK1/2 blocker PD98059 were utilized to explore whether ERK signal was implicated in CXCL1-mediated UCC processes. Results CXCL1 was expressed by HeLa, PHM1-41 cells as well as cervical tissues, in which UCC tissues showed an obviously high level of CXCL1 compared with non-cancerous tissues. Additionally, of the cancer tissues, CXCL1 high-level expression was notably relevant to poor clinical stages. In vitro, the growth and migration of HeLa cells were enhanced in the presence of exogenous CXCL1. Gain-function assays revealed that CXCL1 overexpression promoted growth and migration response to HeLa cells via autocrine/paracrine manners. Moreover, CXCL1 also led to the inhibition of apoptosis in HeLa cells. Finally, CXCL1 overexpression in HeLa cells influenced the expression of ERK signal-related genes including ERK, p-ERK, cyclin D1 and Bax, and cell malignant behaviors derived from CXCL1 overexpresion were further interrupt in the presence of PD98059. Conclusion Our findings provided the potential roles of CXCL1 as a promoter and the novel understanding of the functional relation of CXCL1 with ERK signal pathway in UCC.


Cancer ◽  
1993 ◽  
Vol 72 (1) ◽  
pp. 154-159 ◽  
Author(s):  
Tsutomu Hirao ◽  
Yasuki Sakamoto ◽  
Masaharu Kamada ◽  
Shin-Ichi Hamada ◽  
Toshihiro Aono

2005 ◽  
Vol 37 (3) ◽  
pp. 191 ◽  
Author(s):  
Suzy Kim ◽  
Hong-Gyun Wu ◽  
Jin Hee Shin ◽  
Hye Jin Park ◽  
In Ah Kim ◽  
...  

1987 ◽  
Vol 23 (6) ◽  
pp. 1038
Author(s):  
J U Chung ◽  
B I Choi ◽  
S H Kim ◽  
M C Han ◽  
C W Kim

2010 ◽  
Vol 999 (999) ◽  
pp. 1-11
Author(s):  
P. Ulivi ◽  
C. Arienti ◽  
W. Zoli ◽  
M. Scarsella ◽  
S. Carloni ◽  
...  

2018 ◽  
Vol 18 (17) ◽  
pp. 1483-1493
Author(s):  
Ricardo Imbroisi Filho ◽  
Daniel T.G. Gonzaga ◽  
Thainá M. Demaria ◽  
João G.B. Leandro ◽  
Dora C.S. Costa ◽  
...  

Background: Cancer is a major cause of death worldwide, despite many different drugs available to treat the disease. This high mortality rate is largely due to the complexity of the disease, which results from several genetic and epigenetic changes. Therefore, researchers are constantly searching for novel drugs that can target different and multiple aspects of cancer. Experimental: After a screening, we selected one novel molecule, out of ninety-four triazole derivatives, that strongly affects the viability and proliferation of the human breast cancer cell line MCF-7, with minimal effects on non-cancer cells. The drug, named DAN94, induced a dose-dependent decrease in MCF-7 cells viability, with an IC50 of 3.2 ± 0.2 µM. Additionally, DAN94 interfered with mitochondria metabolism promoting reactive oxygen species production, triggering apoptosis and arresting the cancer cells on G1/G0 phase of cell cycle, inhibiting cell proliferation. These effects are not observed when the drug was tested in the non-cancer cell line MCF10A. Using a mouse model with xenograft tumor implants, the drug preventing tumor growth presented no toxicity for the animal and without altering biochemical markers of hepatic function. Results and Conclusion: The novel drug DAN94 is selective for cancer cells, targeting the mitochondrial metabolism, which culminates in the cancer cell death. In the end, DAN94 has been shown to be a promising drug for controlling breast cancer with minimal undesirable effects.


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