Prolyl hydroxylase-2 inhibits liver tumor cell proliferation and cyclin D1 expression in a hydroxylase-dependent manner

2016 ◽  
Vol 77 ◽  
pp. 129-140 ◽  
Author(s):  
Yifeng Tao ◽  
Feng Lin ◽  
Ruidong Li ◽  
Jie Shen ◽  
Zhengxin Wang
Keyword(s):  
Cell Proliferation ◽  
Tumor Cell ◽  
Cyclin D1 ◽  
Liver Tumor ◽  
Prolyl Hydroxylase ◽  
Dependent Manner ◽  
Tumor Cell Proliferation ◽  
Liver Tumor Cell

scholarly journals Interruption of Activin A Autocrine Regulation by Antisense Oligodeoxynucleotides Accelerates Liver Tumor Cell Proliferation*

Endocrinology ◽  
1999 ◽  
Vol 140 (7) ◽  
pp. 3125-3132 ◽  
Author(s):  
Kazuaki Takabe ◽  
Jean-Jacques Lebrun ◽  
Yoji Nagashima ◽  
Yasushi Ichikawa ◽  
Masato Mitsuhashi ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tumor Cell ◽  
Liver Tumor ◽  
Activin A ◽  
Antisense Oligodeoxynucleotides ◽  
Tumor Cell Proliferation ◽  
Autocrine Regulation ◽  
Liver Tumor Cell

scholarly journals Metformin Suppressed CXCL8 Expression and Cell Migration in HEK293/TLR4 Cell Line

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Zhihui Xiao ◽  
Wenjun Wu ◽  
Vladimir Poltoratsky
Keyword(s):  
Cell Proliferation ◽  
Cell Migration ◽  
Tumor Cell ◽  
Nuclear Translocation ◽  
High Dose ◽  
Dependent Manner ◽  
Tumor Cell Proliferation ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

Chronic inflammation is associated with cancer. CXCL8 promotes tumor microenvironment construction through recruiting leukocytes and endothelial progenitor cells that are involved in angiogenesis. It also enhances tumor cell proliferation and migration. Metformin, type II diabetes medication, demonstrates anticancer properties via suppressing inflammation, tumor cell proliferation, angiogenesis, and metastasis. This study intended to address the role of metformin in regulation of CXCL8 expression and cell proliferation and migration. Our data indicated that metformin suppressed LPS-induced CXCL8 expression in a dose-dependent manner through inhibiting NF-κB, but not AP-1 and C/EBP, activities under the conditions we used. This inhibitory effect of metformin is achieved through dampening LPS-induced NF-κB nuclear translocation. Cell migration was inhibited by metformin under high dose (10 mM), but not cell proliferation.

scholarly journals Two Gln187 mutants of human soluble APRIL inhibit proliferation of lung carcinoma A549 cells.

2009 ◽  
Vol 56 (4) ◽  
Author(s):  
Shuangshuang Dai ◽  
Yingru Zheng ◽  
Bin Chen ◽  
Min Gao ◽  
Yan Zhang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tumor Cell ◽  
Lung Carcinoma ◽  
Binding Capacity ◽  
Specific Binding ◽  
Active Form ◽  
A549 Cells ◽  
Dependent Manner ◽  
Tumor Cell Proliferation

Soluble APRIL (sAPRIL), the active form of a proliferation-inducing ligand (APRIL), is implicated in the proliferation of tumor cells. Suppressing APRIL function has been considered as a potential strategy for the therapy of APRIL-associated tumors. In the present study, we generated human sAPRIL and its two mutants, Gln187-D-sAPRIL (Gln187 deleted) and Gly187-sAPRIL (Gln187 replaced by Gly). In vitro experiments showed that the two mutants had similar specific binding capacity to lung carcinoma A549 cells compared to the wild-type sAPRIL, and both, especially Gly187-sAPRIL, exhibited significant antagonistic effect on sAPRIL-induced tumor cell proliferation in a dose-dependent manner, which might be predominantly mediated by blocking sAPRIL-induced MEK and ERK phosphorylation but not p38MAPK or JNK signaling. In vivo experiments with nude mice bearing A549 cell-derived xenograft tumor showed that only the Gly187-sAPRIL mutant could significantly suppress the tumor growth. These results suggest that Gln187 may be a crucial amino acid in APRIL-mediated tumor cell proliferation via the MEK-ERK signaling pathway and that the sAPRIL mutants may serve as novel potential antagonists of APRIL for the therapy of APRIL-associated cancers.

scholarly journals RABL6A Promotes G1–S Phase Progression and Pancreatic Neuroendocrine Tumor Cell Proliferation in an Rb1-Dependent Manner

2014 ◽  
Vol 74 (22) ◽  
pp. 6661-6670 ◽  
Author(s):  
Jussara Hagen ◽  
Viviane P. Muniz ◽  
Kelly C. Falls ◽  
Sara M. Reed ◽  
Agshin F. Taghiyev ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tumor Cell ◽  
Neuroendocrine Tumor ◽  
Pancreatic Neuroendocrine Tumor ◽  
S Phase ◽  
Dependent Manner ◽  
Tumor Cell Proliferation ◽  
Phase Progression
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