scholarly journals The cross-talk between tumor cells and activated fibroblasts mediated by lactate/BDNF/TrkB signaling promotes acquired resistance to anlotinib in human gastric cancer

Redox Biology ◽  
2021 ◽  
pp. 102076
Author(s):  
Zhijian Jin ◽  
Yifan Lu ◽  
Xiongyan Wu ◽  
Tao Pan ◽  
Zhenjia Yu ◽  
...  
2018 ◽  
Vol 78 (17) ◽  
pp. 4957-4970 ◽  
Author(s):  
Tatiana A. Karakasheva ◽  
Eric W. Lin ◽  
Qiaosi Tang ◽  
Edmund Qiao ◽  
Todd J. Waldron ◽  
...  

2019 ◽  
Vol 25 (11) ◽  
pp. 3317-3328 ◽  
Author(s):  
Zhijun Zhou ◽  
Guanggai Xia ◽  
Zhen Xiang ◽  
Mingyang Liu ◽  
Zhewei Wei ◽  
...  

2015 ◽  
Vol 48 (2) ◽  
pp. 111-116 ◽  
Author(s):  
Kaiyuan Deng ◽  
Hao Wang ◽  
Xiaoqiang Guo ◽  
Jiazeng Xia

2005 ◽  
Vol 230 (10) ◽  
pp. 731-741 ◽  
Author(s):  
Yongchang Chen ◽  
Ying Wang ◽  
Hao Yu ◽  
Fengwei Wang ◽  
Wenrong Xu

The cross talk between cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA) and RhoA-mediated signal transductions and the effect of this cross talk on biologic features of human prostate and gastric cancer cells were investigated. In the human gastric cancer cell line, SGC-7901, lysophosphatidic acid (LPA) increased RhoA activity in a dosedependent manner. The cellular permeable cAMP analog, 8-chlorophenylthio-cAMP (CPT-cAMP), inhibited the LPA-induced RhoA activation and caused phosphorylation of RhoA at serine188. Immunofluorescence microscopy, Western blotting, and green fluorescent protein (GFP)-tagged RhoA location assay in live cells revealed that RhoA was distributed in both the cytoplasm and nucleus of SGC-7901 cells. Treatment with LPA and/or CPT-cAMP did not induce obvious translocation of RhoA in the cells. The LPA treatment caused formation of F-actin in SGC-7901 cells, and CPT-cAMP inhibited the formation. In a modified Boyden chamber assay, LPA stimulated the migration of SGC-7901 cells, and CPT-cAMP dose-dependently inhibited the stimulating effect of LPA. In soft agar assay, LPA stimulated early proliferation of SGC-7901 cells, and CPT-cAMP significantly inhibited the growth of LPA-stimulated cells. In the prostate cancer cell line, PC-3, LPA caused morphologic changes from polygonal to round, and transfection with plasmid DNA encoding constitutively active RhoA(63L) caused a similar change. Treatment with CPT-cAMP inhibited the changes in both cases. However, in PC-3 cells transfected with a plasmid encoding mutant RhoA188A, LPA induced rounding, but CPT-cAMP could not prevent the change. Results of this experiment indicated that cAMP/PKA inhibited RhoA activation, and serine188 phosphorylation on RhoA was necessary for PKA to exert its inhibitory effect on RhoA activation. The cross talk between cAMP/PKA and RhoA-mediated signal transductions had significant affect on biologic features of gastric and prostate cancer cells, such as morphologic and cytoskeletal change, migration, and anchorage-independent growth. The results may be helpful in implementing novel therapeutic strategies for invasive and metastatic prostate and gastric cancers.


2014 ◽  
Vol 141 (4) ◽  
pp. 647-660 ◽  
Author(s):  
Dandan Yuan ◽  
Liang Chen ◽  
Mingxing Li ◽  
Hongwei Xia ◽  
Yuchen Zhang ◽  
...  

2003 ◽  
Vol 26 (5) ◽  
pp. 403-411 ◽  
Author(s):  
Yongzhan Nie ◽  
Kaichun Wu ◽  
Jinghua Yang ◽  
Fengqi Tian ◽  
Ling Li ◽  
...  

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