scholarly journals GSTΠ stimulates caveolin-1-regulated polyamine uptake via actin remodeling

Oncotarget ◽  
2019 ◽  
Vol 10 (55) ◽  
pp. 5713-5723 ◽  
Author(s):  
Takeshi Uemura ◽  
George Tsaprailis ◽  
Eugene W. Gerner
2014 ◽  
Vol 34 (6) ◽  
Author(s):  
Mario Grossi ◽  
Catarina Rippe ◽  
Ramasri Sathanoori ◽  
Karl Swärd ◽  
Amalia Forte ◽  
...  

We demonstrate that caveolin-1 negatively regulates vascular smooth muscle cell polyamine uptake and show that caveolin-1-regulated polyamine uptake is critical for proliferative advantage of caveolin-1 deficient cells, providing proof-of-principle for targeting this mechanism as a strategy to fight unwanted proliferation.


2011 ◽  
Vol 31 (2) ◽  
pp. 376-383 ◽  
Author(s):  
Baohua Yang ◽  
Chris Radel ◽  
Dalton Hughes ◽  
Sheri Kelemen ◽  
Victor Rizzo

2010 ◽  
Vol 299 (2) ◽  
pp. G517-G522 ◽  
Author(s):  
Takeshi Uemura ◽  
David E. Stringer ◽  
Karen A. Blohm-Mangone ◽  
Eugene W. Gerner

The polyamines spermidine and spermine, and their precursor putrescine, are required for cell growth and cellular functions. The high levels of tissue polyamines are implicated in carcinogenesis. The major sources of exogenous polyamines are diet and intestinal luminal bacteria in gastrointestinal (GI) tissues. Both endocytic and solute carrier-dependent mechanisms have been described for polyamine uptake. Knocking down of caveolin-1 protein increased polyamine uptake in colon cancer-derived HCT116 cells. Dietary supplied putrescine was accumulated in GI tissues and liver in caveolin-1 knockout mice more than wild-type mice. Knocking out of nitric oxide synthase (NOS2), which has been implicated in the release of exogenous polyamines from internalized vesicles, abolished the accumulation of dietary putrescine in GI tissues. Under conditions of reduced endogenous tissue putrescine contents, caused by treatment with the polyamine synthesis inhibitor difluoromethylornithine (DFMO), small intestinal and colonic mucosal polyamine contents increased with dietary putrescine levels, even in mice lacking NOS2. Knocking down the solute carrier transporter SLC3A2 in HCT116-derived Hkh2 cells reduced the accumulation of exogenous putrescine and total polyamine contents in DFMO treated cells, relative to non-DFMO-treated cells. These data demonstrate that exogenous putrescine is transported into GI tissues by caveolin-1- and NOS2-dependent mechanisms, but that the solute carrier transporter SLC3A2 can function bidirectionally to import putrescine under conditions of low tissue polyamines.


2005 ◽  
Vol 173 (4S) ◽  
pp. 385-386
Author(s):  
Gregor Bötticher ◽  
Zsófia Herbert ◽  
Erdogan Sendemir ◽  
Andreas Aschoff ◽  
Gustav Friedrich Jirikowski ◽  
...  

2009 ◽  
Vol 47 (09) ◽  
Author(s):  
C Meyer ◽  
C Stump ◽  
A Müller ◽  
S Dooley
Keyword(s):  

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 84-OR
Author(s):  
WEN ZENG ◽  
KUNYING LIU ◽  
JIANSONG TANG ◽  
HAICHENG LI ◽  
HAIXIA XU ◽  
...  
Keyword(s):  

2018 ◽  
Vol 40 (4) ◽  
pp. 323-327 ◽  
Author(s):  
F Tas ◽  
S Karabulut ◽  
K Erturk ◽  
D Duranyildiz

Aim: Caveolin-1 plays a significant role in the pathogenesis of various carcinomas and its expression affects the survival of cancer patients. However, the molecular function of caveolin-1 and its possible clinical importance has remained uncertain in gastric cancer. No clinical trial has examined serum caveolin-1 levels in gastric cancer patients so far, instead all available results were provided from studies conducted on tissue samples. In the current study, we analyzed the soluble serum caveolin-1 levels in gastric cancer patients, and specified its associations with the clinical factors and prognosis. Material and Methods: Sixty-three patients with pathologically confirmed gastric cancer were enrolled into the trial. Serum caveolin-1 concentrations were detected by ELISA method. Thirty healthy subjects were also included in the study. Results: The median age of patients was 62 years, ranging from 28 to 82 years. The serum caveolin-1 levels in gastric cancer patients were significantly higher than those in control group (p < 0.001). The common clinical parameters including patient age, sex, lesion localization, histopathology, histological grade, disease stage, and various serum tumor markers (e.g. LDH, CEA, and CA 19.9) were not found to be associated with serum caveolin-1 levels (p > 0.05). Similarly, no correlation existed between serum caveolin-1 concentration and chemotherapy responsiveness (p = 0.93). Furthermore, serum caveolin-1 level was not found to have a prognostic role (p = 0.16). Conclusion: Even though it is neither predictive nor prognostic, serum caveolin-1 level may be a valuable diagnostic indicator in patients with gastric cancer. Key


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