The Role of PKC in Retinoic Acid Regulation of Human Mammary Cancer Cell Proliferation

1997 ◽  
Author(s):  
Yunhi Cho ◽  
David Talmage
Keyword(s):  
Cell Proliferation ◽  
Retinoic Acid ◽  
Cancer Cell ◽  
Mammary Cancer ◽  
Cancer Cell Proliferation ◽  
Mammary Cancer Cell ◽  
Human Mammary Cancer

Aberrant microRNA Expression in Radiation-Induced Rat Mammary Cancer: The Potential Role of miR-194 Overexpression in Cancer Cell Proliferation

2012 ◽  
Vol 179 (2) ◽  
pp. 151 ◽  
Author(s):  
Daisuke Iizuka ◽  
Tatsuhiko Imaoka ◽  
Mayumi Nishimura ◽  
Hidehiko Kawai ◽  
Fumio Suzuki ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cancer Cell ◽  
Mammary Cancer ◽  
Potential Role ◽  
Microrna Expression ◽  
Cancer Cell Proliferation ◽  
Radiation Induced

Exercise-induced muscle-derived cytokines inhibit mammary cancer cell growth

2011 ◽  
Vol 301 (3) ◽  
pp. E504-E510 ◽  
Author(s):  
Pernille Hojman ◽  
Christine Dethlefsen ◽  
Claus Brandt ◽  
Jakob Hansen ◽  
Line Pedersen ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cancer Cell ◽  
Mammary Cancer ◽  
Exercise Bout ◽  
Cancer Cell Proliferation ◽  
Caspase Activity ◽  
Humoral Factors ◽  
Mammary Cancer Cell ◽  
Exercise Induced ◽  
Mcf 7

Regular physical activity protects against the development of breast and colon cancer, since it reduces the risk of developing these by 25–30%. During exercise, humoral factors are released from the working muscles for endocrinal signaling to other organs. We hypothesized that these myokines mediate some of the inhibitory effects of exercise on mammary cancer cell proliferation. Serum and muscles were collected from mice after an exercise bout. Incubation with exercise-conditioned serum inhibited MCF-7 cell proliferation by 52% and increased caspase activity by 54%. A similar increase in caspase activity was found after incubation of MCF-7 cells with conditioned media from electrically stimulated myotubes. PCR array analysis (CAPM-0838E; SABiosciences) revealed that seven genes were upregulated in the muscles after exercise, and of these oncostatin M (OSM) proved to inhibit MCF-7 proliferation by 42%, increase caspase activity by 46%, and induce apoptosis. Blocking OSM signaling with anti-OSM antibodies reduced the induction of caspase activity by 51%. To verify that OSM was a myokine, we showed that it was significantly upregulated in serum and in three muscles, tibialis cranialis, gastronemius, and soleus, after an exercise bout. In contrast, OSM expression remained unchanged in subcutaneous and visceral adipose tissue, liver, and spleen (mononuclear cells). We conclude that postexercise serum inhibits mammary cancer cell proliferation and induces apoptosis of these cells. We suggest that one or more myokines secreted from working muscles may be mediating this effect and that OSM is a possible candidate. These findings emphasize that role of physical activity in cancer treatment, showing a direct link between exercise-induced humoral factors and decreased tumor cell growth.

scholarly journals FZD10 Carried by Exosomes Sustains Cancer Cell Proliferation

Cells ◽  
2019 ◽  
Vol 8 (8) ◽  
pp. 777 ◽  
Author(s):  
Scavo ◽  
Depalo ◽  
Rizzi ◽  
Ingrosso ◽  
Fanizza ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cancer Cell ◽  
Culture Medium ◽  
Mrna Level ◽  
Substantial Reduction ◽  
Wnt Signaling Pathway ◽  
Active Role ◽  
Cancer Cell Proliferation ◽  
Long Distance

Extracellular vesicles (EVs) are involved in intercellular communication during carcinogenesis, and cancer cells are able to secrete EVs, in particular exosomes containing molecules, that can be transferred to recipient cells to induce pathological processes and significant modifications, as metastasis, increase of proliferation, and carcinogenesis evolution. FZD proteins, a family of receptors comprised in the Wnt signaling pathway, play an important role in carcinogenesis of the gastroenteric tract. Here, a still unknown role of Frizzled 10 (FZD10) protein was identified. In particular, the presence of FZD10 and FZD10-mRNA in exosomes extracted from culture medium of the untreated colorectal, gastric, hepatic, and cholangio cancer cell lines, was detected. A substantial reduction in the FZD10 and FZD10-mRNA level was achieved in FZD10-mRNA silenced cells and in their corresponding exosomes. Concomitantly, a significant decrease in viability of the silenced cells compared to their respective controls was observed. Notably, the incubation of silenced cells with the exosomes extracted from culture medium of the same untreated cells promoted the restoration of the cell viability and, also, of the FZD10 and FZD10-mRNA level, thus indicating that the FZD10 and FZD10-mRNA delivering exosomes may be potential messengers of cancer reactivation and play an active role in long-distance metastatization.

scholarly journals Exploiting GRK2 Inhibition as a Therapeutic Option in Experimental Cancer Treatment: Role of p53-Induced Mitochondrial Apoptosis

Cancers ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3530
Author(s):  
Jessica Gambardella ◽  
Antonella Fiordelisi ◽  
Gaetano Santulli ◽  
Michele Ciccarelli ◽  
Federica Andrea Cerasuolo ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cancer Cell ◽  
Nude Mice ◽  
Specific Inhibitor ◽  
Cancer Cell Proliferation ◽  
In Vivo Models ◽  
P53 Expression

The involvement of GRK2 in cancer cell proliferation and its counter-regulation of p53 have been suggested in breast cancer even if the underlying mechanism has not yet been elucidated. Furthermore, the possibility to pharmacologically inhibit GRK2 to delay cancer cell proliferation has never been explored. We investigated this possibility by setting up a study that combined in vitro and in vivo models to underpin the crosstalk between GRK2 and p53. To reach this aim, we took advantage of the different expression of p53 in cell lines of thyroid cancer (BHT 101 expressing p53 and FRO cells, which are p53-null) in which we overexpressed or silenced GRK2. The pharmacological inhibition of GRK2 was achieved using the specific inhibitor KRX-C7. The in vivo study was performed in Balb/c nude mice, where we treated BHT-101 or FRO-derived tumors with KRX-C7. In our in vitro model, FRO cells were unaffected by GRK2 expression levels, whereas BHT-101 cells were sensitive, thus suggesting a role for p53. The regulation of p53 by GRK2 is due to phosphorylative events in Thr-55, which induce the degradation of p53. In BHT-101 cells, the pharmacologic inhibition of GRK2 by KRX-C7 increased p53 levels and activated apoptosis through the mitochondrial release of cytochrome c. These KRX-C7-mediated events were also confirmed in cancer allograft models in nude mice. In conclusion, our data showed that GRK2 counter-regulates p53 expression in cancer cells through a kinase-dependent activity. Our results further corroborate the anti-proliferative role of GRK2 inhibitors in p53-sensitive tumors and propose GRK2 as a therapeutic target in selected cancers.

The role of histone deacetylase 7 (HDAC7) in cancer cell proliferation: regulation on c-Myc

2010 ◽  
Vol 89 (3) ◽  
pp. 279-289 ◽  
Author(s):  
Caihua Zhu ◽  
Qin Chen ◽  
Zuoquan Xie ◽  
Jing Ai ◽  
Linjiang Tong ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Histone Deacetylase ◽  
Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Proliferation Regulation

Development of a novel method for the bioanalysis of benfotiamine and sulbutiamine in cancer cells

2016 ◽  
Vol 8 (28) ◽  
pp. 5596-5603 ◽  
Author(s):  
Jaeah Kim ◽  
Christopher P. Hopper ◽  
Kelsey H. Connell ◽  
Parisa Darkhal ◽  
Jason A. Zastre ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Biological Samples ◽  
Cancer Cell Proliferation ◽  
Essential Step ◽  
Novel Method

Quantification of benfotiamine and sulbutiamine, synthetic thiamine analogs, in biological samples is an essential step toward understanding the role of these thiamine analogs on cancer cell proliferation.

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