scholarly journals Growth factor/growth factor receptor loops in autocrine growth regulation of human prostate cancer DU145 cells.

2011 ◽  
Vol 58 (3) ◽  
Author(s):  
Janusz Ligęza ◽  
Joanna Ligęza ◽  
Andrzej Klein
Keyword(s):  
Prostate Cancer ◽  
Growth Factor ◽  
Cell Growth ◽  
Growth Regulation ◽  
Growth Factor Receptor ◽  
Human Prostate ◽  
Main Step ◽  
Autocrine Growth ◽  
Du145 Cells

Autocrine growth factors produced by epithelial cells mediate the development and proliferation of neoplastic human prostate tissue. Various approaches have been used to down-regulate neoplastic growth of prostate cancer using natural flavonoids, soluble receptors, pseudo-ligands, monoclonal antibodies and tyrosine kinase inhibitors (tyrphostins). Selected growth factor/growth factor receptor loops (mainly TGFα/EGFR and IGFs/IGFIR) have been proposed as regulators of prostate cancer cell growth. We have previously determined that blockade of IGFIR or VEGF2R signaling pathways by tyrphostin AG1024 and SU1498 inhibits autocrine growth and viability of DU145 cells in vitro. Recently, we compared the activity of AG1024 and SU1498 with the inhibiting effect of tyrphostin A23 (a selective inhibitor of EGFR). The results described in this paper confirm that DU145 cells do not produce IGFI or EGF. In contrast, DU145 cells produce a great amount of VEGF, much more than TGFα (about 60-fold), and VEGF may be the real autocrine growth factor of the investigated cells. The results indicate that the growth of DU145 may be regulated by at least three autocrine loops: TGFα/EGFR, IGFII/IGFIR and VEGF/VEGFR2. Neither AG1024 nor SU1498 affected the production of TGFα substantially, which excludes the possibility that IGFRs or VEGFR2 inhibitors arrest the growth of these cells by inhibition of synthesis and/or secretion of TGFα. The obtained data indicate that all tree investigated tyrphostins (AG1024, SU1498 and A23) inhibit signal transmission by Akt (PKB), ERK(1/2), Src and STAT in a similar manner. A comparison of the effects of the investigated tyrphostins indicates that TGFα, IGFII and VEGF stimulate cell growth by affecting the same signaling pathway. The hypothesis was confirmed by the effect of the investigated tyrphostins on activation of EGFR. All these inhibitors decreased phosphorylation of EGFR to the same extent, and after the same time of incubation with cell culture. These results strongly suggest that stimulation of EGFR kinase is the main step in the initiation of mitogen signaling in DU145 cells, regardless of the type of ligand (TGFα, IGFs or VEGF) and their specific receptors.

scholarly journals Anticancer activity of midostaurin in hormone refractory human prostate cancer DU145 cells

2016 ◽  
Vol 11 (2) ◽  
pp. 378
Author(s):  
Jin-Jun Sun ◽  
Shi-Feng Kan ◽  
Guan-Xing Sun
Keyword(s):  
Prostate Cancer ◽  
Kinase Inhibitor ◽  
Cancer Cell Line ◽  
Prostate Cancer Cell Line ◽  
Nerve Cells ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Du145 Cells ◽  
Hormone Refractory

<p class="Abstract">We tried a new method of prostate cancer treatment by inducing<em> in vitro</em> differentiation which resulted in reduction of cancer cells growth. A protein kinase inhibitor, midostaurin's ability to trigger the human prostate cancer cell line, DU145 to segregate into nerve cells was studied. Midostaurin (100 nM) suppressed the growth of DU145 cells but without change in the number of dead cells. Midostaurin started to extend neurites on DU145 cells after 24 hours and differentiated into nerve cells by 72 hours. The microtubule was stabilized by tau protein and its mRNA expression showed time-dependent increase in midostaurin-treated DU145 cells. At the same time, the amount of acetylcholinesterase was also increased. The midostaurin-treated DU145 cells showed 40% less activity than control in the colony forming assay. The results suggests that midostaurin can induce differentiation of DU145 cells into nerve cells.</p><p> </p>

scholarly journals Immunity against cancer cells may promote their proliferation and metastasis

2019 ◽  
Vol 117 (1) ◽  
pp. 426-431
Author(s):  
Chih-Wei Lin ◽  
Jia Xie ◽  
Ding Zhang ◽  
Kyung Ho Han ◽  
Geramie Grande ◽  
...  
Keyword(s):  
Immune Response ◽  
Growth Factor ◽  
Cell Growth ◽  
Cancer Patients ◽  
Growth Factor Receptor ◽  
Point Of View ◽  
Breast Cancer Cell Growth ◽  
Agonist Antibody

Herein we present a concept in cancer where an immune response is detrimental rather than helpful. In the cancer setting, the immune system is generally considered to be helpful in curtailing the initiation and progression of tumors. In this work we show that a patient’s immune response to their tumor can, in fact, either enhance or inhibit tumor cell growth. Two closely related autoantibodies to the growth factor receptor TrkB were isolated from cancer patients’ B cells. Although highly similar in sequence, one antibody was an agonist while the other was an antagonist. The agonist antibody was shown to increase breast cancer cell growth both in vitro and in vivo, whereas the antagonist antibody inhibited growth. From a mechanistic point of view, we showed that binding of the agonist antibody to the TrkB receptor was functional in that it initiated downstream signaling identical to its natural growth factor ligand, brain-derived neurotrophic factor (BDNF). Our study shows that individual autoantibodies may play a role in cancer patients.

Inhibitors of Epidermoid Growth Factor Receptor Suppress Cell Growth and Enhance Chemosensitivity of Nasopharyngeal Cancer Cells in vitro

Oncology ◽  
2005 ◽  
Vol 68 (4-6) ◽  
pp. 538-547 ◽  
Author(s):  
Chih-Hung Hsu ◽  
Ming Gao ◽  
Chi-Long Chen ◽  
Pei-Yen Yeh ◽  
Ann-Lii Cheng
Keyword(s):  
Growth Factor ◽  
Cell Growth ◽  
Cancer Cells ◽  
Nasopharyngeal Cancer ◽  
Growth Factor Receptor

scholarly journals Quercetin inhibits angiogenesis through thrombospondin-1 upregulation to antagonize human prostate cancer PC-3 cell growth in vitro and in vivo

2015 ◽  
Vol 35 (3) ◽  
pp. 1602-1610 ◽  
Author(s):  
FEIYA YANG ◽  
XIAN JIANG ◽  
LIMING SONG ◽  
HUIPING WANG ◽  
ZHU MEI ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Growth ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Thrombospondin 1

Peperomin E Induces Apoptosis and Cytoprotective Autophagy in Human Prostate Cancer DU145 Cells In Vitro and In Vivo

Planta Medica ◽  
2021 ◽  
Author(s):  
Min Lin ◽  
Qiannan Zhu ◽  
Yunzhi Li ◽  
Jigang Pan
Keyword(s):  
Prostate Cancer ◽  
Morphological Changes ◽  
Xenograft Model ◽  
Du145 Cell ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Tumor Mouse Model ◽  
Du145 Cells

AbstractPeperomin E was first isolated from Peperomia dindygulensis, an anticarcinogenic herb, and exhibited anticancer activity in many cancer cell lines. To date, it is unknown whether peperomin E has an effect on human prostate cancer DU145 cells in vitro and in vivo. In this study, we used MTT to assess the proliferation inhibition activity of peperomin E in DU145 cells in vitro and observed the cell morphological changes by a phase contrast microscope. A DU145 cell xenograft tumor mouse model was used to evaluate the efficacy of peperomin E in vivo. Apoptosis rates were measured by flow cytometry, and protein expression levels were analyzed by western blot. The results showed that peperomin E significantly inhibited the proliferation of DU145 cells in vitro and reduced the weight and volume of tumors in vivo. Peperomin E also significantly induced the apoptosis and autophagic response of DU145 cells. The autophagic inhibitors LY294002 and chloroquine enhanced peperomin E-mediated inhibition of DU145 cell proliferation and induction of DU145 cell apoptosis. The results also showed that the Akt/mTOR pathway participated in peperomin E-induced autophagy in DU145 cells. In summary, our finding showed that peperomin E had an effect on DU145 cells in vitro and in a nude mouse DU145 cell xenograft model in vivo, demonstrated that peperomin E could significantly induce apoptosis and the autophagic response in DU145 cells and that autophagy played a cytoprotective role in peperomin E-treated DU145 cells. These results suggest that the combination of peperomin E treatment and autophagic inhibition has potential for the treatment of prostate cancer.

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