EXPERIMENTAL IMMUNOLOGY
The effect of mast cells on the biological characteristics of prostate cancer cells
Submission date: 2016-02-25
Final revision date: 2016-05-09
Acceptance date: 2016-05-11
Publication date: 2018-03-30
Cent Eur J Immunol 2018;43(1):1-8
KEYWORDS
ABSTRACT
Aim of the study:
To investigate the effects of mast cells on the proliferation, invasion, and metastasis of prostate cancer cells.
Material and methods:
The mast cell P815 and prostate cancer LNCaP cells were chosen using a Transwell chamber to construct a two-cell cocultured in vitro model to observe the migration of mast cells to prostate cancer cells.
Results:
In the migration experiment, the migration rate of mast cells from the experimental group (%) was 10.167 ±0.833, the mast cell migration rate (%) of the control group was 0.833 ±0.208, and the difference was statistically significant (p < 0.05). The MTT test showed that the OD value of cells in each group over time increased gradually, and 24 h after LNCaP cells were cocultured with different concentrations of mast cells, the OD value was significantly higher than that of the control group (p < 0.05). QRT-PCR and western blot results showed that, compared with the control group, E-cad expression from the experimental group was significantly weakened; N-cad and vimentin expression increased (p < 0.05), and c-kit and SCF expression from experimental group were significantly higher than that of the control group (p < 0.05). After the addition of c-kit neutralising antibodies, compared with the control group, the mast cell migration rate of experimental group decreased significantly and prostate cancer cell proliferation significantly decreased (p < 0.05).
Conclusions:
Mast cells could promote the proliferation of prostate cancer cells and the occurrence of epithelial mesenchymal transition (EMT), which could promote the invasion and metastasis of prostate cancer cells.
To investigate the effects of mast cells on the proliferation, invasion, and metastasis of prostate cancer cells.
Material and methods:
The mast cell P815 and prostate cancer LNCaP cells were chosen using a Transwell chamber to construct a two-cell cocultured in vitro model to observe the migration of mast cells to prostate cancer cells.
Results:
In the migration experiment, the migration rate of mast cells from the experimental group (%) was 10.167 ±0.833, the mast cell migration rate (%) of the control group was 0.833 ±0.208, and the difference was statistically significant (p < 0.05). The MTT test showed that the OD value of cells in each group over time increased gradually, and 24 h after LNCaP cells were cocultured with different concentrations of mast cells, the OD value was significantly higher than that of the control group (p < 0.05). QRT-PCR and western blot results showed that, compared with the control group, E-cad expression from the experimental group was significantly weakened; N-cad and vimentin expression increased (p < 0.05), and c-kit and SCF expression from experimental group were significantly higher than that of the control group (p < 0.05). After the addition of c-kit neutralising antibodies, compared with the control group, the mast cell migration rate of experimental group decreased significantly and prostate cancer cell proliferation significantly decreased (p < 0.05).
Conclusions:
Mast cells could promote the proliferation of prostate cancer cells and the occurrence of epithelial mesenchymal transition (EMT), which could promote the invasion and metastasis of prostate cancer cells.
REFERENCES (23)
1.
Jemal A, Siegel R, Xu J, et al. (2010): Cancer statistics. CA Cancer J Clin 60: 277-300.
2.
Hayat MJ, Howlader N, Reichman ME, et al. (2007): Cancer statistics, trends, and multiple primary cancer analyses from the Surveillance, Epidemiology, and End Results (SEER) Program. Oncologist 12: 20-37.
3.
Clevers H (2004): At the crossroads of inflammation and cancer. Cell 118: 671-674.
5.
De Marzo AM, DeWeese TL, Platz EA, et al. (2004): Pathological and molecular mechanisms of prostate carcinogenesis: implications for diagnosis, detection, prevention, and treatment. Cell Biochem 91: 459-477.
6.
De Marzo AM, Marchi VL, Epstein JI, et al. (1999): Proliferative inflammatory atrophy of the prostate: implications for prostatic carcinogenesis. Am J Pathol 155: 1985-1992.
7.
MacLennan GT, MacLennan GT, Eisenberg R, et al. (2006): The influence of chronic inflammation in prostatic carcinogenesis: A 5-year followupstudy. J Urol 176: 1012-1016.
8.
Daniel NA, Ewing SK, Zmuda JM, et al. (2005): Correlates and prevalence of prostatitis in a large community-base cohort of Order men. Urology 66: 964-970.
9.
Klein EA, Silverman R (2008): Inflammation, infection, and prostate cancer. Curr Opin Urol 18: 315-319.
10.
McDonald PC, Chafe SC, Dedhar S, et al. (2016): Overcoming Hypoxia-Mediated Tumor Progression: Combinatorial Approaches Targeting pH Regulation, Angiogenesis and Immune Dysfunction. Front Cell Dev Biol 4: 27.
11.
Craig M, Ying C, Loberg RD (2008): Co-inoculation of prostate cancer cells with U937 enhances tumor growth and angiogenesis in vivo. J Cell Biochem 103:1-8.
12.
Vyas H, Krishnaswamy GP (2006): Ehrlich’s “Mastzellen”–from aniline dyes to DNA chip arrays: a historical review of developments in mast cell research. Methods Mol Biol 315: 3-11.
13.
Moon TC, St Laurent CD, Morris KE, et al. (2010): Advances in mast cell biology: new understanding of heterogeneity and function. Mucosal Immunol 3: 111-128.
14.
Johansson A, Rudolfsson S, Hammarsten P, et al. (2010): Mast cells are novel independent prognostic markers in prostate cancer and represent a target for therapy. Am J Pathol 177: 1031-1041.
15.
Knapczyk-Stwora K, Grzesiak M, Duda M, et al. (2013): Effect of flutamide on folliculogenesis in the fetal porcine ovary – regulation by Kit ligand/c-Kit and IGF1/IGF1R systems. Anim Reprod Sci 142: 160-167.
16.
Copeland NG, Gilbert DJ, Cho BC, et al. (1990): Mastcell growth factor maps near the steel locus on mouse chromosome 10 and is deleted in a number of steel alleles. Cell 63: 175-183.
17.
Figueira MI, Correia S, Vaz CV, et al. (2016): Estrogens down-regulate the stem cell factor (SCF)/c-KIT system in prostate cells: Evidence of antiproliferative and proapoptotic effects. Biochem Pharmacol 99: 73-87.
18.
Riemann A, Schneider B, Gekle M, et al. (2011): Acidic Environment Leads to ROS-Induced MAPK Signaling in Cancer Cells. PLoS One 6: e22445.
19.
Gupta S, Takebe N, Lorusso P, et al. (2010): Targeting the Hedgehog pathway in cancer. Ther Adv Med Oncol 2: 237-250.
20.
Chen CD, Sawyers CL (2002): NF-kappaB activates prostate-specific antigen expression and is upregulated in androgen-independent prostate cancer. Mol Cell Biol 22: 2862-2870.
21.
Hsu A, Bray TM, Ho E, et al. (2010): Anti-inflammatory activity of soy and tea in prostate cancer prevention. Exp Biol Med 235: 659-667.
22.
Mitselou A, Galani V, Skoufi U, et al. (2016): Syndecan-1, Epithelial-Mesenchymal Transition Markers (E-cadherin/-catenin) and Neoangiogenesis-related Proteins (PCAM-1 and Endoglin) in Colorectal Cancer. Anticancer Res 36: 2271-2280.
23.
Xie F, Liu J, Li C, et al. (2016): Simvastatin blocks TGF-1-induced epithelial-mesenchymal transition in human prostate cancer cells. Oncol Lett 11: 3377-3383.
Share
RELATED ARTICLE
| eISSN: | 1644-4124 |
| ISSN: | 1426-3912 |
We process personal data collected when visiting the website. The function of obtaining information about users and their behavior is carried out by voluntarily entered information in forms and saving cookies in end devices. Data, including cookies, are used to provide services, improve the user experience and to analyze the traffic in accordance with the Privacy policy. Data are also collected and processed by Google Analytics tool (more).
You can change cookies settings in your browser. Restricted use of cookies in the browser configuration may affect some functionalities of the website.
You can change cookies settings in your browser. Restricted use of cookies in the browser configuration may affect some functionalities of the website.
