Dataset Information

PCa_Secretome_PC3vsPC3nKR - Secretome profiling of PC3/nKR cells, a novel highly migrating prostate cancer subline derived from PC3 cells

ABSTRACT: Prostate cancer (PCa) is the most common cancer in American men. The American Cancer Society’s estimates for prostate cancer in the United States for 2017 are estimated 161.360 new cases and 26,730 deaths from PCa. To study metastatic properties to bone, PC-3 cell line is mainly used classical human prostatic carcinoma cell line, established and characterized its tumorigenicity from a human prostatic adenocarcinoma metastatic to bone is reported. In addition, PC-3/nkR cell line, natural killer(NK) cells-resistant, was isolated from mammary tumor xenograft studies in mice from PC-3 was implanted to nude mice and fecund to be tumorigenic in the early 2000s. In this study, we investigated secreted proteins of the conditioned media of PC-3 and PC-3/nkR cell lines using comparative proteomics technology to identify the molecular mechanism related to metastatic processes related to PC-3/nkR. Our study showed PC-3/nkR cells are new highly migrated and NK cells-resistant cell-line compared to PC-3 cells, as novel highly malignant tumor cells to study mechanisms of PCa metastatic.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Epithelial Cell Of Prostate

DISEASE(S): Prostate Adenocarcinoma

SUBMITTER: Oh Kwang Kwon

LAB HEAD: Sangkyu Lee

PROVIDER: PXD008184 | Pride | 2019-08-19

REPOSITORIES: Pride

ACCESS DATA

Dataset's files

Source:

			Action	DRS
	20151015_KNUP_Secretome_TMT6_1.raw	Raw
	20151015_KNUP_Secretome_TMT6_2.raw	Raw
	20151016_KNUP_Secretome_TMT6_1_F1.raw	Raw
	20151016_KNUP_Secretome_TMT6_1_F2.raw	Raw
	20151016_KNUP_Secretome_TMT6_1_F3.raw	Raw

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Publications

Secretome profiling of PC3/nKR cells, a novel highly migrating prostate cancer subline derived from PC3 cells.

Jeon Ju Mi JM Kwon Oh Kwang OK Na Ann-Yae AY Sung Eun Ji EJ Cho Il Je IJ Kim Mirae M Yea Sung Su SS Chun So Young SY Lee Jun Hyung JH Ha Yun-Sok YS Kwon Tae Gyun TG Lee Sangkyu S

PloS one 20190812 8

Prostate cancer (PCa) is the most common cancer among men worldwide. Most PCa cases are not fatal; however, the outlook is poor when PCa spreads to another organ. Bone is the target organ in about 80% of patients who experience metastasis from a primary PCa tumor. In the present study, we characterized the secretome of PC3/nKR cells, which are a new subline of PC3 cells that were originally isolated from nude mice that were implanted with PC3 cells without anti-natural killer (NK) cell treatment ...[more]

PMID: 31404090

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Project description:Background: Aldo-keto reductase (AKR) 1C family member 3 (AKR1C3), one of four identified human AKR enzymes, catalyzes steroid, prostaglandin, and xenobiotic metabolism. In the prostate, AKR1C3 is up-regulated in localized and advanced prostate adenocarcinoma, and is associated with prostate cancer (PCa) aggressiveness. Here we provide initial evidence for potential roles of AKR1C3 in PCa progression. Methods: Spatial distribution of AKR1C3 was analyzed using immunohistochemical staining in prostate adenocarcinoma tissue array. Human PCa PC-3 cells were stably transfected with AKR1C3 cDNA to establish PC3-AKR1C3 transfectants. Microarray and bioinformatics analyses were performed to identify pathways that are activated by elevated AKR1C3 expression in PCa cells. Functional confirmation of microarray and bioinformatics results was performed by immunoblot analysis and an in vitro Matrigel angiogenesis assay. Results: Elevated AKR1C3 expression was specifically limited to human prostate adenocarcinoma. Microarray and bioinformatics analysis suggested that elevated AKR1C3 expression in PC-3 cells modulates estradiol and androgen metabolism and activates insulin growth factor (IGF)-1 and Akt signaling pathways. Immunoblots confirmed that phosphorylated levels of IGF-1 receptor (IGF-1R) and Akt are significantly up-regulated in PC3-AKR1C3 as compared to mock transfectants. PC3-AKR1C3 transfectants promoted endothelial cell tube formation in Matrigel as compared to parental PC-3 cells and mock transfectants. Conclusion: Microarray and bioinformatics data followed by biological analyses suggest that elevated AKR1C3 expression in PC-3 cells promotes PCa angiogenesis and aggressiveness. These results suggest AKR1C3 can promote the aggressiveness of PCa through modulating estrogen and androgen metabolism with subsequent activation of growth factor IGF-1 and cytoplasmic Akt signaling pathways. Total RNA from mock- and ACR1C3 transfected PC-3 cells was isolated, with 2 or 3 biological replicates each. Gene expression data from AKR1C3 transfected PC-3 cells were compared with mock-transfected data.