scholarly journals Role of GDF15 in methylseleninic acid-mediated inhibition of cell proliferation and induction of apoptosis in prostate cancer cells

PLoS ONE ◽  
2019 ◽  
Vol 14 (9) ◽  
pp. e0222812 ◽  
Author(s):  
Wenbo Zhang ◽  
Cheng Hu ◽  
Xiaojie Wang ◽  
Shanshan Bai ◽  
Subing Cao ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Prostate Cancer Cells ◽  
Methylseleninic Acid ◽  
Induction Of Apoptosis

scholarly journals Essential role of JunD in cell proliferation is mediated via MYC signaling in prostate cancer cells

2019 ◽  
Vol 448 ◽  
pp. 155-167 ◽  
Author(s):  
Bethtrice Elliott ◽  
Ana Cecilia Millena ◽  
Lilya Matyunina ◽  
Mengnan Zhang ◽  
Jin Zou ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Essential Role ◽  
Prostate Cancer Cells

scholarly journals Long non-coding RNA LINC01116 acts as an oncogene in prostate cancer cells through regulation of miR-744-5p/UBE2L3 axis

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Shengjie Yu ◽  
Huihong Yu ◽  
Yuanfeng Zhang ◽  
Chuan Liu ◽  
Weili Zhang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Migration And Invasion ◽  
Prostate Cancer Cells ◽  
Cancer Cell Growth ◽  
Non Coding Rna ◽  
The Relationship ◽  
Long Non Coding Rna

Abstract Background Long non-coding RNA (lncRNA) has been confirmed to exert a critical effect on the progression of tumors, including prostate cancer. Previous literature has demonstrated LINC01116 involves in activities of multiple cancers. However, the underlying role of LINC01116 in prostate cancer remains unclear. Methods qRT-PCR measured the expression of LINC01116 in prostate cancer cells. EdU experiment was used to detect cell proliferation. Transwell assays detected cell migration and invasion. Immunofluorescence staining and western blot assays were utilized to measure EMT progress. The binding relationship between RNAs was confirmed by a series of mechanism assays. In addition, rescue experiments were conducted to verify the relationship among RNAs. Results LINC01116 was found to be highly expressed in prostate cancer cells. Functional assays indicated that inhibition of LINC01116 could suppress cell proliferation, migration, invasion and EMT progress. Also, miR-744-5p was proven to bind with LINC01116. Moreover, UBE2L3 was verified as the target gene of miR-744-5p. In rescue assays, we discovered that inhibited miR-744-5p or overexpressed UBE2L3 could offset the suppressive influence of silencing LINC01116 on prostate cancer cells. Conclusion Our study suggested that lncRNA LINC01116 acted as an oncogene in prostate cancer and accelerated prostate cancer cell growth through regulating miR-744-5p/UBE2L3 axis.

scholarly journals PHF19 mediated regulation of proliferation and invasiveness in prostate cancer cells

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Payal Jain ◽  
Cecilia Ballare ◽  
Enrique Blanco ◽  
Pedro Vizan ◽  
Luciano Di Croce
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Target Genes ◽  
Embryonic Stem ◽  
Prostate Cancer Cells ◽  
Genome Wide ◽  
A Genome ◽  
Matrix Organization

The Polycomb-like protein PHF19/PCL3 associates with PRC2 and mediates its recruitment to chromatin in embryonic stem cells. PHF19 is also overexpressed in many cancers. However, neither PHF19 targets nor misregulated pathways involving PHF19 are known. Here, we investigate the role of PHF19 in prostate cancer cells. We find that PHF19 interacts with PRC2 and binds to PRC2 targets on chromatin. PHF19 target genes are involved in proliferation, differentiation, angiogenesis, and extracellular matrix organization. Depletion of PHF19 triggers an increase in MTF2/PCL2 chromatin recruitment, with a genome-wide gain in PRC2 occupancy and H3K27me3 deposition. Transcriptome analysis shows that PHF19 loss promotes deregulation of key genes involved in growth, metastasis, invasion, and of factors that stimulate blood vessels formation. Consistent with this, PHF19 silencing reduces cell proliferation, while promotes invasive growth and angiogenesis. Our findings reveal a role for PHF19 in controlling the balance between cell proliferation and invasiveness in prostate cancer.

scholarly journals The Role of S100A4 for Bone Metastasis in Prostate Cancer Cells

2020 ◽  
Author(s):  
Bongjun Kim ◽  
Haemin Kim ◽  
Suhan Jung ◽  
Jun-Oh Kwon ◽  
Min-Kyong Song ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Bone Metastasis ◽  
Cancer Cells ◽  
Cell Surface Receptor ◽  
Prostate Cancer Cells ◽  
S100a4 Protein ◽  
Knock Down ◽  
Pc3 Cells

Abstract Background: Prostate cancers frequently metastasize to bone, where the best microenvironment for distant colonization is provided. Since osteotropic metastasis of prostate cancer is a critical determinant of patients’ survival, searches for preventive measures are ongoing in the field. Therefore, it is important to dissect the mechanisms of each step of bone metastasis, including the epithelial-mesenchymal transition (EMT) and cross-talk between metastatic niches and cancer cells.Methods: In this study, we established a highly bone-metastatic subline of human prostate cancer cells by selecting bone-homing population of PC3 cells after cardiac injection of eight-week-old male BALB/c-nude mice. Then we assessed the proliferation, EMT, and migration properties of the subline (mtPC3) cells in comparison with the parental PC3 cells. To investigate the role of S100A4, we performed gene knock-down by lentiviral transduction, or treated cells with recombinant S100A4 protein or a S100A4-neutralizing antibody. The effect of cancer cells on osteoclastogenesis was evaluated after treatment of pre-osteoclasts with conditioned medium (CM) from cancer cells.Results: The mtPC3 cells secreted a markedly high level of S100A4 protein and showed elevated cell proliferation and mesenchymal properties. The increased proliferation and EMT of mtPC3 cells was inhibited by S100A4 knock-down, but was not affected by exogenous S100A4. Furthermore, S100A4 released from mtPC3 cells stimulated osteoclast development via the cell surface receptor RAGE. Down-regulation or neutralization of S100A4 in the CM of mtPC3 cells attenuated cancer-induced osteoclastogenesis. Conclusion: Altogether, our results suggest that intracellular S100A4 promotes cell proliferation and EMT in tumor cells, and that secreted S100A4 activates osteoclastogenesis, contributing to osteolytic bone metastasis. Thus, S100A4 upregulation in cancer cells highly metastatic to bone might be a key element in regulating bone metastasis.

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