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Gadolinium inhibits prostate cancer PC3 cell migration and suppresses osteoclast differentiation in vitro
Peng Wang1, Xiao-Min Zou, Jian Huang
1Peking University School of Pharmaceutical Sciences, 38 Xueyuan Road, Beijing 100191, Peoples Republic of China.
Abstract:
This study examined whether Gd (gadolinium) could suppress prostate cancer cell migration and prostate cancer cell-induced osteoclast differentiation. MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide] and colony forming assay showed that GdCl3 treatment inhibited both cell viability and colony forming ability in PC3 cells more significantly than that in DU145 cells. Annexin/PI (propidium iodide) staining showed an increase in apoptotic death of PC3 cells in the presence of GdCl3. Wound healing and adhesion assay indicated that GdCl3 suppressed PC3 cell migration. Western-blot analysis demonstrated that GdCl3 treatment inhibited phosphorylation of ERK (extracellular-signal-regulated kinase) and p38 MAPK (mitogen-activated protein kinase). Pretreatment with PTx (pertussis toxin), a Gi protein inhibitor, conferred resistance to GdCl3-induced colony formation, ERK and p38 phosphorylation in PC3 cells. Moreover, GdCl3 inhibited PC3 cell-induced osteoclast differentiation. RT-PCR (reverse transcription-PCR) indicated that GdCl3 decreased the expression of RANKL (receptor activator of nuclear factor-κB ligand) in PC3 cells, whereas it increased the expression of OPG (osteoprotegerin) in PC3 and DU145 cells. In conclusion, the present study indicated that GdCl3 inhibited PC3 cell migration mediated by the inactivation of both ERK and p38 MAPK pathways via PTx-sensitive G proteins, and also suppressed PC3 cell-induced osteoclast differentiation via regulating the mRNA expression of OPG and RANKL.
Insights
Gadolinium chloride (GdCl3) inhibits prostate cancer cell migration and osteoclast differentiation. GdCl3 affects cell viability, apoptosis, and key signaling pathways like ERK and p38 MAPK.
Area of Science:
- Oncology
- Biochemistry
- Cell Biology
Background:
- Prostate cancer metastasis involves cell migration and bone remodeling.
- Osteoclast differentiation plays a crucial role in bone metastasis of prostate cancer.
- Gadolinium (Gd) has shown potential in cancer research.
Purpose of the Study:
- To investigate the effects of GdCl3 on prostate cancer cell migration.
- To determine GdCl3's impact on prostate cancer cell-induced osteoclast differentiation.
- To elucidate the underlying molecular mechanisms of GdCl3's action.
Main Methods:
- Cell viability assays (MTT, colony forming assay)
- Apoptosis assays (Annexin/PI staining)
- Cell migration assays (wound healing, adhesion assay)
- Western-blot analysis for ERK and p38 MAPK phosphorylation
- Reverse transcription-PCR (RT-PCR) for RANKL and OPG expression
Main Results:
- GdCl3 significantly inhibited viability and colony formation in PC3 cells.
- GdCl3 induced apoptosis and suppressed migration of PC3 cells.
- GdCl3 inhibited ERK and p38 MAPK phosphorylation via PTx-sensitive G proteins.
- GdCl3 suppressed PC3 cell-induced osteoclast differentiation by downregulating RANKL and upregulating OPG mRNA.
Conclusions:
- GdCl3 inhibits prostate cancer cell migration by inactivating ERK and p38 MAPK pathways through PTx-sensitive G proteins.
- GdCl3 suppresses prostate cancer cell-induced osteoclast differentiation by modulating RANKL and OPG expression.
- GdCl3 demonstrates potential as a therapeutic agent for prostate cancer metastasis.
