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Roles of DPY30 in the Proliferation and Motility of Gastric Cancer Cells.

Lee YJ, Han ME, Baek SJ, Kim SY, Oh SO - PLoS ONE (2015)

Bottom Line: Various types of histone methylation have been associated with cancer progression.Depending on the methylation site in histone proteins, its effects on transcription are different.Its knockdown by siRNA decreased the proliferation, migration, and invasion of gastric cancer cells, whereas its overexpression showed the opposite effects.

View Article: PubMed Central - PubMed

Affiliation: Departments of Anatomy, School of Medicine, Pusan National University, Busan, Republic of Korea.

ABSTRACT
Various types of histone methylation have been associated with cancer progression. Depending on the methylation site in histone proteins, its effects on transcription are different. DPY30 is a common member of SET1/MLL histone H3K4 methyltransferase complexes. However, its expression and roles in gastric cancer have been poorly characterized. To determine whether DPY30 has pathophysiological roles in gastric cancer, its expression and roles were examined. Immunohistochemistry and real time PCR showed up-regulation of DPY30 expression in some gastric cancer cell lines and patients' tissues. Its knockdown by siRNA decreased the proliferation, migration, and invasion of gastric cancer cells, whereas its overexpression showed the opposite effects. These results indicate that DPY30 has critical roles in the proliferation, migration, and invasion of gastric cancer cells, and suggest DPY30 might be a therapeutic target in gastric cancer.

No MeSH data available.


Related in: MedlinePlus

WRAD components regulated proliferation of gastric cancer cells.(A) The mRNA levels of WDR5, RBBP5 and ASH2L in HFE145, SNU1, SNU16, SNU216 and SNU638 cells were determined by real-time PCR, using specific primers for WDR5, RBBP5 and ASH2L. GAPDH was used to normalize data. (B) Knockdown efficiency was determined by real-time PCR. Knockdown efficiency was determined after transfecting cells with 100 nM WDR5, RBBP5 and ASH2L siRNA or scrambled (SCR). (C) Effects of WDR5, RBBP5 and ASH2L knockdown on cell proliferation. A cell viability assay was used to measure cell proliferation in the presence of 1% FBS. 24 hrs after transduction, cell viability assays were performed. Values are the means ± SDs of three independent experiments performed in triplicate. *, p < 0.01 (Student’s t test, versus HFE145 (A) or SCR (B-C)).
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pone.0131863.g003: WRAD components regulated proliferation of gastric cancer cells.(A) The mRNA levels of WDR5, RBBP5 and ASH2L in HFE145, SNU1, SNU16, SNU216 and SNU638 cells were determined by real-time PCR, using specific primers for WDR5, RBBP5 and ASH2L. GAPDH was used to normalize data. (B) Knockdown efficiency was determined by real-time PCR. Knockdown efficiency was determined after transfecting cells with 100 nM WDR5, RBBP5 and ASH2L siRNA or scrambled (SCR). (C) Effects of WDR5, RBBP5 and ASH2L knockdown on cell proliferation. A cell viability assay was used to measure cell proliferation in the presence of 1% FBS. 24 hrs after transduction, cell viability assays were performed. Values are the means ± SDs of three independent experiments performed in triplicate. *, p < 0.01 (Student’s t test, versus HFE145 (A) or SCR (B-C)).

Mentions: Because DPY30 is a component of WARDs, we examined expressions and roles of other components of WARDs. Real-time PCR showed that mRNA levels of WDR5 and RBBP5 in SNU1, SNU16, SNU216 and SNU638 were similar to those of HFE145. However, the mRNA level of ASH2L were significantly higher (fold change > 3) in SNU1 and SNU16 than in HFE145 cells (Fig 3A) as DPY30 in Fig 1E. In order to investigate whether WRAD components are associated with proliferation of gastric cancer cells, we knockdowned each WRAD component using their specific siRNA and monitored knockdown efficiencies by real-time PCR (Fig 3B). Each siRNA (100 nM) decreased the mRNA levels in SNU1 and SNU16 cells as compared with SCR by 65%-75%. Knockdown of WDR5 and RBBP5 inhibited the proliferation of SNU1 and SNU16 cells as compared with SCR by 30–48% (Fig 3C). However, ASH2L inhibited the proliferation of SNU1 and SNU16, in which the expression level of ASH2L was high, as compared with SCR by 85% and 75%, respectively.


Roles of DPY30 in the Proliferation and Motility of Gastric Cancer Cells.

Lee YJ, Han ME, Baek SJ, Kim SY, Oh SO - PLoS ONE (2015)

WRAD components regulated proliferation of gastric cancer cells.(A) The mRNA levels of WDR5, RBBP5 and ASH2L in HFE145, SNU1, SNU16, SNU216 and SNU638 cells were determined by real-time PCR, using specific primers for WDR5, RBBP5 and ASH2L. GAPDH was used to normalize data. (B) Knockdown efficiency was determined by real-time PCR. Knockdown efficiency was determined after transfecting cells with 100 nM WDR5, RBBP5 and ASH2L siRNA or scrambled (SCR). (C) Effects of WDR5, RBBP5 and ASH2L knockdown on cell proliferation. A cell viability assay was used to measure cell proliferation in the presence of 1% FBS. 24 hrs after transduction, cell viability assays were performed. Values are the means ± SDs of three independent experiments performed in triplicate. *, p < 0.01 (Student’s t test, versus HFE145 (A) or SCR (B-C)).
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Related In: Results  -  Collection

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pone.0131863.g003: WRAD components regulated proliferation of gastric cancer cells.(A) The mRNA levels of WDR5, RBBP5 and ASH2L in HFE145, SNU1, SNU16, SNU216 and SNU638 cells were determined by real-time PCR, using specific primers for WDR5, RBBP5 and ASH2L. GAPDH was used to normalize data. (B) Knockdown efficiency was determined by real-time PCR. Knockdown efficiency was determined after transfecting cells with 100 nM WDR5, RBBP5 and ASH2L siRNA or scrambled (SCR). (C) Effects of WDR5, RBBP5 and ASH2L knockdown on cell proliferation. A cell viability assay was used to measure cell proliferation in the presence of 1% FBS. 24 hrs after transduction, cell viability assays were performed. Values are the means ± SDs of three independent experiments performed in triplicate. *, p < 0.01 (Student’s t test, versus HFE145 (A) or SCR (B-C)).
Mentions: Because DPY30 is a component of WARDs, we examined expressions and roles of other components of WARDs. Real-time PCR showed that mRNA levels of WDR5 and RBBP5 in SNU1, SNU16, SNU216 and SNU638 were similar to those of HFE145. However, the mRNA level of ASH2L were significantly higher (fold change > 3) in SNU1 and SNU16 than in HFE145 cells (Fig 3A) as DPY30 in Fig 1E. In order to investigate whether WRAD components are associated with proliferation of gastric cancer cells, we knockdowned each WRAD component using their specific siRNA and monitored knockdown efficiencies by real-time PCR (Fig 3B). Each siRNA (100 nM) decreased the mRNA levels in SNU1 and SNU16 cells as compared with SCR by 65%-75%. Knockdown of WDR5 and RBBP5 inhibited the proliferation of SNU1 and SNU16 cells as compared with SCR by 30–48% (Fig 3C). However, ASH2L inhibited the proliferation of SNU1 and SNU16, in which the expression level of ASH2L was high, as compared with SCR by 85% and 75%, respectively.

Bottom Line: Various types of histone methylation have been associated with cancer progression.Depending on the methylation site in histone proteins, its effects on transcription are different.Its knockdown by siRNA decreased the proliferation, migration, and invasion of gastric cancer cells, whereas its overexpression showed the opposite effects.

View Article: PubMed Central - PubMed

Affiliation: Departments of Anatomy, School of Medicine, Pusan National University, Busan, Republic of Korea.

ABSTRACT
Various types of histone methylation have been associated with cancer progression. Depending on the methylation site in histone proteins, its effects on transcription are different. DPY30 is a common member of SET1/MLL histone H3K4 methyltransferase complexes. However, its expression and roles in gastric cancer have been poorly characterized. To determine whether DPY30 has pathophysiological roles in gastric cancer, its expression and roles were examined. Immunohistochemistry and real time PCR showed up-regulation of DPY30 expression in some gastric cancer cell lines and patients' tissues. Its knockdown by siRNA decreased the proliferation, migration, and invasion of gastric cancer cells, whereas its overexpression showed the opposite effects. These results indicate that DPY30 has critical roles in the proliferation, migration, and invasion of gastric cancer cells, and suggest DPY30 might be a therapeutic target in gastric cancer.

No MeSH data available.


Related in: MedlinePlus