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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

DPY30 regulated the invasion of gastric cancer cells.(A-B) A Matrigel invasion assay was used to measure gastric cancer cell invasion. Presented results are representative of the results obtained. 10% FBS was used to induce invasion, and mitomycin C (0.01 μg/ml) was added to remove effects of proliferation. Invasion assays were performed two days after transfection with 100 nM ORF-targeting DPY30 or SCR siRNA. After culture for one day, invasion assay was carried out for the DPY30-over and mock cells. Bar = 100 μm. (C) Invasive cells were counted and results are displayed as a bar graph. Values are the means ± SDs of three independent experiments performed in triplicate. *, p < 0.01 (Student’s t test, versus SCR or Mock).
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pone.0131863.g005: DPY30 regulated the invasion of gastric cancer cells.(A-B) A Matrigel invasion assay was used to measure gastric cancer cell invasion. Presented results are representative of the results obtained. 10% FBS was used to induce invasion, and mitomycin C (0.01 μg/ml) was added to remove effects of proliferation. Invasion assays were performed two days after transfection with 100 nM ORF-targeting DPY30 or SCR siRNA. After culture for one day, invasion assay was carried out for the DPY30-over and mock cells. Bar = 100 μm. (C) Invasive cells were counted and results are displayed as a bar graph. Values are the means ± SDs of three independent experiments performed in triplicate. *, p < 0.01 (Student’s t test, versus SCR or Mock).

Mentions: We next examined whether DPY30 regulates the migration of gastric cancer cells. Knockdown of DPY30 decreased the FBS-induced migrations of SNU1 and SNU16 cells versus SCR by 35% and 45%, respectively (Fig 4). In contrast, DPY30 overexpression increased the FBS-induced migrations of SNU216 and SNU638 cells versus mock cells by 2.5 and 2.2 fold, respectively (Fig 4). These results led us to examine the role of DPY30 in the invasion of gastric cancer cells. In a Matrigel invasion assay, DPY30 siRNA inhibited the FBS-induced invasions of SNU1 and SNU16 cells versus SCR siRNA by 65% and 84%, respectively (Fig 5A and 5C). Furthermore, DPY30 overexpression increased the FBS-induced invasions of SNU216 and SNU638 cells versus mock cells by 3.2 and 2.9 fold, respectively (Fig 5B and 5C). These results show that DPY30 promotes the migration and invasion of gastric cancer cells.


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)

DPY30 regulated the invasion of gastric cancer cells.(A-B) A Matrigel invasion assay was used to measure gastric cancer cell invasion. Presented results are representative of the results obtained. 10% FBS was used to induce invasion, and mitomycin C (0.01 μg/ml) was added to remove effects of proliferation. Invasion assays were performed two days after transfection with 100 nM ORF-targeting DPY30 or SCR siRNA. After culture for one day, invasion assay was carried out for the DPY30-over and mock cells. Bar = 100 μm. (C) Invasive cells were counted and results are displayed as a bar graph. Values are the means ± SDs of three independent experiments performed in triplicate. *, p < 0.01 (Student’s t test, versus SCR or Mock).
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pone.0131863.g005: DPY30 regulated the invasion of gastric cancer cells.(A-B) A Matrigel invasion assay was used to measure gastric cancer cell invasion. Presented results are representative of the results obtained. 10% FBS was used to induce invasion, and mitomycin C (0.01 μg/ml) was added to remove effects of proliferation. Invasion assays were performed two days after transfection with 100 nM ORF-targeting DPY30 or SCR siRNA. After culture for one day, invasion assay was carried out for the DPY30-over and mock cells. Bar = 100 μm. (C) Invasive cells were counted and results are displayed as a bar graph. Values are the means ± SDs of three independent experiments performed in triplicate. *, p < 0.01 (Student’s t test, versus SCR or Mock).
Mentions: We next examined whether DPY30 regulates the migration of gastric cancer cells. Knockdown of DPY30 decreased the FBS-induced migrations of SNU1 and SNU16 cells versus SCR by 35% and 45%, respectively (Fig 4). In contrast, DPY30 overexpression increased the FBS-induced migrations of SNU216 and SNU638 cells versus mock cells by 2.5 and 2.2 fold, respectively (Fig 4). These results led us to examine the role of DPY30 in the invasion of gastric cancer cells. In a Matrigel invasion assay, DPY30 siRNA inhibited the FBS-induced invasions of SNU1 and SNU16 cells versus SCR siRNA by 65% and 84%, respectively (Fig 5A and 5C). Furthermore, DPY30 overexpression increased the FBS-induced invasions of SNU216 and SNU638 cells versus mock cells by 3.2 and 2.9 fold, respectively (Fig 5B and 5C). These results show that DPY30 promotes the migration and invasion of gastric cancer cells.

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