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CMTM3 inhibits cell migration and invasion and correlates with favorable prognosis in gastric cancer.

Su Y, Lin Y, Zhang L, Liu B, Yuan W, Mo X, Wang X, Li H, Xing X, Cheng X, Dong B, Hu Y, Du H, Zhu Y, Ding N, Li J, Liu W, Ma Y, Qiu X, Ji J, Han W - Cancer Sci. (2013)

Bottom Line: Restoration of CMTM3 significantly affected migration and invasion of AGS and SGC-7901 cells (P < 0.001).In vivo experiments showed that peritoneal disseminated metastases were significantly suppressed by CMTM3 (P < 0.001).We further showed that the expression of MMP2 and the phosphorylation of Erk1/2 were decreased when CMTM3 was restored.

View Article: PubMed Central - PubMed

Affiliation: Department of Immunology, School of Basic Medical Sciences, Peking University Health Science Center, Peking University Center for Human Disease Genomics, Beijing, China; Key Laboratory of Medical Immunology, Ministry of Health, Beijing, China.

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(a) Overexpression of CMTM3 in SGC-7901 and AGS gastric cancer cells was detected by Western blot analysis. Different MOIs (0, 60, 120, and 240) of adenovirus were used. (b) Effect of CMTM3 on cell migration was observed by wound healing assay. Photographs were taken at indicated time points after the scratch (magnification, ×100). (c, d) Effects of CMTM3 on cell migration (c) and invasion (d) were detected by Transwell assay (magnification, ×100). The statistical graph indicates the mean ± SD and P-value of the number of cells per five random high power fields (magnification, ×400) counted from three independent experiments. (e) Ability of cell migration and invasion in vivo was detected by a peritoneal spreading model in nude mice. Photographs were taken after the mice were killed. Arrows indicate tumor nodules. NS, not significant. *P < 0.05; ***P < 0.001.
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fig02: (a) Overexpression of CMTM3 in SGC-7901 and AGS gastric cancer cells was detected by Western blot analysis. Different MOIs (0, 60, 120, and 240) of adenovirus were used. (b) Effect of CMTM3 on cell migration was observed by wound healing assay. Photographs were taken at indicated time points after the scratch (magnification, ×100). (c, d) Effects of CMTM3 on cell migration (c) and invasion (d) were detected by Transwell assay (magnification, ×100). The statistical graph indicates the mean ± SD and P-value of the number of cells per five random high power fields (magnification, ×400) counted from three independent experiments. (e) Ability of cell migration and invasion in vivo was detected by a peritoneal spreading model in nude mice. Photographs were taken after the mice were killed. Arrows indicate tumor nodules. NS, not significant. *P < 0.05; ***P < 0.001.

Mentions: CMTM3 is downregulated in gastric cancer cell lines and primary tissues both at mRNA and protein levels. To know the function of CMTM3 in gastric cancer, we infected cells with adenovirus and confirmed the expression of CMTM3 in AGS and SGC-7901 cells by Western blotting (Fig.2a). We first tested the effect of CMTM3 on cell proliferation and apoptosis, and found that CMTM3 did not significantly affect cell growth or apoptosis in AGS and SGC-7901 cells (data not shown). To evaluate whether CMTM3 had any effect on cell mobility or invasion ability, we carried out the wound healing assay using AGS and SGC-7901 cells. After observing for 36–48 h after the scratch, we found that cells in the CMTM3 group were distinctively less migrated than those in the Mock group (Fig.2a). Strikingly, in SGC-7901 cells, the Mock group healed the wounded area in 36 h, whereas the CMTM3 group was unable to heal in the same time period. The relative migration rates were statistically significant (P < 0.001) (Fig.2b). These results showed that the migratory capacity of both cells lines was suppressed by CMTM3. To confirm this conclusion, we used a Transwell system with or without Matrigel to detect cell migration and invasion. As shown in Figure2(c,d), CMTM3 groups showed a markedly lower migratory and invasive capacity compared to the Mock groups, suggesting that CMTM3 might decrease the abilities of cell motility and invasion. Overall, the results suggest that CMTM3 inhibits migration and invasion of gastric cancer cells in vitro.


CMTM3 inhibits cell migration and invasion and correlates with favorable prognosis in gastric cancer.

Su Y, Lin Y, Zhang L, Liu B, Yuan W, Mo X, Wang X, Li H, Xing X, Cheng X, Dong B, Hu Y, Du H, Zhu Y, Ding N, Li J, Liu W, Ma Y, Qiu X, Ji J, Han W - Cancer Sci. (2013)

(a) Overexpression of CMTM3 in SGC-7901 and AGS gastric cancer cells was detected by Western blot analysis. Different MOIs (0, 60, 120, and 240) of adenovirus were used. (b) Effect of CMTM3 on cell migration was observed by wound healing assay. Photographs were taken at indicated time points after the scratch (magnification, ×100). (c, d) Effects of CMTM3 on cell migration (c) and invasion (d) were detected by Transwell assay (magnification, ×100). The statistical graph indicates the mean ± SD and P-value of the number of cells per five random high power fields (magnification, ×400) counted from three independent experiments. (e) Ability of cell migration and invasion in vivo was detected by a peritoneal spreading model in nude mice. Photographs were taken after the mice were killed. Arrows indicate tumor nodules. NS, not significant. *P < 0.05; ***P < 0.001.
© Copyright Policy - open-access
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4317871&req=5

fig02: (a) Overexpression of CMTM3 in SGC-7901 and AGS gastric cancer cells was detected by Western blot analysis. Different MOIs (0, 60, 120, and 240) of adenovirus were used. (b) Effect of CMTM3 on cell migration was observed by wound healing assay. Photographs were taken at indicated time points after the scratch (magnification, ×100). (c, d) Effects of CMTM3 on cell migration (c) and invasion (d) were detected by Transwell assay (magnification, ×100). The statistical graph indicates the mean ± SD and P-value of the number of cells per five random high power fields (magnification, ×400) counted from three independent experiments. (e) Ability of cell migration and invasion in vivo was detected by a peritoneal spreading model in nude mice. Photographs were taken after the mice were killed. Arrows indicate tumor nodules. NS, not significant. *P < 0.05; ***P < 0.001.
Mentions: CMTM3 is downregulated in gastric cancer cell lines and primary tissues both at mRNA and protein levels. To know the function of CMTM3 in gastric cancer, we infected cells with adenovirus and confirmed the expression of CMTM3 in AGS and SGC-7901 cells by Western blotting (Fig.2a). We first tested the effect of CMTM3 on cell proliferation and apoptosis, and found that CMTM3 did not significantly affect cell growth or apoptosis in AGS and SGC-7901 cells (data not shown). To evaluate whether CMTM3 had any effect on cell mobility or invasion ability, we carried out the wound healing assay using AGS and SGC-7901 cells. After observing for 36–48 h after the scratch, we found that cells in the CMTM3 group were distinctively less migrated than those in the Mock group (Fig.2a). Strikingly, in SGC-7901 cells, the Mock group healed the wounded area in 36 h, whereas the CMTM3 group was unable to heal in the same time period. The relative migration rates were statistically significant (P < 0.001) (Fig.2b). These results showed that the migratory capacity of both cells lines was suppressed by CMTM3. To confirm this conclusion, we used a Transwell system with or without Matrigel to detect cell migration and invasion. As shown in Figure2(c,d), CMTM3 groups showed a markedly lower migratory and invasive capacity compared to the Mock groups, suggesting that CMTM3 might decrease the abilities of cell motility and invasion. Overall, the results suggest that CMTM3 inhibits migration and invasion of gastric cancer cells in vitro.

Bottom Line: Restoration of CMTM3 significantly affected migration and invasion of AGS and SGC-7901 cells (P < 0.001).In vivo experiments showed that peritoneal disseminated metastases were significantly suppressed by CMTM3 (P < 0.001).We further showed that the expression of MMP2 and the phosphorylation of Erk1/2 were decreased when CMTM3 was restored.

View Article: PubMed Central - PubMed

Affiliation: Department of Immunology, School of Basic Medical Sciences, Peking University Health Science Center, Peking University Center for Human Disease Genomics, Beijing, China; Key Laboratory of Medical Immunology, Ministry of Health, Beijing, China.

Show MeSH
Related in: MedlinePlus