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Wnt5a-Ror2 signaling in mesenchymal stem cells promotes proliferation of gastric cancer cells by activating CXCL16-CXCR6 axis.

Takiguchi G, Nishita M, Kurita K, Kakeji Y, Minami Y - Cancer Sci. (2016)

Bottom Line: Wnt5a-Ror2 signaling has been shown to play important roles in promoting aggressiveness of various cancer cells in a cell-autonomous manner.However, little is known about its function in cancer-associated stromal cells, including mesenchymal stem cells (MSCs).Interestingly, it was found that expression of CXCL16 in MSCs is augmented by Wnt5a-Ror2 signaling, and that recombinant chemokine (C-X-C motif) ligand (CXCL)16 protein can enhance proliferation of MKN45 cells in the absence of MSCs.

View Article: PubMed Central - PubMed

Affiliation: Division of Cell Physiology, Department of Physiology and Cell Biology, Graduate School of Medicine, Kobe University, Kobe, Japan.

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Expression of Ror2 in mesenchymal stem cells (MSCs) is required for the ability of MSCs to promote proliferation of MKN45‐Luc cells in coculture. (a) Suppressed expression of Ror2 in MSCs treated with siRNAs for Ror2. Cells were transfected with either control (ctrl) siRNA or three different siRNAs against Ror2 (#1, #2, #3) and cultured for 5 or 9 days. Expression levels of Ror2 mRNA were measured by quantitative RT‐PCR analyses. (b,c) MKN45‐Luc cells were cultured singly (monoculture) or cocultured with siRNA‐transfected MSCs either directly (b) or indirectly (c). After 9 days in culture, luciferase activities were measured. Data are expressed as mean ± SD (n = 3). *P < 0.005; **P < 0.001, t‐test.
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cas12871-fig-0002: Expression of Ror2 in mesenchymal stem cells (MSCs) is required for the ability of MSCs to promote proliferation of MKN45‐Luc cells in coculture. (a) Suppressed expression of Ror2 in MSCs treated with siRNAs for Ror2. Cells were transfected with either control (ctrl) siRNA or three different siRNAs against Ror2 (#1, #2, #3) and cultured for 5 or 9 days. Expression levels of Ror2 mRNA were measured by quantitative RT‐PCR analyses. (b,c) MKN45‐Luc cells were cultured singly (monoculture) or cocultured with siRNA‐transfected MSCs either directly (b) or indirectly (c). After 9 days in culture, luciferase activities were measured. Data are expressed as mean ± SD (n = 3). *P < 0.005; **P < 0.001, t‐test.

Mentions: It was found that expression levels of both Ror2 and Wnt5a were relatively high in MSCs, but were marginal if any in MKN45‐Luc cells (Fig. S2). Thus, we then examined a possible role of Wnt5a‐Ror2 signaling in MSCs in promoting proliferation of MKN45‐Luc cells. Suppressed expression of Ror2 or Wnt5a in MSCs resulted in the inhibition of promoted proliferation of MKN45‐Luc cells by direct or indirect coculture with MSCs (Figs 2,S3). Furthermore, proliferation and viability of MSCs were unaffected by suppressed expression of Ror2 in the cells as assessed by WST assay (Fig. S4a). These results suggest that Wnt5a‐Ror2 signaling in MSCs might play a role in promoting proliferation of MKN45 cells.


Wnt5a-Ror2 signaling in mesenchymal stem cells promotes proliferation of gastric cancer cells by activating CXCL16-CXCR6 axis.

Takiguchi G, Nishita M, Kurita K, Kakeji Y, Minami Y - Cancer Sci. (2016)

Expression of Ror2 in mesenchymal stem cells (MSCs) is required for the ability of MSCs to promote proliferation of MKN45‐Luc cells in coculture. (a) Suppressed expression of Ror2 in MSCs treated with siRNAs for Ror2. Cells were transfected with either control (ctrl) siRNA or three different siRNAs against Ror2 (#1, #2, #3) and cultured for 5 or 9 days. Expression levels of Ror2 mRNA were measured by quantitative RT‐PCR analyses. (b,c) MKN45‐Luc cells were cultured singly (monoculture) or cocultured with siRNA‐transfected MSCs either directly (b) or indirectly (c). After 9 days in culture, luciferase activities were measured. Data are expressed as mean ± SD (n = 3). *P < 0.005; **P < 0.001, t‐test.
© Copyright Policy - creativeCommonsBy-nc
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4814243&req=5

cas12871-fig-0002: Expression of Ror2 in mesenchymal stem cells (MSCs) is required for the ability of MSCs to promote proliferation of MKN45‐Luc cells in coculture. (a) Suppressed expression of Ror2 in MSCs treated with siRNAs for Ror2. Cells were transfected with either control (ctrl) siRNA or three different siRNAs against Ror2 (#1, #2, #3) and cultured for 5 or 9 days. Expression levels of Ror2 mRNA were measured by quantitative RT‐PCR analyses. (b,c) MKN45‐Luc cells were cultured singly (monoculture) or cocultured with siRNA‐transfected MSCs either directly (b) or indirectly (c). After 9 days in culture, luciferase activities were measured. Data are expressed as mean ± SD (n = 3). *P < 0.005; **P < 0.001, t‐test.
Mentions: It was found that expression levels of both Ror2 and Wnt5a were relatively high in MSCs, but were marginal if any in MKN45‐Luc cells (Fig. S2). Thus, we then examined a possible role of Wnt5a‐Ror2 signaling in MSCs in promoting proliferation of MKN45‐Luc cells. Suppressed expression of Ror2 or Wnt5a in MSCs resulted in the inhibition of promoted proliferation of MKN45‐Luc cells by direct or indirect coculture with MSCs (Figs 2,S3). Furthermore, proliferation and viability of MSCs were unaffected by suppressed expression of Ror2 in the cells as assessed by WST assay (Fig. S4a). These results suggest that Wnt5a‐Ror2 signaling in MSCs might play a role in promoting proliferation of MKN45 cells.

Bottom Line: Wnt5a-Ror2 signaling has been shown to play important roles in promoting aggressiveness of various cancer cells in a cell-autonomous manner.However, little is known about its function in cancer-associated stromal cells, including mesenchymal stem cells (MSCs).Interestingly, it was found that expression of CXCL16 in MSCs is augmented by Wnt5a-Ror2 signaling, and that recombinant chemokine (C-X-C motif) ligand (CXCL)16 protein can enhance proliferation of MKN45 cells in the absence of MSCs.

View Article: PubMed Central - PubMed

Affiliation: Division of Cell Physiology, Department of Physiology and Cell Biology, Graduate School of Medicine, Kobe University, Kobe, Japan.

Show MeSH
Related in: MedlinePlus