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MicroRNA-135a acts as a putative tumor suppressor by directly targeting very low density lipoprotein receptor in human gallbladder cancer.

Zhou H, Guo W, Zhao Y, Wang Y, Zha R, Ding J, Liang L, Yang G, Chen Z, Ma B, Yin B - Cancer Sci. (2014)

Bottom Line: Moreover, very low density lipoprotein receptor (VLDLR), which is often upregulated in GBC tissues, was identified as a direct functional target of miR-135a-5p.Furthermore, the p38 MAPK pathway was proven to be involved in miR-135a-VLDLR downstream signaling.Together, these results suggested that the miR-135a-VLDLR-p38 axis may contribute to GBC cell proliferation.

View Article: PubMed Central - PubMed

Affiliation: Department of General Surgery, Huashan Hospital, Fudan University, Shanghai, China.

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MicroRNA-135a (miR-135a) inhibited gallbladder cancer (GBC) cell proliferation in vitro and in vivo. (a,b) Cell counting (CCK-8) and colony formation assays of GBC-SD and EH-GB1 cells stably expressing miR-135a or GFP control. *P < 0.05 (Lenti-GFP vs Lenti-miR-135a). (c) Tumor formation in nude mice with GBC-SD cells stably expressing miR-135a or GFP control and the tumor weight. *P < 0.05 (Lenti-GFP vs Lenti-miR-135a).
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fig02: MicroRNA-135a (miR-135a) inhibited gallbladder cancer (GBC) cell proliferation in vitro and in vivo. (a,b) Cell counting (CCK-8) and colony formation assays of GBC-SD and EH-GB1 cells stably expressing miR-135a or GFP control. *P < 0.05 (Lenti-GFP vs Lenti-miR-135a). (c) Tumor formation in nude mice with GBC-SD cells stably expressing miR-135a or GFP control and the tumor weight. *P < 0.05 (Lenti-GFP vs Lenti-miR-135a).

Mentions: MicrRNA-135a-5p mimic transfection could inhibit the proliferation and colony formation ability of GBC-SD and EH-GB1 cells (Fig. S2b,c), and arrest the cells in G1/S phase (Fig. S3a). Caspase-Glo 3/7 Assay (Promega) showed that miR-135a-5p could slightly upregulate caspase 3/7 activity (Fig. S3b), whereas SA-β-gal staining showed that miR-135a-5p had no obvious influence on GBC cellular senescence (Fig. S3c). We then established stable GBC-SD and EH-GB1 cells overexpressing miR-135a via lentivirus (Fig. S2d), and found that the proliferation rates of lenti-miR-135a GBC cells were significantly decreased compared with those cells infected with lenti-GFP (Fig. 2a,b). The cells stably expressing miR-135a or GFP were s.c. injected into nude mice. After 6 weeks, the mice were killed and the xenografts were evaluated. The tumors derived from the miR-135a cells were much smaller than those from the GFP cells (Fig. 2c). In sum, miR-135a-5p could inhibit the proliferation of GBC cells both in vitro and in vivo.


MicroRNA-135a acts as a putative tumor suppressor by directly targeting very low density lipoprotein receptor in human gallbladder cancer.

Zhou H, Guo W, Zhao Y, Wang Y, Zha R, Ding J, Liang L, Yang G, Chen Z, Ma B, Yin B - Cancer Sci. (2014)

MicroRNA-135a (miR-135a) inhibited gallbladder cancer (GBC) cell proliferation in vitro and in vivo. (a,b) Cell counting (CCK-8) and colony formation assays of GBC-SD and EH-GB1 cells stably expressing miR-135a or GFP control. *P < 0.05 (Lenti-GFP vs Lenti-miR-135a). (c) Tumor formation in nude mice with GBC-SD cells stably expressing miR-135a or GFP control and the tumor weight. *P < 0.05 (Lenti-GFP vs Lenti-miR-135a).
© Copyright Policy - open-access
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4317855&req=5

fig02: MicroRNA-135a (miR-135a) inhibited gallbladder cancer (GBC) cell proliferation in vitro and in vivo. (a,b) Cell counting (CCK-8) and colony formation assays of GBC-SD and EH-GB1 cells stably expressing miR-135a or GFP control. *P < 0.05 (Lenti-GFP vs Lenti-miR-135a). (c) Tumor formation in nude mice with GBC-SD cells stably expressing miR-135a or GFP control and the tumor weight. *P < 0.05 (Lenti-GFP vs Lenti-miR-135a).
Mentions: MicrRNA-135a-5p mimic transfection could inhibit the proliferation and colony formation ability of GBC-SD and EH-GB1 cells (Fig. S2b,c), and arrest the cells in G1/S phase (Fig. S3a). Caspase-Glo 3/7 Assay (Promega) showed that miR-135a-5p could slightly upregulate caspase 3/7 activity (Fig. S3b), whereas SA-β-gal staining showed that miR-135a-5p had no obvious influence on GBC cellular senescence (Fig. S3c). We then established stable GBC-SD and EH-GB1 cells overexpressing miR-135a via lentivirus (Fig. S2d), and found that the proliferation rates of lenti-miR-135a GBC cells were significantly decreased compared with those cells infected with lenti-GFP (Fig. 2a,b). The cells stably expressing miR-135a or GFP were s.c. injected into nude mice. After 6 weeks, the mice were killed and the xenografts were evaluated. The tumors derived from the miR-135a cells were much smaller than those from the GFP cells (Fig. 2c). In sum, miR-135a-5p could inhibit the proliferation of GBC cells both in vitro and in vivo.

Bottom Line: Moreover, very low density lipoprotein receptor (VLDLR), which is often upregulated in GBC tissues, was identified as a direct functional target of miR-135a-5p.Furthermore, the p38 MAPK pathway was proven to be involved in miR-135a-VLDLR downstream signaling.Together, these results suggested that the miR-135a-VLDLR-p38 axis may contribute to GBC cell proliferation.

View Article: PubMed Central - PubMed

Affiliation: Department of General Surgery, Huashan Hospital, Fudan University, Shanghai, China.

Show MeSH
Related in: MedlinePlus