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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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Related in: MedlinePlus

Reintroduction of very low density lipoprotein receptor (VLDLR) abrogated microRNA-135a (miR-135a)-induced inhibition of proliferation in gallbladder cancer (GBC) cells. (a,b) Cell counting (CCK-8) and colony formation assays of GBC-SD and EH-GB1 cells stably expressing miR-135a or lenti-GFP were infected with lenti-VLDLR or corresponding lenti-GFP. *P < 0.05 (Lenti-GFP vs Lenti-miR-135a); **P < 0.05 (Lenti-GFP vs Lenti-VLDR+miR-135a). (c) Protein levels of VLDLR, ERK(1/2), SAPK/JNK, and p38 and their phosphorylation (p−) levels were detected by Western blot assays after GBC-SD and EH-GB1 cells stably expressing miR-135a or lenti-GFP were infected with lenti-VLDLR or corresponding lenti-GFP.
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fig04: Reintroduction of very low density lipoprotein receptor (VLDLR) abrogated microRNA-135a (miR-135a)-induced inhibition of proliferation in gallbladder cancer (GBC) cells. (a,b) Cell counting (CCK-8) and colony formation assays of GBC-SD and EH-GB1 cells stably expressing miR-135a or lenti-GFP were infected with lenti-VLDLR or corresponding lenti-GFP. *P < 0.05 (Lenti-GFP vs Lenti-miR-135a); **P < 0.05 (Lenti-GFP vs Lenti-VLDR+miR-135a). (c) Protein levels of VLDLR, ERK(1/2), SAPK/JNK, and p38 and their phosphorylation (p−) levels were detected by Western blot assays after GBC-SD and EH-GB1 cells stably expressing miR-135a or lenti-GFP were infected with lenti-VLDLR or corresponding lenti-GFP.

Mentions: To further address the critical role of VLDLR in miR-135a-5p-induced suppression of GBC cell proliferation, we constructed a lentiviral expression vector of VLDLR ORF without the 3′-UTR, and established the stable GBC cells using this vector. The infection of lentivirus carrying VLDLR-ORF antagonized the inhibition of miR-135a-5p on GBC cells proliferation (Fig 4a,b), with VLDLR protein recovery in Lenti-miR-135a cells (Fig 4c). Furthermore, it was shown that enforced expression of VLDLR could counteract the miR-135a-5p-induced G1/S arrest (Fig. S3a). These results suggested that VLDLR is a functional target of miR-135a-5p in GBC cells.


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)

Reintroduction of very low density lipoprotein receptor (VLDLR) abrogated microRNA-135a (miR-135a)-induced inhibition of proliferation in gallbladder cancer (GBC) cells. (a,b) Cell counting (CCK-8) and colony formation assays of GBC-SD and EH-GB1 cells stably expressing miR-135a or lenti-GFP were infected with lenti-VLDLR or corresponding lenti-GFP. *P < 0.05 (Lenti-GFP vs Lenti-miR-135a); **P < 0.05 (Lenti-GFP vs Lenti-VLDR+miR-135a). (c) Protein levels of VLDLR, ERK(1/2), SAPK/JNK, and p38 and their phosphorylation (p−) levels were detected by Western blot assays after GBC-SD and EH-GB1 cells stably expressing miR-135a or lenti-GFP were infected with lenti-VLDLR or corresponding lenti-GFP.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig04: Reintroduction of very low density lipoprotein receptor (VLDLR) abrogated microRNA-135a (miR-135a)-induced inhibition of proliferation in gallbladder cancer (GBC) cells. (a,b) Cell counting (CCK-8) and colony formation assays of GBC-SD and EH-GB1 cells stably expressing miR-135a or lenti-GFP were infected with lenti-VLDLR or corresponding lenti-GFP. *P < 0.05 (Lenti-GFP vs Lenti-miR-135a); **P < 0.05 (Lenti-GFP vs Lenti-VLDR+miR-135a). (c) Protein levels of VLDLR, ERK(1/2), SAPK/JNK, and p38 and their phosphorylation (p−) levels were detected by Western blot assays after GBC-SD and EH-GB1 cells stably expressing miR-135a or lenti-GFP were infected with lenti-VLDLR or corresponding lenti-GFP.
Mentions: To further address the critical role of VLDLR in miR-135a-5p-induced suppression of GBC cell proliferation, we constructed a lentiviral expression vector of VLDLR ORF without the 3′-UTR, and established the stable GBC cells using this vector. The infection of lentivirus carrying VLDLR-ORF antagonized the inhibition of miR-135a-5p on GBC cells proliferation (Fig 4a,b), with VLDLR protein recovery in Lenti-miR-135a cells (Fig 4c). Furthermore, it was shown that enforced expression of VLDLR could counteract the miR-135a-5p-induced G1/S arrest (Fig. S3a). These results suggested that VLDLR is a functional target of miR-135a-5p in GBC cells.

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