Targeting GAPLINC decreased CD44 expression and tumor growth in vivo.

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Presentation transcript:

Targeting GAPLINC decreased CD44 expression and tumor growth in vivo. Targeting GAPLINC decreased CD44 expression and tumor growth in vivo. A and B, knockdown of GAPLINC inhibited growth of xenograft in nude mice. Human gastric cancer MGC803 cells with GAPLINC stable knockdown or negative control were injected subcutaneously into the left hip to establish xenograft model. At the last time point (17 days after first injection), tumors in both groups were measured both in situ (A) and after resection (B), shown for both groups. C, statistical analysis of tumor volume in MGC803GAPLINC-KD (knockdown) and MGC803vector (control) groups (values also shown in Supplementary Table S5). Knockdown of GAPLINC significantly delayed tumor progression as compared with the control group. D, RT-qPCR of GAPLINC and CD44 in xenografts treated with GAPLINC stable knockdown clone and control clone. It can be observed that knockdown of GAPLINC dramatically decreased the level of CD44. E, Western blot analysis of xenografts in MGC803GAPLINC-KD and MGC803vector groups suggest decreased expression of CD44 protein upon stable knockdown of GAPLINC. F, RT-qPCR of miR211-3p in xenografts in MGC803GAPLINC-KD and MGC803vector groups. It can be observed that knockdown of GAPLINC dramatically increased the level of miR211-3p (P value indicated, Student t test). G, schematic representation showing GAPLINC-mediated cell proliferation and invasion in gastric cancer. The miR211-3p has dual target specificity for both GAPLINC and CD44, which leads to degradation of the bound RNA. The high expression of GAPLINC competes to bind miR211-3p, which reduces the degradation of CD44 mRNA and leads to increased translation of the functional CD44 protein. The CD44 oncoprotein has well-established roles in promoting cancer proliferation, migration, and angiogenesis, which mediates the oncogenic effects of GAPLINC in gastric cancer. Ye Hu et al. Cancer Res 2014;74:6890-6902 ©2014 by American Association for Cancer Research