Author of

• 11454

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  P2.01 - Poster Session 2 - Cancer Biology (ID 145)

  • Event: WCLC 2013
  • Type: Poster Session
  • Track: Biology
  • Presentations: 1
  • Moderators:
  • Coordinates: 10/29/2013, 09:30 - 16:30, Exhibit Hall, Ground Level

  • 11474

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    P2.01-020 - Down-regulation of Somatostatin Receptor 2 decreases cell proliferation in Lung Cancer (ID 1889)

    09:30 - 09:30  |  Author(s): J. Miao
    • Abstract

    Background
    Somatostatin receptors (SSTRs) have been shown to be overexpressed in 80-90% of all neuroendocrine tumors, including SCLCs. Previous reports have shown that SSTR2 activation modulates cell proliferation by acting through the ERK signaling cascade. We hypothesized that down regulation of SSTR2 will inhibit cell proliferation in lung cancer cell lines that overexpresses this receptor.

    Methods
    SSTR2 expression was assessed by western blot analysis in 28 lung cancer cell lines. H520 (SCC) and H727 (Carcinoid) were used as an in vitro model for studying the effects of targeted down-regulation of SSTR2 by shRNA. Several SSTR2 null-colonies of these cell lines were generated by antibiotic selection. Cell proliferation was measured at four different time points using MTS metabolic assay. In addition, we evaluated the effect of SSTR2 down regulation in colony formation potential of our lung cancer cell lines.

    Results
    Western blot analysis of 28 lung cancer cell lines showed expression of SSTR2 in 17/18 (94%) of SCLCs including carcinoids, 3/6 (50%) of NSCLCs, and 0/4 (0%) of non-immortalized human bronchial cells. Post transfection analysis by western blot revealed a significant decrease in SSTR2 protein expression in multiple SSTR2 null-colonies. We observed a 37% decrease in cell growth in H520 and a 38% decrease in H727 by day 6 with p values of 0.007 and 0.002 respectively. In addition, down regulation of SSTR2 resulted in reduction in the number of colonies formed by both cell lines.

    Conclusion
    These results demonstrate that that knocking down SSTR2 in lung cancer cells induces a marked decrease in cell proliferation. Ongoing studies are focused on understanding the effect of knocking down SSTR2 on oncogenic traits of lung cancer cells including cell survival, apoptosis, migration and invasion and the cellular mechanisms underpinning our original observation.