Page 155 - D. Cancer biology
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GPR110 PLAYS A CRITICAL ROLE IN REGULATION OF TRIPLE-
                            NEGATIVE BREAST CANCER PROGRESSION

                                                    1
                                                                  1
                                           Hye-Jung Nam , Eun-Ji Lim , Yi Zhao , Su-Jae Lee 1
                                                            1
                   1 Department of Life Science, Research Institute for Natural Sciences, Hanyang University, Seoul 04763, Republic of Korea
                BACKGROUND                                                    AIM
   Triple negative breast cancer (TNBC) which is a group  Adhesion GPCRs(aGPCRs) have been reported to play
   of breast cancer correlates with aggressive behaviors  an important role in biological processes and cancer
   and poor clinical outcomes. TNBC remains intractable  progression in various cancers. However, aGPCR
   to targeted therapies because lacking of estrogen    mechanism of action remain unclear in breast cancer.
   receptor (ER), progesterone receptor (PR) and human  Therefore, In this study we aim to explore the
   epidermal growth factor receptor2 (HER2) expression.  functional role and mechanism of GPR110, as a
   Thus, development of targeted therapies becomes a    member of aGPCR, in TNBC.
   significant issue in the treatment of TNBC.
                                              METHODS

    Human tissue microarray, qRT-PCR, western blotting analysis, invasion assay and sphere formation assay
      were used to demonstrate the regulatory mechanism of GPR110
    The microarray data of GPR110 Patients were analyzed by gene set enrichment analysis(GSEA)

                                               RESULTS

   Figure 1                                      Figure 2



















   Figure3                                       Figure 4



















         CONCLUSION                         REFERENCES                      Contact information

   Our findings demonstrate a crucial   Structure, function and therapeutic     Hye-Jung Nam
   role of GPR110 and its downstream     potential of adhesion GPCRs.    Laboratory of Molecular Biochemistry,
   effectors in maintaining the TNBC type  https://doi.org/10.1016/B978-0-12-  Department of Life Science, Hanyang University,
                                                                         222, Seoul 04763 Korea.
   features, and we suggest that GPR110  816228-6.00002-7                E-mail: namhj1231@naver.com
   would be a putative therapeutic target
   for TNBC treatment.                  GPCRs profiling and identification     Su-Jae Lee
                                         of GPR110 as a potential new    Laboratory of Molecular Biochemistry,
                                                                         Department of Life Science, Hanyang University,
                                         target in HER2+ breast cancer.   222, Seoul 04763 Korea.
                                         https://doi.org/10.1007/s10549-018-  Phone: 82-2220-4554
                                         4751-9                          E-mail: sj0420@hanyang.ac.kr
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