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Poster lunch

774 - miR93 regulates epithelial-to-mesenchymal transition process in metastatic colorectal cancer by targeting EphA4 (552P)


18 Nov 2017


Poster lunch


Translational Research;  Colon and Rectal Cancer


Sheng Gao


Annals of Oncology (2017) 28 (suppl_10): x173-x176. 10.1093/annonc/mdx679


S. Gao1, B. Jiang1, H. Liu1, S. Hou1, L. Wu2, Z. Yang2, J. Shen3, L. Zhou2, S. Zheng2, W. Bai1

Author affiliations

  • 1 Colorectal Cancer, Shanxi Cancer Hospital/Institute, 030001 - Taiyuan/CN
  • 2 Surgery, Zhejiang University School of Medicine, Hangzhou/CN
  • 3 General Surgery, Licheng County People’s Hospital, Licheng/CN


Abstract 774


Regulating epithelial-to-mesenchymal transition (EMT) in cancer cells has been widely considered as an approach to combat cancer progression and therapeutic resistance, whereas a limited number of broadly comprehensive investigations of miRNAs involved in metastatic colorectal cancer (mCRC) have been conducted. In this study, we investigated the roles and mechanisms of EMT process in mCRC.


We used ISH and RT-qPCR to measure expression of miR93 in CRC tissues, nontumor tissues and metastatic liver tissues. CRC cell lines were transduced with lentiviruses expressed miR93. Its inhibitor sequence targeted miR93 or a scrambled sequence (control). Proliferation, metastasis, invasion and colony formation and growth of CRC cells which overexpress miR93 or its inhibitor in severe combined immune-deficient mice were analysed. Western blot, and luciferase assays were used to measure expression of Eph tyrosine kinase receptor (EphA4) and related signalling molecules.


In this study, we demonstrated that miR93 regulated EMT process by targeting EphA4 in mCRC. CRC tissues and metastatic liver tissues had increased levels of miR93 compared with the nontumor tissues and cells, and miR93 can regulate EMT process. Overexpression of miR93 increased proliferation of CRC cells, metastasis, invasion and colony formation in vitro, whereas miR93 depletion reduced these parameters. In nude mice, overexpression of miR93 by CRC cells increased liver metastasis and overexpression of the miR93 inhibitor reduced it. Then we identified by microarray analysis that the direct and functional target genes of miR93 was EphA4. Knockdown of EphA4 phenocopied the effect of miR-93 and ectopic expression of EphA4 restored the effect of miR93 on proliferation, migration, invasion and liver metastasis in CRC cells.


Our findings revealed miR93 regulates EMT process by targeting EphA4 to affect liver metastasis in CRC. miR93 inhibited tumor metastasis by directly targeting EphA4, a crucial factor in regulating EMT. Collectively, this study provides new insights into exploring the therapeutic potential of miR93, which is able to regulate EMT process to affect tumor metastasis, and warrant further study in clinical settings.

Clinical trial identification

The present study was supported in part by grants from the Health and Family Planning Commission of Shanxi Province (No.2015049), the Applied Basic Research Programs of Shanxi Science and Technology Department (No.201601D011128).

Legal entity responsible for the study

The Health and Family Planning Commission of Shanxi Province, the Applied Basic Research Programs of Shanxi Science and Technology Department


The Health and Family Planning Commission of Shanxi Province, the Applied Basic Research Programs of Shanxi Science and Technology Department


All authors have declared no conflicts of interest.

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