Zhu Sheng Zhang , Lu Jian Bo , Wang Jing Ye , Li Ru Yi , Jiang Qiong , He Jin Song , Li Meng . Experimental Study on Neuroendocrine Differentiation of Colon Cancer Cell Line HCT-116 Induced by Epidermal Growth Factor[J]. Journal of Kunming Medical University, 2017, 38(07): 45-49.
Citation: Zhu Sheng Zhang , Lu Jian Bo , Wang Jing Ye , Li Ru Yi , Jiang Qiong , He Jin Song , Li Meng . Experimental Study on Neuroendocrine Differentiation of Colon Cancer Cell Line HCT-116 Induced by Epidermal Growth Factor[J]. Journal of Kunming Medical University, 2017, 38(07): 45-49.

Experimental Study on Neuroendocrine Differentiation of Colon Cancer Cell Line HCT-116 Induced by Epidermal Growth Factor

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基金: 云南省科技厅-昆明医科大学应用基础研究联合专项基金资助项目 (2008CD004R);

  • Received Date: 2017-04-02
  • Objective To induce and block to induce neuroendocrine differentiation of colon adenocarcinoma cell HCT-116 by using the epidermal growth factor (EGF) and epidermal growth factor receptor (EGFR) inhibitor Cetuximab, and further explore the intrinsical changes and association with the characteristics of colonic cancer cells HCT-116 in proliferation, apoptosis, possible mechanism, and the adjustment factors of neuroendocrine differentiation. Methods HE and immunohistochemical stains were conducted to observe morphological characters of colonic cancer cultured cells HCT-116 and tumor in the nude mouse by expression of Cg A, Ki-67, Bcl-2, Syn, CEA, CA19-9, COX2, CDX2. Cell growth curve of HCT-116 was drawn by MTT, flow cytometry technique was used to determine the cell cycle of HCT-116, and Low Density Plate Clone Test was applied to measure the cloned forming rate of HCT-116. Results Morphology of HCT-116 in the induced courses was similar. EGF acted on cultured HCT-116 cells to strengthen the expression of Cg A, Ki-67 and Bcl-2, to increase cell proliferation rate and proliferation activity in cell cycle of S and G2 phase. The colony formation rate was also increased significantly compared with the control group. Difference with cetuximab group was statistically significant (P <0.001) . Changes of proliferation index of Ki-67 in cultured HCT-116 cells was statistically significant in EGF group compared with the other groups (P<0.01) . The differential expression of NSE, CEA, CA19-9, CDX2, COX2, and Syn in each group was no statistically significant (P>0.05) . Conclusion EGF can induce neuroendocrine differentiation in cultured HCT-116 cells NED, increase cell proliferation activity, strengthen antiapoptotic ability of colonic cancer cells. EGFR can block EGF to induce HCT-116 NED, and inhibit changes of relevant biological features. However, CEA, CA19-9, COX2, and CDX2 do not regulate NED, proliferation, and apoptosis.
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