Authors

Mingde ni1, Xiuping Li2, HongMei Liu3, Zuojuan ZHang4, aicHun Li1, *

Departments

1Department of Tuberculosis, Linyi People's Hospital, Linyi, PR China - 2Department of Eastern Division of Surgery, Linyi People's Hospital, PR China - 3Department of Obstetrics and Gynecology, Linyi Jinluo Hospital, Qianfoshan Hospital, PR China - 4Department of Respiration, Linyi People's Hospital, PR China

Abstract

Objective: To explore the mechanism of trophoblast cell surface antigen 2 (TROP2) promoting the proliferation of chronic obstructive pulmonary airway basal cells through the ERK/MAPK signalling pathway.

Methods: Fifty cases of COPD tissue and normal lung tissue were randomly selected between May 2016 to May 2017 in our hospital to detect the expression of trophoblast cell surface antigen 2 (TROP2) in COPD tissue and normal lung tissue. Airway basal cells were cultured, while basal cells were constructed. Four groups were set up to observe and compare the overexpression/silence ofTROP2 on cell proliferation in each group and the effect of TROP2 on airway basal cell proliferation in COPD via the ERK/MAPK signalling pathway: a blank control group (control), a pcDNA 3.1 group (constructing pcDNA 3.1 plasmids), a pcDNA.3-TROP2 group (over-expressingTROP2), and an siRNA-TROP2 group (silencing TROP).

Results: The expression rate of TROP2 in COPD airway epithelium was 52.00% (26/50), significantly higher than that in normal airway epithelium by 8.00% (4/50) (P<0.05). At 48 h and 72 h, the cell proliferation ability of pcDNA3.1-TROP2 group was significantly stronger than that of the pcDNA3.1 group (P<0.05), and there was no significant difference in cell proliferation ability between pcDNA3.1 group and blank control group (P>0.05). At 0 h and 24 h, there was no significant difference between the pcDNA3.1-TROP2 group, the blank control group and the pcDNA3.1 group (P>0.05). At 24 h, 48 h and 72 h, the cell proliferation ability of siRNA-TROP2 group was significantly weaker than that of the pcDNA.3 group (P<0.05), and the cell proliferation ability of pcDNA3.1 group was not significant compared with that of the blank control group (P>0.05). There was no significant difference between the siRNA-TROP2 group, the blank control group and the pcDNA3.1 group at 0 h (P>0.05). After overexpression of TROP2, the expression of p-ERK1/2 in the pcDNA3.1-TROP2 group was significantly higher than that in the blank control group and the pcDNA3.1 group (P<0.05), and the expression of p-ERK1/2 in the blank control group and pcDNA3.1 group was not significant (P>0.05). There was no significant difference in ERK1/2 expression in the three groups (P>0.05).

Conclusion: Overexpression of TROP2 can promote the proliferation of chronic obstructive lung airway basal cells through the ERK/MAPK signalling pathway.

Keywords

TROP2, ERK/MAPK signalling pathway, COPD, airway basal cells, proliferation.

DOI:

10.19193/0393-6384_2020_6_545