The v-Crk avian sarcoma virus CT10 oncogene homolog-like (
CRKL) protein is important in
cancer progression. However, its expression pattern and
biological roles in human
endometrial carcinoma remain unexplored. The potential mechanism of CRKL-induced
cancer progression is still unclear. The present study aimed to explore the expression pattern and
biological roles of CRKL in human
endometrial carcinoma. Using immunohistochemistry, it was observed that the
CRKL protein was overexpressed in 50.5% (44/87) of
endometrial carcinoma tissues. Plasmid transfection of CRKL into Ishikawa cells was performed, and CRKL overexpression promoted cell proliferation, colony formation and cell cycle transition in the transfected cells. In addition, CRKL overexpression inhibited cell apoptosis in Ishikawa cells treated with
cisplatin, with decreased
caspase-3 and
caspase-9 cleavage. Further analysis revealed that CRKL upregulated the expression of
cyclin D1,
cyclin E,
B cell lymphoma (Bcl)-2 and
survivin, and downregulated Bcl-2 associated X
protein expression. In conclusion, the present study demonstrated that CRKL overexpression in
endometrial carcinoma contributes to malignant cell growth and resistance to apoptosis, possibly through Bcl-2.