Upregulation of ECT2 Predicts Adverse Clinical Outcomes and Increases 5-Fluorouracil Resistance in Gastric Cancer Patients
Author(s) -
Hua Zhang,
Yuan Geng,
Chunhui Sun,
Jin Yu
Publication year - 2021
Publication title -
journal of oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.228
H-Index - 54
eISSN - 1687-8469
pISSN - 1687-8450
DOI - 10.1155/2021/2102890
Subject(s) - downregulation and upregulation , medicine , cancer research , gene knockdown , viability assay , gene silencing , cancer , metastasis , cell , western blot , oncology , cell culture , biology , gene , biochemistry , genetics
Background The abnormal expression and prognosis prediction of epithelial cell transforming sequence 2 (ECT2) in gastric cancer (GC) has been reported. However, the effect of ECT2 on 5-fluorouracil (5-Fu) resistance in GC is unclear. This research aims to solve the abovementioned problems.Methods Gene expression was detected by RT-qPCR and Western blot analysis. Cell viability was evaluated by the colony formation assay, MTT assay, and flow cytometric analysis. Transwell and wound healing assays were used to detect cell metastasis.Results Upregulation of ECT2 was found in stomach adenocarcinoma (STAD) and GC tissues. In addition, high ECT2 expression can predict adverse clinical outcomes in GC patients. More importantly, ECT2 knockdown weakened the resistance of 5-FU in GC cells. ECT2 silencing reduced the cell migratory and invasive abilities of GC cells treated with 5-FU. We also found that downregulation of ECT2 increased 5-FU sensitivity in GC cells by downregulating P-gp, MRP1, and Bcl-2.Conclusion Upregulation of ECT2 can predict adverse clinical outcomes and increase 5-FU resistance in GC patients.
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