LiuFeng,Jianxin Zhong,Jianbin Sun,Hailong Wu. Effects of MIF on proliferation, migration, and STAT1 pathway of colon cancer cells. Oncol Transl Med, 2020, 6: 121-125. |
Effects of MIF on proliferation, migration, and STAT1 pathway of colon cancer cells |
Received:April 16, 2020 Revised:June 19, 2020 |
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KeyWord:colon cancer; migration inhibitory factor; signal transducer and activator of transcription 1; cell proliferation; cell migration |
Author Name | Affiliation | E-mail | LiuFeng | Wuhan Puai Hospital, Tongji Medical College, Huazhong University of Science and Technology | lf5806@sina.com | Jianxin Zhong | Wuhan Puai Hospital, Tongji Medical College, Huazhong University of Science and Technology | | Jianbin Sun | Wuhan Puai Hospital, Tongji Medical College, Huazhong University of Science and Technology | | Hailong Wu | Wuhan Puai Hospital, Tongji Medical College, Huazhong University of Science and Technology | |
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Abstract: |
Objective This study aimed to investigate how macrophage migration inhibitory factor (MIF) regulates
the interaction of signal transducer and activator of transcription 1 (STAT1) with CD74, and affects colon
cancer proliferation and invasion.
Methods After transfecting MIF small interfering RNA into the SW480 cell line, the expression of STAT1
and CD74 mRNA was detected by qRT-PCR and western blotting. Transwell and MTT assays were
performed to detect the colon cancer cell invasion and proliferation ability. Co-immunoprecipitation was
used to detect the interaction between CD74 and STAT1 proteins in the treated and control groups.
Results The cellular biological assays (MTT and Transwell) showed that the proliferation and invasion
ability of colon cancer cells decreased after MIF knockdown; the results showed significant statistical
difference (P < 0.05). The results of the co-immunoprecipitation assay suggested that MIF knockdown in
colon cancer cells could inhibit the binding of CD74 and STAT1 proteins; statistical difference was observed
between the two groups (P < 0.05).
Conclusion MIF can increase the proliferation and invasion of colon cancer cells by promoting the
combination of CD74 and STAT1. |
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