ABSTRACT
Aim To investigate whether the Enphorbia lunulata Bge extract regulates the proliferation, migration and invasion of colorectal cancer cells induced by interleukin-1β(IL-1β)through miR-30a-5p/nuclear factor κB(NF-κB). Methods HT29 cells were divided into NC group, IL-1β group, low-dose(2.5 mg·L-1)+IL-1β group, middle-dose(5 mg·L-1)+IL-1β group, high-dose(10 mg·L-1)+IL-1β group, miR-NC+IL-1β group, miR-30a-5p+IL-1β group, anti-miR-NC+high-dose+IL-1β group, anti-miR-30a-5p+high-dose+IL-1β group. Cell counting kit-8 method was used to detect cell proliferation activity in each group, clone formation experiment was applied to assess cell clones, Transwell method was employed to monitor cell migration and invasion, Western blot was performed to determine the protein expression level, and qRT-PCR was employed to detect the expression level of miR-30a-5p. Results Compared with the NC group, the proliferation activity, cell clone number, migration and invasion number of colorectal cancer cell HT29 in IL-1β group increased, and the expression level of miR-30a-5p decreased(all P<0.01). Compared with the IL-1β group, the proliferation activity, the number of cell clones, the number of migration and invasion of colorectal cancer cell HT29 decreased, and the expression level of miR-30a-5p increased(all P<0.01); The expression level of p-p65 in the high-dose+IL-1β group was lower than that in the IL-1β group(P<0.01). The proliferation activity, cell clone number, migration and invasion number of colorectal cancer cell HT29 in the miR-30a-5p+IL-1β group were lower than those in the miR-NC+IL-1β group(all P<0.01). The proliferation activity, cell clone number, migration and invasion number of colorectal cancer cell HT29 in the anti-miR-30a-5p+high-dose+IL-1β group were higher than those of anti-miR-NC+high-dose+IL-1β group(all P<0.01). Conclusions Enphorbia lunulata Bge extract can inhibit the proliferation, migration and invasion of colorectal cancer cells induced by IL-1β by up-regulating miR-30a-5p and down-regulating the activity of NF-κB signaling pathway.
