IndraLab

Statements

TNFAIP3 activates Neoplasm Invasiveness. 7 / 7
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"This assertion is corroborated by experimental validations indicating that the knockdown or overexpression of TNFAIP3 in ESCC‐TRCs yields contrasting outcomes: knockdown diminishes migration and invasion while enhancing apoptosis, whereas overexpression promotes migration and invasion."
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"On the other hand, TNFAIP3 is necessary for trophoblast invasion; although its upregulation is crucial during the early stages of pregnancy, the results are dangerous in the third trimester."
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"The results of Transwell assays demonstrated that TNFAIP3 knockdown significantly impaired the migration and invasion of EC109‐TRCs and EC109 cells (Figures 6C and S6E,F)."
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"In addition, the knockdown of TNFAIP3 restores the significant decrease in invasion and proliferation in miR-605-5p-inhibitor-transfected lung cancer cells."
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"The overexpression of TNFAIP3 significantly increased the migration and invasion capacities of KYSE150‐TRCs, as demonstrated by Transwell assays."
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"Additionally, the overexpression of TNFAIP3 enhances the proliferation, migration and invasion of KYSE150‐TRCs, confirming our earlier speculation that TNFAIP3 is the key molecule responsible for the growth‐inhibitory effect of ZSH‐2208 on ESCC‐TRCs.3 DISCUSSION."
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"Tubulogenesis and Trewells experiments showed that TNFAIP3 gene knockout/knockdown inhibited the angiogenesis, migration, and invasion of HUVEC cells promoted by FGFR1 activation."
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