Open Access
ARTICLE
IKIP downregulates THBS1/FAK signaling to suppress migration and invasion by glioblastoma cells
1 Department of Neurosurgery, The Affiliated Hospital of Southwestern Medical University, Luzhou, China
2 Department of Neurosurgery, Sichuan University West China Hospital, Chengdu, China
* Corresponding Authors: HAO LIU. Email: ; NIANDONG ZHENG. Email:
Oncology Research 2024, 32(7), 1173-1184. https://doi.org/10.32604/or.2024.042456
Received 30 May 2023; Accepted 04 February 2024; Issue published 20 June 2024
Abstract
Background: Inhibitor of NF-κB kinase-interacting protein (IKIP) is known to promote proliferation of glioblastoma (GBM) cells, but how it affects migration and invasion by those cells is unclear. Methods: We compared levels of IKIP between glioma tissues and normal brain tissue in clinical samples and public databases. We examined the effects of IKIP overexpression and knockdown on the migration and invasion of GBM using transwell and wound healing assays, and we compared the transcriptomes under these different conditions to identify the molecular mechanisms involved. Results: Based on data from our clinical samples and from public databases, IKIP was overexpressed in GBM tumors, and its expression level correlated inversely with survival. IKIP overexpression in GBM cells inhibited migration and invasion in transwell and wound healing assays, whereas IKIP knockdown exerted the opposite effects. IKIP overexpression in GBM cells that were injected into mouse brain promoted tumor growth but inhibited tumor invasion of surrounding tissue. The effects of IKIP were associated with downregulation of THBS1 mRNA and concomitant inhibition of THBS1/FAK signaling. Conclusions: IKIP inhibits THBS1/FAK signaling to suppress migration and invasion of GBM cells.Keywords
Supplementary Material
Supplementary Material FileCite This Article
This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.