KITENIN promotes glioma invasiveness and progression, associated with the induction of EMT and stemness markers

Abstract

KITENIN (KAI1 COOH-terminal interacting tetraspanin) promotes tumor invasion and metastasis in various cancers. This study assessed the association between KITENIN expression and advanced glioma grade in patients. In vitro assays revealed that KITENIN knockdown inhibited the invasion and migration of glioma cells, whereas KITENIN overexpression promoted their invasion and migration. In orthotopic mouse tumor models, mice transplanted with KITENIN-transfected glioma cells had significantly shorter survival than mice transplanted with mock-transfected cells. Patients with low KITENIN expression showed a significantly longer progression-free survival than patients with high KITENIN expression. KITENIN induced the expression of the epithelial-mesenchymal transition (EMT) markers (N-cadherin, ZEB1, ZEB2, SNAIL and SLUG) as well as the glioma stemness markers (CD133, ALDH1 and EPH-B1). Taken together, these findings showed that high levels of KITENIN increased glioma invasiveness and progression, associated with the up-regulation of EMT and stemness markers.

RETRACTED: CRNDE Promotes Malignant Progression of Glioma by Attenuating miR-384/PIWIL4/STAT3 Axis

“…As reported earlier, cyclin D1, VEGFA, SLUG, MMP-9, Bcl-2, bcl-xL, and caspase 3 are involved in regulating glioma cells proliferation, migration, invasion, and apoptosis. [26][27][28][29][30] Meanwhile, STAT3 could promote tumor cells progression via modulating these genes. [31][32][33][34][35][36][37] The expressions of p-STAT3, cyclin D1, VEGFA, SLUG, MMP-9, Bcl-2, and bcl-xL were robustly rescued in miR-384+PIWIL4 (non-3′UTR) group than that in miR-384+PIWIL4 group; the expression of cleaved caspase 3 in miR-384+PIWIL4 (non-3′UTR) group was blocked versus with that in miR-384+PIWIL4 group (Figure 6f).…”

Regulation of Osteosclerosis by Inoculated Cd133+ PC3 Cells in Bone‐marrow Microenvironmental Niches

“…During the last decades, research has identified CSCs as central players in cancer metastasis. CSCs are a small population of cells responsible for initiation of tumor burden and therapeutic refractoriness . Acquisition of self‐renewal capacity and stemness properties at the time of tumorigenesis is an essential prerequisite for further accumulation of oncogenic transformations and eventual development of cancer .…”

“…CSCs are a small population of cells responsible for initiation of tumor burden and therapeutic refractoriness. (27) Acquisition of self-renewal capacity and stemness properties at the time of tumorigenesis is an essential prerequisite for further accumulation of oncogenic transformations and eventual development of cancer. (28) Here, we sought to identify CSC-like cells by inducing ectopic overexpression of CD133 in two PC cell lines (PC3 and DU145).…”

Cyclin‑dependent kinase 10 prevents glioma metastasis via modulation of Snail expression

“…Since it was demonstrated that CDK10 overexpression affected the metastasis of glioma, further experiments aimed to reveal the underlying mechanism. EMT is considered to be highly relevant to glioma metastasis, which occurs at the invasive front of glioma tissues (18). A previous study demonstrated that the expression status of EMT markers was closely associated with mesenchymal differentiation in gliosarcoma, a rare form of glioblastoma characterized by a biphasic mode of glial and mesenchymal differentiation (22).…”

“…It is well established that EMT serves a crucial role in the metastasis of various types of cancer. The shift to EMT-associated protein expression is regarded as an important mechanism in the promotion of motility in glioma cancer cells (18,19). Therefore, the expression statuses of EMT protein markers were analyzed by western blot analysis.…”