Abstract
<title>Abstract</title> <p>MicroRNA-155 (miR-155) has been implicated in glioblastoma (GBM) progression. However, its role remains unclear because previous studies have largely relied on transient modulation approaches and have reported context-dependent effects. Here, we generated stable miR-155 knockout (K/O) U87 and T98G GBM cell lines using CRISPR/Cas9 and examined the effects of sustained miR-155 loss on proliferative and malignancy-associated phenotypes. miR-155 K/O reduced cell viability and clonogenic growth in both cell lines. Ki-67 expression decreased, whereas p21 expression increased in miR-155-deficient cells. Western blot analysis showed increased TP53INP1, p53, and p21 levels, accompanied by Bax induction and Bcl-2 reduction. Confocal imaging demonstrated enhanced nuclear localization of TP53INP1. In contrast, the effects of miR-155 depletion on malignancy-associated markers were heterogeneous between U87 and T98G cells, with TWIST showing the most consistent decrease among the examined markers. Migration was modestly reduced in both cell lines, whereas anti-invasive effects were limited and not consistently observed, particularly in T98G cells. These findings indicate that stable miR-155 deletion suppresses GBM cell proliferation through TP53INP1/p53/p21 activation, while exerting limited effects on other malignancy-related traits.</p>