<p>Silencing Of MAGI1 Promotes The Proliferation And Inhibits Apoptosis Of Glioma Cells Via The Wnt/β-Catenin And PTEN/AKT Signaling Pathways</p>

Abstract

Background: Membrane-associated guanylate kinase (MAGUK) with inverted orientation protein 1 (MAGI1) is a novel member of the MAGUK family with a vital role in tumor progression related to invasion and metastasis. However, the function of MAGI1 in glioma is currently unknown. We therefore analyzed the expression of MAGI1 protein in human glioma samples, glioma cell lines and glioma stem cells (GSCs), and explored its effects on glioma cell proliferation and apoptosis. Methods: MAGI1 expression in glioma tissues was examined by Western blotting and realtime polymerase chain reaction and its relationships with clinical pathological features were analyzed. The effects of MAGI1 knockdown on the proliferation of glioma cell lines and GSCs were detected by CCK8 and colony-formation assays, and apoptosis was assessed by flow cytometry. We also investigated the effects of MAGI1 silencing on protein expression levels of epithelial-mesenchymal transition biomarkers, as well as β-catenin, cyclin D1, PTEN and phospho-Akt by Western blotting. Results: MAGI1 was significantly downregulated in glioma tissues and its expression was related to cancer progression. Silencing of MAGI1 in both glioma cell lines and GSCs enhanced proliferation and inhibited apoptosis. MAGI1 knockdown also significantly increased the expression levels of N-cadherin, vimentin, β-catenin, cyclin D1 and phospho-Akt and reduced the expression of E-cadherin and PTEN. Conclusions: Our results indicated that MAGI1 might play a vital role in glioma progression and may represent a potential therapeutic target for the treatment of glioma.

Long Non-coding RNA TMEM220-AS1 Suppressed Hepatocellular Carcinoma by Regulating the miR-484/MAGI1 Axis as a Competing Endogenous RNA

“…Some studies have indicated that in estrogen receptor-positive breast cancer, MAGI1 is a new potential tumor suppressor gene (Alday-Parejo et al, 2020). Via the Wnt/β-Catenin and PTEN/AKT signaling pathways, MAGI1 silencing inhibits apoptosis of glioma cells and promotes proliferation (Lu et al, 2019). Moreover, by regulating PTEN, MAGI1 curbed the invasion and migration of HCC (Zhang and Wang, 2011).…”

Long Non-Coding RNA TMEM220-AS1 Suppressed Hepatocellular Carcinoma by Regulating the miR-484/MAGI1 Axis as a Competing Endogenous RNA

“…The downstream target genes of miR-484 was predicted using MIRDB, MAGI1 with the highest score was chosen to forsubsequentresearch. Some studies indicated that, in estrogen receptor positive breast cancer, MAGI1 is a new potential tumor suppressor gene [29].Via the Wnt/β-Catenin and PTEN/AKT signaling pathways, MAGI1 silencing inhibited apoptosis of glioma cells and promoted the proliferation [30]. Moreover, via regulating PTEN, MAGI1 curbed invasion and migration of HCC [31].Our study con rmed that MAGI1 was the downstream target gene of miR-484, and TMEM220-AS1 released MAGI1 through competitive binding of miR-484, thereby regulating the progression of HCC.…”

MAGI1, a Scaffold Protein with Tumor Suppressive and Vascular Functions

“…Three studies performed in glioma cells showed similar outcomes; the study of Lu et al demonstrated that MAGI1 played an essential role during glioma progression; its silencing in different glioma cell lines enhanced proliferation and inhibited apoptosis, increased Wnt/β-catenin signaling, enhanced AKT phosphorylation, and reduced E-cadherin and PTEN expression. Conversely, overexpression of MAGI1 significantly inhibited tumor growth in vivo [57]. Another study found that overexpressing MAGI1 inhibits proliferation, migration, and invasion of glioma cells by regulating cell growth and EMT through AKT, matrix metalloproteinase 2 (MMP2) and MMP9, and the E-cadherin/N-cadherin/vimentin pathway [58].…”