MiR‐34a inhibits the proliferation, migration, and invasion of oral squamous cell carcinoma by directly targeting SATB2

Abstract

In various kinds of carcinomas, the special AT-rich sequence-binding protein 2 (SATB2) with its atypical expression promotes the metastasis and progression of the tumor, though in the oral squamous cell carcinoma (OSCC) its inherent mechanism and the status of SATB2 remain unclear. The role played by the SATB2 expression in the OSCC cell lines and tissue samples in the target of miR-34a downstream is the intended endeavor of this study. In te OSCCs the miR-34a expression was determined by quantitative real-time polymerase chain reaction (q-PCR), while the SATB2 expression in the cell lines and tissue samples in OSCC was analyzed with the q-PCR and the western blot. Studies in both in vitro and in vivo of the effects of miR-34a on the initiation of OSCC were conducted. As a direct target of the miR-34a the SATB2 was verified with the luciferase reporter assay. In cases where the miR-34a levels were low, the SATB2 in OSCCs seemed to be overexpressed. Besides, both in the in vitro and in vivo a suppression of migration, invasion, and cell growth was caused by miR-34a by down regulating the SATB2 expression. The SATB2 being a direct target of miR-34a was confirmed by the cotransfection of miR-34a mimics specifically the decrease in the expression of luciferase of SATB2-3′UTR-wt reporter.As a whole, our study confirmed the inhibition of miR-34a in the invasion, proliferation, and migration of the OSCCs, playing a potential tumor suppressor role with SATB2 as its downstream target.

Increased ACTL6A occupancy within mSWI/SNF chromatin remodelers drives human squamous cell carcinoma

“…Amplification or overexpression of ACTL6A leads to full occupancy of BAF complexes, giving rise to two mechanisms promoting SCC initiation and maintenance. ll promotes the survival and chemoresistance of SCCs partly by interacting with DNp63a (Chung et al, 2010;Ge et al, 2020b;Seong et al, 2015;Yu et al, 2017) (Figure 6D). Several other ACTL6A-dependent PRC target genes belong to the FOX family, members of which are often repressed by polycomb and poised for activation (Golson and Kaestner, 2016).…”

SATB2 Overexpression Promotes the Proliferation, Migration and Invasion of Oral Squamous Cell Carcinoma by Up-Regulating NOX4

“…SATB2 overexpression in HN4 cells promoted proliferation, migration, and invasion, as well as facilitating EMT and activating the Janus kinase (JAK)/STAT3 signaling pathway. These ndings suggest that SATB2 overexpression in important for progression in oncogenesis, like the role of SATB1 in breast cancer [23]. Because of the limited number of patients enrolled in this study, more patients from multiple institutions are needed to de nitively establish SATB2's overexpression pattern as well as its diagnostic utility in OSCC.…”

“…It has been reported that IL-6 promotes head and neck tumor metastasis and EMT via the STAT3/SNAIL signaling pathway [24]. Like SATB1 in breast cancer [23], IL-6 promotes growth and invasion of breast cancer cells through STAT3dependent up-regulation of the NOTCH signaling pathway [20,24,25].…”

Increased ACTL6A Occupancy Within mSWI/SNF Chromatin Remodelers Drives Human Squamous Cell Carcinoma

“…Besides WNT7B , other ACTL6A-dependent PRC targets known to play roles in SCC oncogenesis included TWIST1 , which is associated with epithelial–mesenchymal transition (EMT) in esophageal and head-and-neck SCCs (Jouppila-Matto et al, 2011; Lee et al, 2012); and SATB2 (special AT-rich binding protein 2), which promotes survival and chemoresistance of head-and-neck SCC cells in part by interacting with Δ Np63 α (Chung et al, 2010) and also drives carcinogenesis of oral SCC, colorectal cancer and osteosarcoma (Ge et al, 2020b; Seong et al, 2015; Yu et al, 2017) (Figure 5D). Several other ACTL6A- dependent PRC target genes belong to the forkhead box (FOX) family, members of which are often repressed by polycomb and poised for activation (Golson and Kaestner, 2016) (Figure 5D).…”