Maternally expressed 3 inhibits the biological activity of oral squamous cell carcinoma SCC25 and CAL27 cell lines

Abstract

The abnormal expression of long non-coding RNA (lncRNA) maternally expressed 3 (MEG3) is closely related to several tumor diagnosis and progression, such as endometrial carcinoma and ovarian cancer. However, the role of MEG3 in oral squamous cell carcinoma (OSCC) is rarely reported. The current study aimed to evaluate the expression of lncRNA MEG3 in OSCC tissues and cell lines and its effect on the biological behavior of OSCC cell lines. The expression of lncRNA MEG3 in the OSCC tissues and cell lines was detected by reverse transcription-quantitative (RT-q) PCR. The relationship between MEG3 expression and the clinicopathologic characteristics and prognosis of patients with OSCC was analyzed. The lncRNA MEG3 overexpression plasmid and control plasmid were transfected into SCC25 and CAL27 cell lines using the lipofectin method. MTT assay was performed to detect the growth and proliferation of the cell lines. Transwell chamber test was used to detect changes in cell migration and invasion. Flow cytometry was employed to detect changes in apoptosis. Western blotting and RT-qPCR were conducted to detect the expression of the p53 gene. The expression of lncRNA MEG3 in the OSCC tissues and cell lines was significantly compared with normal tissues and cell lines, respectively. The expression level of MEG3 was related to clinical stage, lymph node metastasis, distant metastasis and survival status. Overexpression of lncRNA MEG3 inhibited the proliferation, migration, and invasion of SCC25 and CAL27 cell lines, induced apoptosis and promoted the expression of p53 gene. lncRNA MEG3 played the role of a tumor inhibitor gene and significantly inhibited the biological activity of OSCC cell lines, which may provide a novel idea for molecular targeted therapy of OSCC.

Long noncoding RNAMEG3 inhibits oral squamous cell carcinoma progression via GATA3

“…We found that GSK126 treatment indeed significantly inhibited H3K27me3 modification of the MEG3 gene locus and promoted MEG3 expression in OSCC cells, suggesting that the downregulation of MEG3 expression in OSCC cells was mediated by H3K27me3 modification of the MEG3 gene locus. Several reports have demonstrated that MEG3 inhibits proliferation, migration, invasion, and promotes apoptosis of OSCC cells [14][15][16]. In the present work, it was authenticated that overexpression of MEG3 resulted in the suppression of proliferation and invasion of OSCC cells, which is consistent with previous studies [14 -16].…”

“…MEG3 is usually acts as a tumor‐suppressive lncRNA, which is downregulated in tumor tissues and cells [ 9 , 10 , 11 , 12 , 13 ]. Several studies have shown that MEG3 expression is inhibited in OSCC tissues [ 14 , 15 , 16 ]. Consistent with this, we found that MEG3 expression was downregulated in OSCC tissues by analyzing TCGA data and the 72 pairs samples collected in this study.…”

“…Several reports have demonstrated that MEG3 inhibits proliferation, migration, invasion, and promotes apoptosis of OSCC cells [ 14 , 15 , 16 ]. In the present work, it was authenticated that overexpression of MEG3 resulted in the suppression of proliferation and invasion of OSCC cells, which is consistent with previous studies [ 14 , 15 , 16 ].…”

“…In previous studies, MEG3 expression was reported to be downregulated in OSCC tissues [ 14 , 15 , 16 ]. Overexpression of MEG3 could inhibit proliferation, migration, invasion, and promote apoptosis of OSCC cells [ 14 , 15 , 16 ]. However, the mechanism underlying MEG3 downregulation in OSCC has not been well characterized.…”

DCBLD1 Overexpression Is Associated With a Poor Prognosis in Head and Neck Squamous Cell Carcinoma

“…Combining HPA data and qPCR results, it was found that DCBLD1 proteins were moderately expressed in OSCC tissues but were absent in normal oral tissues. SCC25 and CAL27 cancer cell lines are derived from human OSCC commonly used in HNSCC studies (24), while gingival fibroblasts originated from the gingival tissues resected in normal people after the removal of impacted teeth. The qPCR results indicated that the expression of DCBLD1 mRNA in OSCC cells was higher than that in normal gingival fibroblasts, which further suggested that high DCBLD1 expression might associate with the development or progression of HNSCC.…”