Long non-coding RNA MRPL23-AS1 suppresses anoikis in salivary adenoid cystic carcinoma in vitro

被引:11
作者
Li, Yin-Ran [1 ,2 ,3 ,4 ,5 ,6 ]
Fu, Min [1 ,2 ,3 ,4 ,5 ,6 ]
Song, Ye-Qing [1 ,2 ,3 ,4 ,5 ]
Li, Sheng-Lin [1 ,2 ,3 ,4 ,5 ,6 ]
Ge, Xi-Yuan [1 ,2 ,3 ,4 ,5 ,6 ]
机构
[1] Peking Univ, Cent Lab, Sch & Hosp Stomatol, Beijing, Peoples R China
[2] Natl Ctr Stomatol, Beijing, Peoples R China
[3] Natl Clin Res Ctr Oral Dis, Natl Engn Res Ctr Oral Biomat & Digital Med Devic, Beijing, Peoples R China
[4] Minist Hlth, Res Ctr Engn & Technol Computerized Dent, Beijing Key Lab Digital Stomatol, Beijing, Peoples R China
[5] NMPA Key Lab Dent Mat, Beijing, Peoples R China
[6] Peking Univ, Dept Oral & Maxillofacial Surg, Sch & Hosp Stomatol, Beijing, Peoples R China
基金
北京市自然科学基金; 中国国家自然科学基金;
关键词
anoikis; LncRNA; MRPL23-AS1; p19INK4D; salivary adenoid cystic carcinoma; DISTANT METASTASES; MESENCHYMAL TRANSITION; HEAD; NECK; INHIBITORS; CELLS; DIFFERENTIATION; GALECTIN-3; APOPTOSIS; P19INK4D;
D O I
10.1111/odi.14156
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
Distant lung metastasis is the main factor that affects the survival rate of patients with salivary adenoid cystic carcinoma (SACC). Anoikis resistance is a feature of tumor cells that easily metastasize. The long non-coding RNA (lncRNA) MRPL23 antisense RNA 1 (MPRL23-AS1) is related to lung metastasis in SACC, but its role in anoikis resistance is unknown. After altering MPRL23-AS1 expression in SACC cells, anoikis resistance was detected by calcein AM/PI staining and annexin V/PI flow cytometry. The apoptosis marker activated caspase-3 and the bcl-2/bax ratio were detected by Western blotting. The relationship between MPRL23-AS1 and the promoter of the potential downstream target gene p19INK4D was identified by chromatin immunoprecipitation (ChIP)-PCR assay. p19INK4D expression in patient tissues was determined using qRT-PCR and immunohistochemistry. The functional experiments showed that MPRL23-AS1 could promote anoikis resistance in vitro. MRPL23-AS1 recruited the EZH2 to the promoter region of p19INK4D, inhibited p19INK4D expression, and promoted tumor cell anoikis resistance. p19INK4D overexpression did not affect anoikis in attached cells; however, it attenuated the anoikis resistance effect of MPRL23-AS1 in suspension cells. p19INK4D expression was significantly lower in SACC tissues than in normal tissues. The novel MRPL23-AS1/p19INK4D axis may be a potential SACC biomarker or therapeutic target.
引用
收藏
页码:1588 / 1601
页数:14
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