Liu Xilin, Song Xianji, Li Hong
Department of Hand Surgery, China Japan Union Hospital of Jilin University, Changchun, 130033, Jilin, China.
Orthopaedic Surgery, China Japan Union Hospital of Jilin University, Changchun, 130033, Jilin, China.
Cancer Cell Int. 2021 Jan 11;21(1):43. doi: 10.1186/s12935-020-01737-3.
Ectopic expression of transcription elongation factor A (SII)-like 7 (TCEAL7) has been observed in several kinds of cancers, but its role in melanoma is still unclear. This study was carried out to investigate TCEAL7 role in melanoma progression, and uncover the underlying mechanisms.
TCEAL7 expression levels in melanoma tissues and cells were determined by using real-time quantitative PCR (RT-PCR) and western blotting. CCK-8, transwell chambers, flow cytometry, starch assay and tumorigenesis assay were applied to detect cell growth, invasion, apoptosis, migration and tumorigenesis, respectively.
A low expression level of TCEAL7 was observed in melanoma tissues and cells, which was associated with malignant clinical process and poor prognosis. TCEAL7 negatively modulated AKT1, AKT2, c-Myc, N-cadherin and PCNA expression and inhibited cancer progression via decreasing AKT1 and c-Myc levels. In addition, TCEAL7 was negatively modulated by miR-758-3p which promoted melanoma progression. Moreover, overexpression of TCEAL7 abolished miR-758-3p role in promoting melanoma progression.
This study demonstrated that TCEAL7, regulated by miR-758-3p inhibited melanoma progression through decreasing the expression levels of c-Myc and AKT1.
转录延伸因子A（SII）样7（TCEAL7）的异位表达已在多种癌症中被观察到，但其在黑色素瘤中的作用仍不清楚。本研究旨在探讨TCEAL7在黑色素瘤进展中的作用，并揭示其潜在机制。
采用实时定量PCR（RT-PCR）和蛋白质免疫印迹法检测黑色素瘤组织和细胞中TCEAL7的表达水平。分别应用CCK-8、Transwell小室、流式细胞术、淀粉测定法和肿瘤发生试验检测细胞生长、侵袭、凋亡、迁移和肿瘤发生情况。
在黑色素瘤组织和细胞中观察到TCEAL7低表达水平，这与恶性临床过程和不良预后相关。TCEAL7通过降低AKT1和c-Myc水平负向调节AKT1、AKT2、c-Myc、N-钙黏蛋白和增殖细胞核抗原（PCNA）的表达并抑制癌症进展。此外，TCEAL7受到促进黑色素瘤进展的miR-758-3p的负向调节。而且，TCEAL7的过表达消除了miR-758-3p在促进黑色素瘤进展中的作用。
本研究表明，受miR-758-3p调控的TCEAL7通过降低c-Myc和AKT1的表达水平抑制黑色素瘤进展。
