Downregulation of TRIM28 inhibits growth and increases apoptosis of nude mice with non‑small cell lung cancer xenografts

Abstract

TRIM28 is a well-known transcriptional co-repressor of Kruppel-associated box zinc finger proteins. The authors previously demonstrated that TRIM28 small interfering (si)RNA decreases cell proliferation and inhibits cell cycle progression in non-small cell lung cancer (NSCLC) cell lines. The present study further demonstrated that the stable silencing of TRIM28 expression by a specific siRNA lentivirus vector significantly inhibited the growth and exerted obvious anti-tumor effects in nude mice. The results of the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling assay indicated that TRIM28 knockdown increased apoptosis. Furthermore, TRIM28 knockdown decreased the expression of B cell lymphoma (Bcl)-2 and increased the expression of Bcl-2 associated X, apoptosis regulator and p53 at the gene and protein levels. Auto-antibodies to TRIM28 were present in 12.32% of the sera of the patients with NSCLC. The results suggest that TRIM28 knockdown may be effective against NSCLC, and TRIM28 antibodies have the potential to act as novel diagnostic and therapeutic tools.

Disruption of RING and PHD Domains of TRIM28 Evokes Differentiation in Human iPSCs

“…Here, we show that during differentiation of iPSC due to TRIM28 depletion, there is a significant shift in cellular signaling. We demonstrate that silencing TRIM28 leads to upregulation of processes related to the regulation of apoptosis, differentiation into a multicellular organism, positive regulation of the developmental process, and regulation of the cell cycle, which is also confirmed by earlier evidence [9,74,75].…”

C1QTNF6 regulated by miR‐29a-3p promotes proliferation and migration in stage I lung adenocarcinoma

“…Previous reports showed that 30%-35% stage I NSCLC patients treated with surgery may progress to local recurrence or distant metastasis within five years [ 4 ]. The 5-year survival rate is 83.9% in stage IA and 66.3% in stage IB NSCLC [ 5 ]. Lung adenocarcinoma (LUAD) is the most common histologic type of NSCLC with morbidity and mortality persistently elevated over past decades [ 6 ].…”

Expression and Significance of TRIM 28 in Squamous Carcinoma of Esophagus

“…They believed that TRIM28 played a pivotal role in cervical cancer cell proliferation and might serve as a potential therapeutic target. In non-small cell lung cancer (NSCLC) cell lines, Liu L [9] demonstrated that the stable silencing of TRIM28 expression by a specific siRNA lentivirus vector significantly inhibited the growth and exerted obvious anti-tumor effects in nude mice. Furthermore, TRIM28 expression was significantly correlated with several clinicopathological characteristics of patients with breast cancer (BC), such as p53 mutation, tumor recurrence and Elston grade of the tumor [11].…”

“…As one of the evolutionarily conserved TRIM family proteins, TRIM28 has been proved to accelerate cell proliferation and metastasis in a variety of human cancers. Studies have shown, for example, that TRIM28 knockdown may be effective against NSCLC, and the knockdown of TRIM28 expression by lenti-siRNA/TRIM28 may inhibit tumor growth and induce cell apoptosis in vivo [9, 10]. Hao L found that TRIM28 is frequently elevated in multiple tumor types and is associated with aggressive clinical features of breast cancer.…”