Anticancer potential of TUG1 knockdown in cisplatin-resistant osteosarcoma through inhibition of MET/Akt signalling.

J Drug Target

Department of Orthopedics, Zhejiang Hospital, Hangzhou, People's Republic of China.

Published: February 2020

Development of cisplatin (DDP)-resistance is a major challenge that largely limits the efficacy of chemotherapy for osteosarcoma. LncRNA Taurine up-regulated gene 1 (TUG1) is a recently identified oncogenic lncRNA that has been involved in chemo-resistance of various cancers. In this study, over-expression of TUG1 was found in two osteosarcoma cell lines resistant to DDP (Saos-2/DDP, MG-63/DDP). Knockdown of TUG1 inhibited the DDP-resistance and promoted the cytotoxicity and apoptosis induced by DDP in Saos-2/DDP and MG-63/DDP cells. TUG1 knockdown also markedly inhibited the expression level of MET and p-Akt. In conclusion, knockdown of TUG1 suppressed cell growth and increased apoptotic rate under DDP treatment possibly via regulating MET/Akt signalling pathway.

Download full-text PDF

Source
http://dx.doi.org/10.1080/1061186X.2019.1644651DOI Listing

Publication Analysis

Top Keywords

tug1 knockdown
8
met/akt signalling
8
ddp saos-2/ddp
8
saos-2/ddp mg-63/ddp
8
knockdown tug1
8
tug1
6
anticancer potential
4
potential tug1
4
knockdown
4
knockdown cisplatin-resistant
4

Similar Publications

Purpose: This study aimed to explore the relationship between m6A demethylase ALKBH5 and long noncoding RNA TUG1 (TUG1), as well as their effects on proliferation, migration, and angiogenesis in gastric cancer (GC) cells.

Methods: The Cancer Genome Atlas (TCGA) database was utilized to analyze the relative expression levels of ALKBH5, TUG1, and vascular endothelial growth factor A (VEGFA). Survival analyses of TUG1, ALKBH5, and VEGFA were performed using the Gene Expression Profiling Interactive Analysis (GEPIA) and Kaplan-Meier databases.

View Article and Find Full Text PDF

Microglia, the central nervous system's primary immune cells, play a key role in the progression of cerebral ischemic stroke, particularly through their involvement in pyroptosis. The long non-coding RNA taurine up-regulated gene 1 (Tug1) is elevated during ischemic stroke and is critical in driving post-stroke neuroinflammation. However, the underlying molecular mechanisms remain unclear.

View Article and Find Full Text PDF

Background: The purpose of this study was to probe the specific role of long noncoding RNA taurine upregulation 1 (LncRNA TUG1) in viral myocarditis (VMC).

Methods: The mouse model of VMC was induced by Coxsackievirus type B3 (CVB3). LncRNA TUG1 was subsequently silenced, and micro-140-3p (miR-140-3p) was overexpressed in VMC mice.

View Article and Find Full Text PDF

Acute myeloid leukemia (AML) is a fatal malignancy with rising incidence and low cure rates. This study aims to investigate the effect of alkB homolog 5 (ALKBH5)-mediated N6-methyladenosine (m6A) modification on adriamycin (ADR) resistance in AML. First, the levels of ALKBH5, taurine upregulated 1 (TUG1), YTH N6-methyladenosine RNA binding protein F2 (YTHDF2), euchromatic histone lysine methyltransferase 2 (EHMT2), and SH3 domain-binding glutamate-rich protein-like (SH3BGRL) were measured.

View Article and Find Full Text PDF

Epitranscriptomic mA modifications during reactivation of HIV-1 latency in CD4 T cells.

mBio

November 2024

Department of Microbiology and Immunology, Carver College of Medicine, The University of Iowa, Iowa City, Iowa, USA.

Article Synopsis
  • The presence of latently infected CD4 T cells remains a challenge to curing HIV-1, even with effective antiretroviral therapy.
  • Research shows that the mA modification of RNA plays a crucial role in regulating HIV-1 infection, affecting viral stability and immune response.
  • In a study using a model of HIV-1 latency, an increase in mA levels was observed during reactivation, highlighting its potential importance in overcoming HIV-1 latency.
View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!