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LINC00958 Involves in Bladder Cancer Through Sponging miR-378a-3p to Elevate IGF1R
Yupeng Cui1, Mao Xie1, Zhiyu Zhang1
1Department of Urology, Yantai Yuhuangding Hospital, Affiliated to Qingdao University, Yantai, China.
Abstract:
LINC00958 is involved in bladder cancer, but its mechanism of action remains indistinct. This study further analyzed its potential targets, aiming to search for therapeutic targets. miR-378a-3p was predicted to bind to LINC00958 and IGF1R, which was verified by double-luciferase reporter analysis. The levels of LINC00958 and miR-378a-3p in bladder cancer tissues and cells, and their correlation were further analyzed. Then LINC00958, miR-378a-3p, and IGF1R in bladder cancer cells were up- or downregulated, and their effects on cell viability, migration, and invasion of cells were detected, respectively. LINC00958 binds to miR-378a-3p whose target gene was IGF1R. The expression of miR-378a-3p was negative relative with the level of LINC00958 and IGF1R. Overexpressed miR-378a-3p restrained the activity, migration, and invasion of bladder cancer cells, which was the same as the effects of silent LINC00958 and downregulated IGF1R. Nonetheless, upregulated LINC00958 rescued the antitumor effect of overexpressed miR-378a-3p, whereas miR-378a-3p inhibitor acted as a cancer promoter to reverse the inhibition of downregulated IGF1R on cell activity, migration, and invasion. LINC00958 accelerated the propagation and metastasis of bladder cancer cells through sponging miR-378a-3p to elevate IGF1R, which might trigger a new direction for the treatment of bladder cancer.
Insights
Long non-coding RNA LINC00958 promotes bladder cancer by interacting with miR-378a-3p to increase Insulin-like Growth Factor 1 Receptor (IGF1R) expression. This mechanism highlights LINC00958 as a potential therapeutic target for bladder cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Long non-coding RNA (lncRNA) LINC00958 has been implicated in bladder cancer, but its precise role and molecular mechanisms require elucidation.
- Identifying novel therapeutic targets is crucial for improving bladder cancer treatment outcomes.
Purpose of the Study:
- To investigate the mechanism of action of LINC00958 in bladder cancer.
- To explore the potential of targeting the LINC00958/miR-378a-3p/IGF1R axis for bladder cancer therapy.
Main Methods:
- Bioinformatic prediction of interactions between LINC00958, miR-378a-3p, and IGF1R.
- Experimental validation using double-luciferase reporter assays.
- Analysis of expression levels of LINC00958, miR-378a-3p, and IGF1R in bladder cancer tissues and cells.
- In vitro functional assays to assess the effects of modulating these molecules on cell viability, migration, and invasion.
Main Results:
- LINC00958 directly binds to miR-378a-3p, and IGF1R is identified as a target gene of miR-378a-3p.
- Expression of miR-378a-3p was inversely correlated with LINC00958 and IGF1R levels in bladder cancer.
- Overexpression of miR-378a-3p or downregulation of LINC00958/IGF1R inhibited bladder cancer cell proliferation, migration, and invasion.
- Upregulation of LINC00958 reversed the antitumor effects of miR-378a-3p, while miR-378a-3p inhibition promoted cancer progression.
Conclusions:
- LINC00958 promotes bladder cancer progression and metastasis by acting as a molecular sponge for miR-378a-3p, leading to increased IGF1R expression.
- The LINC00958/miR-378a-3p/IGF1R axis represents a promising therapeutic strategy for bladder cancer.
