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In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
Long Intergenic Non-Protein Coding RNA 01089 Weakens Tumor Proliferation, Migration, and Invasion by Sponging
Dongdong Zhang1, Xingdong Cai2, Songwang Cai1
1Department of Thoracic Surgery, The First Affiliated Hospital, Jinan University, Guangzhou 510632, People's Republic of China.
Background:
Long non-coding RNAs (lncRNAs), a class of endogenous non-coding RNAs, play an important role in the development and metastasis of non-small cell lung cancer (NSCLC). However, the function and mechanism of action of long intergenic non-protein coding RNA 1089 (LINC01089) in NSCLC remains unclear. This study aimed to identify the role of LINC01089 in cell proliferation, migration, and invasion of NSCLC.
Methods:
Expression of LINC01089 and the relationship between LINC01089 and overall survival (OS) in NSCLC were determined using GEPIA 2.0. Similarly, microRNAs (miRNAs) that showed increased expression in NSCLC and correlated with OS were identified using the online OncomiR cancer database. Target miRNAs of LINC01089 were predicted using starBase. Cell models of LINC01089 and miR-3187-3p overexpression were constructed using transfection. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was performed to analyze the expression of LINC01089 and miR-3187-3p. MTS assay was used to assess cell proliferation. Transwell was used for migration and invasion assays.
Results:
LINC01089 expression was significantly reduced in NSCLC tissues and cells. Gain-of-function studies further demonstrated that LINC01089 overexpression inhibited proliferation, migration, and invasion of lung cancer cell lines, A549 and SK-MES-1. Based on starBase prediction and subsequent verification, we revealed that miR-3187-3p is a target miRNA of LINC01089. Additionally, miR-3187-3p expression was significantly increased in NSCLC tissues and cells. Overexpression of miR-3187-3p promoted proliferation, migration, and invasion of A549 and SK-MES-1 cells, thereby reversing the effect of LINC01089.
Conclusion:
LINC01089 attenuates tumor proliferation, migration, and invasion by sponging miR-3187-3p in NSCLC. LINC01089 acts as a tumor suppressor and represents a potential therapeutic target in NSCLC.
Insights
Long non-coding RNA 1089 (LINC01089) suppresses non-small cell lung cancer (NSCLC) growth by inhibiting miR-3187-3p. This finding positions LINC01089 as a potential therapeutic target for NSCLC treatment.
Area of Science:
- Molecular Biology
- Oncology
Background:
- Long non-coding RNAs (lncRNAs) are implicated in non-small cell lung cancer (NSCLC) development and metastasis.
- The specific role of long intergenic non-protein coding RNA 1089 (LINC01089) in NSCLC remains largely unknown.
Purpose of the Study:
- To investigate the function and mechanism of LINC01089 in NSCLC cell proliferation, migration, and invasion.
- To determine the relationship between LINC01089 expression and overall survival in NSCLC patients.
Main Methods:
- Utilized GEPIA 2.0 and OncomiR database for expression analysis and survival correlation.
- Employed starBase for miRNA target prediction and constructed cell models for LINC01089 and miR-3187-3p.
- Performed qRT-PCR, MTS assays, and Transwell assays to evaluate gene expression, proliferation, migration, and invasion.
Main Results:
- LINC01089 expression was significantly downregulated in NSCLC tissues and cells.
- Overexpression of LINC01089 inhibited proliferation, migration, and invasion in NSCLC cell lines (A549, SK-MES-1).
- Identified miR-3187-3p as a direct target of LINC01089; miR-3187-3p overexpression promoted NSCLC cell proliferation, migration, and invasion, counteracting LINC01089's effects.
Conclusions:
- LINC01089 functions as a tumor suppressor in NSCLC by sponging miR-3187-3p.
- LINC01089 represents a promising therapeutic target for NSCLC.
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