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Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
miR-1238 inhibits cell proliferation by targeting LHX2 in non-small cell lung cancer
Xiangguang Shi1,2, Lei Zhan1,2, Can Xiao3
1Soochow University Laboratory of Cancer Molecular Genetics, Medical College of Soochow University, Suzhou, China.
Abstract:
In human cancers, dysregulated expression of LIM-homeobox gene 2 (LHX2) and downregulation of miR-1238 has been reported separately. However, the relationship between them remains unclear. We investigated the functional contribution of miR-1238 to the regulation of LHX2 in non-small cell lung cancer (NSCLC). Here, computational algorithms predicted that the 3'-untranslated region (3'-UTR) of LHX2 is a target of miR-1238. Luciferase assays validated that miR-1238 directly bound to 3'-UTR of LHX2. qRT-PCR and western blot analyses further confirmed that overexpression of miR-1238 mimic in NSCLC A549 and LTEP-α-2 cells inhibited endogenous expression of LHX2 mRNA and protein. Moreover, ectopic expression of miR-1238 in NSCLC A549 and LTEP-α-2 cells suppressed cellular viability and proliferation. siRNA-induced knockdown of LHX2 copied the phenotype of miR-1238 overexpression in NSCLC A549 and LTEP-α-2 cells and LHX2 knockdown inhibited cell cycle. In addition, miR-1238 expression was frequently decreased in human NSCLC tissues and reversely correlated with LHX2 expression, which was increased in NSCLC tissues. Collectively, our findings demonstrate that miR-1238 inhibit the proliferation of NSCLC cells at least partly via repression of LHX2, shedding light on the mechanistic interaction of miR-1238 and LHX2 in NSCLC carcinogenesis. Furthermore, our data suggest that expression of miR-1238 could be a promising therapeutic strategy for NSCLC treatment.
Insights
MicroRNA-1238 (miR-1238) suppresses non-small cell lung cancer (NSCLC) growth by inhibiting LIM-homeobox gene 2 (LHX2). This study reveals miR-1238 as a potential therapeutic target for NSCLC.
Area of Science:
- Molecular Biology
- Oncology
- Genetics
Background:
- Dysregulated LIM-homeobox gene 2 (LHX2) and downregulated miR-1238 are observed in human cancers.
- The specific relationship between miR-1238 and LHX2 in non-small cell lung cancer (NSCLC) remains largely unexplored.
Purpose of the Study:
- To investigate the functional role of miR-1238 in regulating LHX2 expression within NSCLC.
- To elucidate the mechanistic link between miR-1238 and LHX2 in the context of NSCLC development and progression.
Main Methods:
- Computational prediction and luciferase assays to confirm direct binding of miR-1238 to the LHX2 3'-untranslated region (3'-UTR).
- Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blot analysis to assess LHX2 expression following miR-1238 mimic transfection.
- Cell viability, proliferation, and cell cycle assays in NSCLC cell lines (A549, LTEP-α-2) with manipulated miR-1238 and LHX2 levels.
Main Results:
- miR-1238 directly targets the 3'-UTR of LHX2, inhibiting its mRNA and protein expression in NSCLC cells.
- Overexpression of miR-1238 suppressed NSCLC cell viability, proliferation, and induced cell cycle arrest.
- Knockdown of LHX2 mimicked the suppressive effects of miR-1238, indicating LHX2's role in mediating miR-1238's function.
- Decreased miR-1238 and increased LHX2 expression were observed in human NSCLC tissues, showing an inverse correlation.
Conclusions:
- miR-1238 inhibits NSCLC proliferation, at least partially, by repressing LHX2 expression.
- The miR-1238/LHX2 axis represents a significant mechanism in NSCLC carcinogenesis.
- miR-1238 holds promise as a potential therapeutic strategy for NSCLC treatment.
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