MicroRNA-134 reverses multidrug resistance in human lung adenocarcinoma cells by targeting FOXM1
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Updated: Mar 3, 2026

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
Jipeng Li1, Ying Chen1, Mingwei Jin1
1Department of Central Laboratory, Yinzhou People's Hospital, Ningbo, Zhejiang 315040, P.R. China.
Abstract:
Multidrug resistance (MDR) is the primary barrier to the success of chemotherapy for lung adenocarcinoma. MicroRNA (miR)-134, which is downregulated in lung adenocarcinoma, influences cell proliferation, apoptosis and invasion of lung adenocarcinoma. However, the function of miR-134 in the MDR of lung adenocarcinoma remains unclear. In the present study, it was identified that miR-134 expression is significantly downregulated in A549/cisplatin MDR lung adenocarcinoma cells, as compared with A549 parental cells. miR-134 regulates the sensitivity of lung adenocarcinoma cells to certain anticancer drugs. Furthermore, it was demonstrated that forkhead box M1 and multidrug resistance-associated protein 1 are functional targets of miR-134. These data revealed an important role for miR-134 in the regulation of MDR in lung adenocarcinoma.
Insights
MicroRNA-134 (miR-134) is downregulated in lung adenocarcinoma, impacting multidrug resistance (MDR). Restoring miR-134 may enhance chemotherapy effectiveness against lung adenocarcinoma by targeting key MDR genes.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Multidrug resistance (MDR) significantly hinders chemotherapy efficacy in lung adenocarcinoma.
- MicroRNA-134 (miR-134) is known to regulate proliferation, apoptosis, and invasion in lung adenocarcinoma, but its role in MDR is not well understood.
Purpose of the Study:
- To investigate the role of miR-134 in the multidrug resistance of lung adenocarcinoma.
- To identify the functional targets of miR-134 involved in MDR.
Main Methods:
- Quantitative analysis of miR-134 expression in A549/cisplatin MDR cells versus A549 parental cells.
- Assessment of miR-134's influence on the sensitivity of lung adenocarcinoma cells to anticancer drugs.
- Identification of downstream targets, including forkhead box M1 (FOXM1) and multidrug resistance-associated protein 1 (MRP1).
Main Results:
- miR-134 expression was significantly downregulated in cisplatin-resistant lung adenocarcinoma cells.
- miR-134 was found to modulate the sensitivity of lung adenocarcinoma cells to chemotherapy drugs.
- FOXM1 and MRP1 were confirmed as functional targets regulated by miR-134.
Conclusions:
- miR-134 plays a crucial role in regulating multidrug resistance in lung adenocarcinoma.
- The findings suggest that miR-134 could be a potential therapeutic target for overcoming MDR in lung adenocarcinoma.
- Targeting miR-134 may offer a novel strategy to improve chemotherapy outcomes for lung adenocarcinoma patients.
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