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MyD88 expression is associated with paclitaxel resistance in lung cancer A549 cells
Fenfen Xiang1, Rong Wu1, Zhenhua Ni2
1Department of Laboratory Medicine, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200062, P.R. China.
Abstract:
The purpose of the present study was to investigate the relationship between myeloid differentiation primary response gene 88 (MyD88) expression and the resistance to paclitaxel of A549 lung cancer cells. In order to achieve MyD88 gene overexpression or knockdown in the A549 cell line, the cells were infected with lentivirus carrying MyD88 gene or shRNA to MyD88. MyD88 mRNA and protein expression was measured by RT-qPCR, immunohistochemistry and western blotting after infection for confirmation. Cell prolife-ration was detected by the WST-1 assay. Flow cytometry was used to measure the cell cycle and apoptosis. The transwell migration assay was used to observe the change of migration of transfected cells. The results showed that the overexpression of MyD88 increased the resistance of lung cancer A549 cells to paclitaxel, while the suppression of MyD88 increased the sensitivity of A549 lung cancer cells to paclitaxel. Following the paclitaxel treatment, a decreased apoptosis and G2 phase ratio, an increased cell migration ratio, and an increased production of IL-8 were found in MyD88‑overexpressed A549 cells. The western blot analysis revealed that Myd88 overexpression resulted in an increased level of Bcl-2 but a decreased level of Bax in A549 cells. These findings suggested that the expression level of MyD88 is closely associated with paclitaxel resistance in A549 lung cancer cells. Thus, the downregulation of MyD88 in A549 cells increased its sensitivity to paclitaxel treatment, whereas the upregulation of MyD88 substantiates its paclitaxel resistance.
Insights
Myeloid differentiation primary response gene 88 (MyD88) expression influences paclitaxel resistance in A549 lung cancer cells. Overexpression of MyD88 enhances resistance, while its suppression increases sensitivity to paclitaxel.
Area of Science:
- Oncology
- Molecular Biology
Background:
- Paclitaxel is a key chemotherapy agent for lung cancer.
- Mechanisms of paclitaxel resistance in A549 cells require further elucidation.
- Myeloid differentiation primary response gene 88 (MyD88) is implicated in cellular signaling pathways.
Purpose of the Study:
- To investigate the association between MyD88 expression and paclitaxel resistance in A549 lung cancer cells.
- To determine the effect of MyD88 modulation on A549 cell sensitivity to paclitaxel.
Main Methods:
- Lentiviral vectors were used for MyD88 gene overexpression and knockdown in A549 cells.
- MyD88 expression levels were confirmed using RT-qPCR, immunohistochemistry, and Western blotting.
- Cell proliferation, cell cycle, apoptosis, migration, and IL-8 production were assessed.
- Western blot analysis evaluated Bcl-2 and Bax protein levels.
Main Results:
- MyD88 overexpression conferred paclitaxel resistance, while MyD88 suppression enhanced sensitivity in A549 cells.
- Overexpression of MyD88 led to decreased apoptosis, altered cell cycle distribution (reduced G2 phase), and increased migration and IL-8 production.
- MyD88 overexpression correlated with increased Bcl-2 and decreased Bax protein levels.
Conclusions:
- MyD88 expression levels are significantly correlated with paclitaxel resistance in A549 lung cancer cells.
- Downregulation of MyD88 enhances sensitivity to paclitaxel, suggesting MyD88 as a potential therapeutic target.
- Upregulation of MyD88 contributes to paclitaxel resistance, highlighting its role in chemotherapy evasion.
