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Downregulated Mucin 1 alleviates paclitaxel resistance in non‑small cell lung cancer cells
1Department of Oncology, The General Hospital of Western Theater Command, Chengdu, Sichuan 610083, P.R. China.
Abstract:
Multidrug resistance of non‑small cell lung cancer (NSCLC) is a common clinical problem, which is one of the main reasons leading to the failure of chemotherapy. Therefore, how to overcome or prevent drug resistance has become a hot and difficult issue in clinical research. The present study was designed to investigate the expression patterns, functions and underlying mechanisms of MUC1 in regulating paclitaxel‑resistant cell line A549/PR in NSCLC. RT‑qPCR and western blot was performed to determine the mRNA and protein level, respectively. CCK‑8 was conducted to determine the cell viability of A549/PR cells. Moreover, flow cytometry assay was applied to examine the apoptosis rate of A549/PR. Herein, the MUC1 was over‑expressed in clinic NSCLC tissues and A549/PR cells. Silence of MUC1 could obviously suppress the proliferation and promote apoptosis of A549/PR cells in treatment of paclitaxel through up‑regulating the expression of Bax and Caspase‑3, and down‑regulating the expression of Bcl‑2, suggesting that chemotherapy combined with the modulation of MUC1 might be characterized as a promising therapeutic approach to overcome paclitaxel‑resistance in NSCLC in the future.
Insights
Multidrug resistance in non-small cell lung cancer (NSCLC) is a major challenge. Targeting MUC1 shows promise in overcoming paclitaxel resistance by suppressing proliferation and promoting apoptosis in NSCLC cells.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Multidrug resistance in non-small cell lung cancer (NSCLC) significantly limits chemotherapy efficacy.
- Overcoming drug resistance is a critical area of clinical research for improving patient outcomes.
Purpose of the Study:
- To investigate the role of MUC1 in paclitaxel resistance in NSCLC.
- To elucidate the mechanisms by which MUC1 influences drug resistance in NSCLC cells.
Main Methods:
- Quantitative reverse transcription PCR (RT-qPCR) and Western blot to assess MUC1 mRNA and protein levels.
- Cell Counting Kit-8 (CCK-8) assay to evaluate cell viability.
- Flow cytometry to determine apoptosis rates.
Main Results:
- MUC1 was found to be overexpressed in clinical NSCLC tissues and paclitaxel-resistant A549/PR cells.
- Silencing MUC1 suppressed proliferation and enhanced apoptosis in A549/PR cells treated with paclitaxel.
- MUC1 silencing modulated the expression of apoptosis-related proteins, including upregulation of Bax and Caspase-3, and downregulation of Bcl-2.
Conclusions:
- MUC1 plays a significant role in paclitaxel resistance in NSCLC.
- Modulating MUC1 expression, in combination with chemotherapy, presents a potential strategy to overcome paclitaxel resistance in NSCLC.
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