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Updated: Apr 17, 2026
Radiosensitivity of Cancer Stem Cells in Lung Cancer Cell Lines
Published on: August 21, 2019
Knockdown of PKM2 Enhances Radiosensitivity of Non-small cell Lung Cancer
Shijiang Wang1, Yan Ma1, Peiguo Wang2
1Department of Radiation Oncology, Shandong Cancer Hospital and Institute, No. 440 Ji Yan Road, Jinan, 250117, People's Republic of China.
Abstract:
Pyruvate kinase isoenzyme M2 (PKM2) is a key enzyme to regulate aerobic glycolysis in tumor cells and can be used as potential target for cancer therapy. Here, we investigated the effect of knockdown of PKM2 on non-small cell lung cancer (NSCLC) responses to ionizing radiation. Our results showed that PKM2 was greatly up-regulated in radioresistant cell lines and PKM2 knockdown leaded to increased radiosensitivity of radioresistant cell lines, which were associated with higher apoptosis rate and endoplasmic reticulum stress according to western blot analysis. Moreover, significant inhibition in tumor size under regular radiotherapy was found in Balb/c-nude mice bearing radioresistant NSCLC tumors with PKM2 knockdown. Our findings suggested that targeting PKM2 could effectively improve the efficacy of radiotherapy.
Insights
Targeting pyruvate kinase isoenzyme M2 (PKM2) enhances cancer therapy. Knocking down PKM2 increases radiosensitivity in non-small cell lung cancer (NSCLC) by promoting apoptosis and endoplasmic reticulum stress, improving radiotherapy efficacy.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Therapy
Background:
- Pyruvate kinase isoenzyme M2 (PKM2) regulates aerobic glycolysis in tumor cells.
- PKM2 is a potential therapeutic target for cancer treatment.
- Understanding PKM2's role in radioresistance is crucial for improving cancer therapy.
Purpose of the Study:
- To investigate the effect of PKM2 knockdown on non-small cell lung cancer (NSCLC) response to ionizing radiation.
- To determine if targeting PKM2 can enhance the efficacy of radiotherapy in NSCLC.
Main Methods:
- PKM2 knockdown in radioresistant NSCLC cell lines.
- Western blot analysis to assess apoptosis and endoplasmic reticulum stress.
- In vivo studies using Balb/c-nude mice bearing NSCLC tumors.
Main Results:
- PKM2 was significantly upregulated in radioresistant NSCLC cell lines.
- PKM2 knockdown increased radiosensitivity of radioresistant NSCLC cells.
- PKM2 knockdown was associated with higher apoptosis rates and endoplasmic reticulum stress.
- In vivo, PKM2 knockdown significantly inhibited tumor growth in mice receiving radiotherapy.
Conclusions:
- PKM2 is upregulated in radioresistant NSCLC and contributes to radioresistance.
- Targeting PKM2 can overcome radioresistance in NSCLC.
- PKM2 is a promising therapeutic target to improve radiotherapy efficacy in NSCLC.
