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Downregulation of hexokinase 2 improves radiosensitivity of breast cancer
Dan Zhang1, Hui Wang1, Wenjing Yu1
1Department of Nuclear Medicine, The First Affiliated Hospital of Anhui Medical University, Hefei 230022, China.
Background:
Hexokinase 2 (HK2) is a major glycolytic enzyme that plays a critical role in the development of tumor metabolism. Triple negative breast cancers (TNBC) have high glycolytic activity and poor prognosis. This study explored the effect of HK2 on radiotherapy (RT) sensitivity of TNBC.
Methods:
The knockdown of HK2 genes in TNBC by lentiviral shRNA was confirmed by quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting. In addition, the boosts of radiation therapy effects of TNBC accompanied by a reduction of HK2 gene were determined by CCK-8, flow cytometry and colonic formation assays. (18F)-fluorodeoxyglucose (18F-FDG) uptake was used to evaluate tumor growth before and after radiation therapy in vivo.
Results:
After administration of lentiviral shHK2, the expressions of HK2 proteins and mRNA were inhibited effectively. Following exposure to different doses of X-rays, the survival rate of cells and colony formation displayed a decreased trend and the cell apoptosis rate increased in the Lv-shHK2 group (P<0.05). In addition, (18F)-fluorodeoxyglucose (18F-FDG) positron emission tomography/computed tomography (PET/CT) imaging showed that compared with control, the maximum standardized uptake value (SUVmax) was lower in the Lv-shHK2 group.
Conclusions:
Downregulation of HK2 improved the radiosensitivity of breast cancer (BC).
Insights
Downregulating Hexokinase 2 (HK2) enhances radiotherapy sensitivity in triple-negative breast cancer (TNBC). This involves reducing tumor cell survival and growth, making radiation therapy more effective for TNBC patients.
Area of Science:
- Biochemistry
- Oncology
- Radiotherapy
Background:
- Hexokinase 2 (HK2) is a key glycolytic enzyme implicated in tumor metabolism.
- Triple-negative breast cancer (TNBC) exhibits high glycolytic activity and a poor prognosis.
- This study investigates the role of HK2 in TNBC radiosensitivity.
Purpose of the Study:
- To determine the effect of HK2 downregulation on the sensitivity of TNBC to radiotherapy.
- To evaluate whether inhibiting HK2 can enhance the efficacy of radiation treatment for TNBC.
Main Methods:
- HK2 gene knockdown in TNBC cells using lentiviral shRNA, confirmed by qRT-PCR and Western blotting.
- Assessment of radiotherapy effects using CCK-8, flow cytometry, and colony formation assays.
- In vivo tumor growth evaluation via (18F)-fluorodeoxyglucose (18F-FDG) uptake using PET/CT imaging.
Main Results:
- Effective inhibition of HK2 mRNA and protein expression was achieved with lentiviral shHK2.
- Reduced cell survival, colony formation, and increased apoptosis were observed in cells with HK2 knockdown following X-ray exposure (P<0.05).
- In vivo imaging showed lower (18F-FDG) uptake (SUVmax) in the Lv-shHK2 group compared to controls.
Conclusions:
- Downregulation of HK2 significantly improves the radiosensitivity of breast cancer.
- Targeting HK2 represents a potential strategy to enhance radiotherapy outcomes in TNBC.
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