Objective: To investigate the function of repair gene LIG4 in radiosensitivity enhancement of rectal cancer cells by curcumin.
Methods: Human rectal cancer cells HT-29 were cultured in normal. LIG4-overexpression HT-29 cells and blank control plasmid HT-29 cells were established by gene transfection. Both kind of HF-29 cells were further randomly divided into curcumin group, radiotherapy group, curcumin plus radiotherapy group (combined group) and control group. The growth inhibition and apoptosis of cells were detected by MTT and Annexin V/PI respectively. Change of tumor volume was observed in nude mouse xenograft model, and the apoptosis of tumor cells was analyzed by TUNEL.
Results: Regarding blank control plasmid HT-29 cells, the growth inhibition rate and apoptosis rate in combined group were significantly higher than those in radiotherapy group(all P<0.05); tumor volume of nude mouse in combined group was significantly smaller than that in radiotherapy group, and the apoptotic index in combined group was significantly higher than that in radiotherapy group (all P<0.05). However, regarding LIG4-overexpression HT-29 cells, the growth inhibition rate and apoptosis rate were not significantly different between combined group and radiotherapy group(all P>0.05); the tumor volume of nude mouse and the apoptotic index were also not significantly different between combined group and radiotherapy group (all P>0.05).
Conclusion: Down-regulation of LIG4 is an important mechanism of radiosensitivity enhancement of rectal cancer cells by curcumin.
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Int J Clin Oncol
January 2025
Department of Radiation Oncology, Kindai University Faculty of Medicine, 377-2, Ohno-Higashi, Osaka-Sayama, Osaka, Japan.
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Dept of Surgical Oncology, Aster International Institute of Oncology, Bangalore, India.
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Clin Transl Radiat Oncol
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Institute of Medical Science & Institute for Cancer Research, Keimyung University, Daegu, Republic of Korea.
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View Article and Find Full Text PDFHeliyon
January 2025
Sir Peter MacCallum Department of Oncology, The University of Melbourne, Australia.
Background: TG02 is a peptide-based cancer vaccine eliciting immune responses to oncogenic codon 12/13 mutations. This phase 1 clinical trial (NCT02933944) assessed the safety and immunological efficacy of TG02 adjuvanted by GM-CSF in patients with -mutant colorectal cancer.
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Prostate
January 2025
AP-HP. Department of Urology, Henri Mondor University Hospital, Creteil, France.
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