{'fraction_non_alphanumeric': 0.021414665801427646, 'fraction_numerical': 0.005840363400389357, 'mean_word_length': 5.2682926829268295, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Involvement of vascular endothelial growth factor (VEGF) secretion in radiation surviving tumor cells derived from breast cancer cell line

Radiotherapy is an effective approach for the treatment of many types of cancer. However, it has been reported that the malignant capacities of tumor cells can be increased in those tumors that survive radiotherapy. Here, we constructed radiation‐ surviving tumor cells (IR cells) by using the human breast cancer cell line MCF7, in the manner of our previous report. We focused on angiogenesis in IR cells, because angiogenesis in breast cancer is highly associated with unfavorable patient prognosistic criteria, such as tumor metastasis and relapse. To analyze angiogenesis in IR cells, we performed a tube formation assay and plasma clot assay by using human umbilical vein endothelial cells (HUVEC). However, IR cells had the same levels of angiogenic activity compared to that of parental cells. On the other hand, the secretion of vascular endothelial growth factor (VEGF) was enhanced by about 1.9‐fold in IR cells as estimated by ELISA. From microarray analysis, the gene expression of NRP1 and CXCL14 was upregulated in IR cells. These results suggest that increased CXCL14 expression prevents angiogenesis in IR cells, even though NRP1 may promote upregulation of VEGF expression by autocrine signaling. Further studies are necessary to clarify the function of upregulated‐VEGF in IR cells, and may elucidate their possible role in controlling the behavior of tumors surviving radiotherapy.