ABSTRACT
Head and neck cancers are the seventh most common type of cancer in the world， among which more than 90% are squamous cell carcinomas（HNSCC）. Radiotherapy is one of the important treatments for HNSCC， and the sensitivity of tumor cells to the therapy is a key factor influencing the efficacy of treatment. p53 is one of the most common mutated genes in HNSCC， and epidermal growth factor receptor（EGFR） is overexpressed in many HNSCC. Both of these genes could enhance cellular DNA repair， which may be related to the radiotherapy resistance of HNSCC. This review focuses on the mechanisms by which tumor cells escape radiation-mediated apoptosis through p53 and EGFR-mediated DNA repair.
ABSTRACT
Radiotherapy is an important means to treat malignant tumors in clinical practice. However, tumor radioresistance not only seriously limits the efficiency of radiotherapy, but also leads to poor prognosis of patients, which may eventually lead to tumor metastasis and recurrence. Circular RNA (circRNA) is a new member of noncoding RNA, which is highly specific, stable and conservative. This paper reviewed with the effect of circRNA on the signal pathways related to radiotherapy resistance by analyzing the perspective of DNA damage repair pathway, EMT (epithelial mesenchymal transition) process, Wnt pathway, tumor stem cells and other pathways, and sorted out the mechanism of circRNA in tumor cell resistance to radiotherapy, which may provide valuable clues for further study of circRNA.
ABSTRACT
Objective: To study the role of pancreatic cancer stem cells in radiotherapy resistance of pancreatic cancer. Methods: CD133+ pancreatic cancer stem cells were obtained by using magnetic cell sorting. MTT and flow cytometry were used to observe the proliferation activity and apoptosis of different cell subsets of pancreatic cancer after radiation treatment. Then flow cytometry, Western blot and qRT-PCR were used to observe the expression changes of CD133 in pancreatic cancer cells after radiation treatment. Finally, the cell cycle distribution of different subgroup cells was observed by flow cytometry. Results: Compared with unselected cells and CD133- cells, CD133+ stem cells had the highest survival rate and the lowest apoptosis rate after radiation treatment. The proportion of CD133+ stem cells increased and the expressions of CD133 protein and RNA increased in pancreatic cancer cells. CD133+ stem cells had the highest ratio of G0/G1 phase compared with unsorted cells and CD133- cells, and the difference was statistically significant. Conclusion: CD133+ pancreatic cancer stem cells are one of the important causes of radiotherapy resistance in pancreatic cancer cells, and the increased proportion of G0/G1 phase may be one of the mechanisms.
ABSTRACT
Distant metastasis is one of the main obstacles to cancer treatment.Overexpression of S1PR1 in malignant tumors enhances cell invasion and migration activity,mediates EMT and induces lymphangiogenesis and angiogenesis via activation of its downstream signaling pathways,eventually results in the occurrence of tumor metastasis.S1PR1 is also closely related to generation of acquired radiotherapy resistance.This article discusses the roles of S1PR1 in tumor metastasis and radiotherapy resistance.
ABSTRACT
@#Objective: To investigate the mechanism of miR-31-5p/tension protein 1 gene (TNS1) axis modulating radiotherapy resistance in breast cancer. Methods: The breast cancer tissues and corresponding para-cancerous tissues of 21 patients with breast cancer, who underwent surgical resection at Department of Cancer Radiotherapy of Nanyang Central Hospital from July 2017 to December 2017, were collected for this study; breast cancer cell lines (MCF-7，MDA-MB-23 and SKBR-3) were also collected; qPCR was applied to detect the expression level of miR-31-5p in breast cancer tissues and cell lines. The radiation resistant cell line MCF-7R was constructed by using 6 MV-X ray radiotherapy treatment. Subsequently, the influence of over-expression/kockdown of miR-31-5p on radiation sensitivity of MCF-7 and MCF-7R cells were detected by colony formation assay, Transwell assay and Annexin V-FITC/PI double staining flow cytometry assay, respectively. Moreover, luciferase reporter assay was used to verify whether TNS1 was a target gene of miR-31-5p. Results: Compared with para-cancerous tissues, normal mammary epithelial MCF-10A cells and MCF-7 cells, miR-31-5p was low-expressed in breast cancer, cell lines and MCF-7R (all P<0.01). Over-expression of miR-31-5p resulted in inhibited invasion and promoted apoptosis of MCF-7R cells (P<0.01), whereas miR-31-5p knockdown got opposite results in MCF-7 cells. Moreover, luciferase reporter assay confirmed that TNS1 was a target gene of miR-31-5p. Over-expression of miR-31-5p inhibited invasion and increased radio-sensitivity, apoptosis of MCF-7R cell via targeting TNS1 (P<0.01), whereas knockdown of miR-31-5p significantly promoted the invasion but reduced apoptosis of MCF-7R cells (all P<0.01), and further up-regulated the radio-sensitivity of MCF-7R cells. Conclusion: miR-31-5p/TNS1 axis regulates the radiotherapy resistance of breast cancer, and over-expression of miR-31-5p may reverse the resistance of MCF-7R to radiotherapy.