The survival rate of cancer patients was improved due to the development of cancer treatment techniques, and thus the fertility protection for young female cancer patients has attracted increasing attention. Radiotherapy, as one of the comprehensive cancer treatment, could cause ovarian damage in adolescent and child-bearing women, which leads to fertility decline and a series of side effects. Radiation can cause ovarian damage not only by acting on biological macromolecules directly, but also by increasing oxidative stress between oocytes and ovarian granulosa cells indirectly. At present, the fertility preservation of female cancer patients undergoing radiotherapy mainly includes physical protection, drug protection and biological protection. Recently, the development of new technologies for the preservation of fertility in female cancer patients has also brought new hope, including factors such as protective effects, patient age, and the selection of specific cancer treatment measures, which are the main considerations in the selection process of fertility preservation measures. This article reviews the research progress on radiation-induced ovarian damage, with a focus on the introduction of the fertility preservation measures and new technologies for young female tumor patients receiving radiotherapy.

Objective:To screen the key miRNA downstream of TLR2 and explore the function of the miR-21.Methods:Wild type (WT) and TLR2 KO mice were irradiated with 60Co γ-ray to compare their survivals. The downstream miRNAs of TLR2 signaling pathway were screened by RNA sequence in BMCs, and their expressions were verified by QT-PCR. Cell lines with overexpression or knockdown of a miRNA were established to evaluate the function of miRNA. Results:The radiosensitivity of TLR2 KO mice was higher than that of TLR2 WT mice( χ2=4.490, 13.100, 7.928, P<0.05). The bone marrow transplantation experiment proved that the increased radiosensitivity of TLR2 KO mice was related to BMCs ( χ2=4.291, P<0.05). A total of 55 differentially expressed genes were screened by RNA sequence ([log2 Fold Change]>0.95, Q<0.05), of which 28 were up-regulated and 27 were down-regulated. QT-PCR assay determined that miR-21 was down-regulated in BMCs of TLR2 KO ( t=9.420, P<0.01) and MyD88 KO ( t=10.700, P<0.01) mice. It was proved by QT-PCR that the expressions of IL-6 ( t=13.790, P<0.05) and TNF-α ( t=14.280, P<0.05) were increased in a TLR2 dependent manner after PAM3CSK4 stimulation. Overexpression of miR-21 promoted viability of EL4 cells ( t=5.951, P<0.05) and NIH/3T3 cells ( t=4.786, P<0.05) and reduced BMCs apoptosis in WT ( t=4.842, P<0.05) and TLR2 KO ( t=10.520, P<0.05) mice after radiation. Inhibition of miR-21 decreased the viability of EL4 cells ( t=4.815, P<0.05) and NIH/3T3 cells ( t=4.042, P<0.05). Conclusions:miR-21 plays a key regulatory role in the process of TLR2 radioprotection, which may be related to the up-regulation of IL-6 and TNF-α.