同期放化疗诱导的凋亡结直肠癌细胞通过外泌体lncRNA促进结直肠癌活细胞侵袭转移的实验研究

近年来，放化疗导致肿瘤细胞生物学行为变化的负面问题开始受到重视。我们的前期研究发现，同期放化疗可导致残余存活结直肠癌细胞侵袭转移能力增强，其机制尚不完全清楚。最近，其他学者的研究发现，凋亡细胞的外泌体也可影响存活肿瘤细胞的增殖和治疗敏感性。我们的预实验研究证实，放化疗诱导的凋亡肿瘤细胞也可通过外泌体lncRNA影响存活肿瘤细胞的侵袭转移特性。为进一步探索上述现象，本项目拟通过细胞实验、动物模型研究和临床肿瘤标本验证的方法，探讨同期放化疗诱导的凋亡结直肠癌细胞通过外泌体lncRNA途径影响存活癌细胞侵袭转移的关键分子机制，为阐明放化疗等常用肿瘤治疗方法在诱导肿瘤细胞凋亡的同时所引发的负面问题提供科学依据；同时，研究结果将为探索合理的干预措施调变放化疗后肿瘤细胞的生物学特性，以进一步减少放化疗后的结直肠癌转移和复发打下基础，具有潜在的临床应用价值。

The opposite effects of chemoradation have attracted more and more attention in recent years. The results of our previous studies showed that the residual colorectal cancer cells after chemoradiation had enhanced invasive and metastatic ability. But the detailed mechanisms were not well understood. Recently, it was reported that the apoptotic cancer cells can promote the growing and treatment resistance of living cells through exosomes. The results of our preliminary studies showed the similar phenomenon that chemoradiation-induced apoptotic colorectal cancer cells can enhance the invasion and migration of living colorectal cancer cells via exosomes. In this study, detailed mechanisms of this.phenomenon will be explored by cell experiments, animal models and clinical tumor samples. The results of this study will provide scientific proofs to elaborate the opposite effects of chemoradiation and set a foundation for reducing the metastasis and recurrences of colorectal cancer after chemoradiation by effective interventions.