RESUMEN
@# T-Vec（talimogene laherparepvec）是由Ⅰ型单纯疱疹病毒（HSV-1）改造而来的一种溶瘤病毒，能够选择性地在恶性肿 瘤细胞中复制而不伤及其他正常细胞。T-Vec在治疗晚期黑色素瘤患者的Ⅲ期临床试验中显示出良好的安全性和肿瘤治疗效 果，已于2015年经美国FDA批准用于治疗晚期黑色素瘤。为了提高T-Vec的疗效，扩大其应用范围，T-Vec联合其他抗肿瘤疗法 以及应用于其他肿瘤的临床试验仍在陆续开展。近期，T-Vec联合免疫检查点抑制剂在治疗晚期黑色素瘤的临床试验中取得新 进展，临床数据显示T-Vec联合疗法具有更强的抗肿瘤活性。此外，T-Vec在治疗头颈癌、胰腺癌、肝癌等肿瘤的临床研究中也取 得了一定进展。本文对近年来T-Vec治疗肿瘤的临床试验的相关研究进展做一综述。
RESUMEN
Several microRNAs (miRNAs) have been reported as oncogenes or tumor suppressors in many cancers, including gastric cancer (GC). However, the role and molecular mechanism of miR-3129 in GC is largely unknown. We aimed to explore the function and the underlying molecular mechanism of miR-3129 in GC. Cancer tissues and corresponding adjacent tissues were collected from 50 patients with GC, and the expression of miR-3129 was detected by RT-qPCR. The expression of miR-3129 and pRb in human GC cell line SCG7091 was altered by transient transfection. Thereafter, MTT and flow cytometry assays were used to analyze cell viability and cell cycle. The expression of cyclin E, CDK2, CDK2 inhibitors (p16 and 21), and pRb were detected by RT-qPCR and western blot. A significant up-regulation of miR-3129 was observed in GC tissues compared to adjacent tissues. Overexpression of miR-3129 significantly improved cell viability after 4 days of post-transfection. Flow cytometry assay results showed that the miR-3129 overexpression arrested more SGC7901 cells at S phase. Moreover, overexpression of miR-3129 down-regulated the expression of CDK2 inhibitors while it up-regulated the expression levels of cyclin E, CDK2, and pRb. Interestingly, we found that pRb inhibition reversed the effect of miR-3129 inhibitor on cell proliferation in SGC7901 cells, increased cell viability, reduced cells at G0/1 phase, and modulated the expression of proliferation-related factors. Our results revealed that miR-3129 functioned as an oncogene through positive regulation of pRb and may prove to be a promising option for molecular therapy of GC.