Department of Gastrointestinal Surgery, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China (mainland).
Department of Cardiovascular Surgery II, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China (mainland).
Med Sci Monit. 2021 May 29;27:e928375. doi: 10.12659/MSM.928375.
BACKGROUND The aim of this study was to investigate the effect of ribosomal protein L22 (RPL22) on gastric cancer (GC) cell proliferation, migration, and apoptosis, and its correlation with the murine double minute 2-protein 53 (MDM2-p53) signaling pathway. MATERIAL AND METHODS The RPL22 expression in GC tissues and cells was detected by quantitative reverse transcription-polymerase chain reaction and western blotting. RPL22 was overexpressed in the MKN-45 cells by the transfection of a vector, pcDNA3.1 (pcDNA)-RPL22, whereas it was silenced in the MGC-803 cells by the transfection of short interfering (si) RNA (si-RPL22). Flow cytometric analysis, cell viability assays, wound healing assays, and transwell assays were utilized to explore the influences of RPL22 on the apoptosis, proliferation, migration, and invasion. Nutlin-3 (an MDM2-p53 inhibitor) was used to inhibit MDM2-p53 signaling. RESULTS The RPL22 expression was downregulated in GC tissues and cells. It was significantly lower in the advanced GC tissues than in the early GC tissues, and was significantly lower in the lymphatic metastatic tissues than in the non-lymphatic metastatic tissues. The transfection of si-RPL22 accelerated the ability of GC cells to proliferate and metastasize, whereas apoptosis was dampened. The transfection of pcDNA-RPL22 exerted the opposite effect on the GC cells; MDM2 expression was upregulated in RPL22-silenced GC cells, while the expression of p53 was downregulated. In vitro, treatment with nutlin-3 reversed the promoting effects of si-RPL22 on GC progression. CONCLUSIONS In vitro, the silencing of RPL22 aggravates GC by regulating the MDM2-p53 signaling pathway.
本研究旨在探讨核糖体蛋白 L22（RPL22）对胃癌（GC）细胞增殖、迁移和凋亡的影响，及其与鼠双微体 2 蛋白 53（MDM2-p53）信号通路的相关性。
通过定量逆转录聚合酶链反应和 Western blot 检测 GC 组织和细胞中的 RPL22 表达。通过转染载体 pcDNA3.1（pcDNA）-RPL22 过表达 MKN-45 细胞中的 RPL22，通过转染小干扰（si）RNA（si-RPL22）沉默 MGC-803 细胞中的 RPL22。通过流式细胞术分析、细胞活力测定、划痕愈合试验和 Transwell 试验探讨 RPL22 对细胞凋亡、增殖、迁移和侵袭的影响。使用 Nutlin-3（MDM2-p53 抑制剂）抑制 MDM2-p53 信号通路。
RPL22 在 GC 组织和细胞中表达下调。晚期 GC 组织中 RPL22 的表达明显低于早期 GC 组织，淋巴转移组织中 RPL22 的表达明显低于非淋巴转移组织。转染 si-RPL22 加速了 GC 细胞的增殖和转移能力，而凋亡受到抑制。转染 pcDNA-RPL22 对 GC 细胞产生相反的影响；沉默 RPL22 的 GC 细胞中 MDM2 表达上调，而 p53 表达下调。体外，Nutlin-3 处理逆转了 si-RPL22 对 GC 进展的促进作用。
体外，沉默 RPL22 通过调节 MDM2-p53 信号通路加重 GC。
