Gastroenterology Department, The 3(rd) Affiliated Hospital of Chengdu Medical College, Pidu District People's Hospital, Chengdu, China.
Gastroenterology Department, The 3(rd) Affiliated Hospital of Chengdu Medical College, Pidu District People's Hospital, Chengdu, China.
Tissue Cell. 2021 Dec;73:101644. doi: 10.1016/j.tice.2021.101644. Epub 2021 Sep 21.
Long non-coding RNA (lncRNA) LINC00467 plays a proto-oncogenic role in non-small cell lung cancer. However, its effect and modulatory mechanism in gastric cancer (GC) are unknown. Thereby, we elucidated the mechanism of LINC00467 in GC. LINC00467 level in GC tissues was assessed by bioinformatic analysis, and clinicopathological parameters from GC patients were collected. The levels of LINC00467, integrin subunit beta 3 (ITGB3), proliferating cell nuclear antigen (PCNA), cleaved caspase-3 and cleaved poly (ADP-ribose) polymerase 1 (PARP1) in tissue samples or treated GC cells were assessed by quantitative real-time polymerase chain reaction (qRT-PCR), fluorescence in situ hybridization (FISH), or Western blot. The viability, proliferation and apoptosis of GC cells were detected by methyl thiazolyl tetrazolium assay, colony formation assay, and flow cytometry. Levels of LINC00467 and ITGB3 were up-regulated in GC, and highly expressed LINC00467 was positively associated with tumor size, differentiation, N stage, and T stage in GC patients. LINC00467 was enriched in cytoplasm of GC cells, and overexpressed LINC00467 promoted the viability and proliferation as well as levels of ITGB3 and PCNA, while suppressing the apoptosis and levels of cleaved caspase-3 and cleaved PARP1 in GC cells. Besides, the effects of shLINC00467 on inhibiting cell viability, proliferation of GC cells and PCNA level and promoting apoptosis as well as levels of cleaved caspase-3 and cleaved PARP1 were all partially reversed by overexpressed ITGB3. Overexpressed LINC00467 enhanced the viability and proliferation but inhibited apoptosis of GC cells via increasing ITGB3 level.
长链非编码 RNA（lncRNA）LINC00467 在非小细胞肺癌中发挥原癌基因的作用。然而，其在胃癌（GC）中的作用和调节机制尚不清楚。因此，我们阐明了 LINC00467 在 GC 中的作用机制。通过生物信息学分析评估 GC 组织中 LINC00467 的水平，并收集 GC 患者的临床病理参数。通过定量实时聚合酶链反应（qRT-PCR）、荧光原位杂交（FISH）或 Western blot 评估组织样本或经处理的 GC 细胞中 LINC00467、整合素亚基β 3（ITGB3）、增殖细胞核抗原（PCNA）、裂解的半胱天冬酶-3 和裂解的多聚（ADP-核糖）聚合酶 1（PARP1）的水平。通过噻唑蓝比色法、集落形成实验和流式细胞术检测 GC 细胞的活力、增殖和凋亡。LINC00467 和 ITGB3 在 GC 中上调，高表达的 LINC00467 与 GC 患者的肿瘤大小、分化、N 期和 T 期呈正相关。LINC00467 富含于 GC 细胞的细胞质中，过表达 LINC00467 可促进 GC 细胞的活力和增殖以及 ITGB3 和 PCNA 的水平，同时抑制 GC 细胞的凋亡和 cleaved caspase-3 和 cleaved PARP1 的水平。此外，shLINC00467 对抑制 GC 细胞活力、增殖和 PCNA 水平以及促进凋亡和 cleaved caspase-3 和 cleaved PARP1 水平的作用均可部分被过表达的 ITGB3 逆转。过表达的 LINC00467 通过增加 ITGB3 水平增强 GC 细胞的活力和增殖，同时抑制凋亡。
