Li Fang, Tan Bibo, Chen Zihao, Zhao Qun, Li Shi, Ding Pingan, Liu Chang, Wang Xiaoxiao, Li Xiaoya, Li Yong
Department of Pathology, The Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
The Third Department of Surgery, The Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
J Gastrointest Oncol. 2022 Dec;13(6):2809-2822. doi: 10.21037/jgo-22-1069.
Gastric cancer (GC) is a globally prevalent gastrointestinal tumor. Long non-coding RNAs (lncRNAs) are a new type of transcript which has become a hotspot of current research; however, the function of most lncRNAs in the advancement of GC is still not clear. The focus of this research was to elucidate the role and expression of lncRNA CNALPTC1 in GC.
In GC cells and tissues, the detection of CNALPTC1 expression was carried out using quantitative real-time polymerase chain reaction (qRT-PCR), and the link between its expression and clinicopathological features was investigated. The impacts of inhibition and upregulation of CNALPTC1 on the physiological behavior of GC cells were observed. Furthermore, through bioinformatics analysis and prediction of microRNA (miRNA) targeted to CNALPTC1 and target genes interacting with miRNA, the effects on invasion, proliferation, and migration of GC cells were investigated.
The elevated expression level of CNALPTC1 was observed in GC tissues and cell lines. The analysis indicated that gene silencing of CNALPTC1 resulted in inhibition, whereas upregulation of CNALPTC1 resulted in the promotion of invasion, proliferation, and migration of GC cells, respectively. In addition, we observed that CNALPTC1 functions as a molecular sponge for miR-6788-5p, and the level of expression of CNALPTC1 exhibited a negative correlation with miR-6788-5p. Moreover, it was revealed that the miR-6788-5p's direct target was PAK1, which could reverse the inhibitory function of miR-6788-5p.
Our research revealed that the CNALPTC1 promotes GC development by negatively regulating the miR-6788-5p/PAK1 pathway. GC therapy may be improved by conducting targeted studies of the CNALPTC1/miR-6788-5p/PAK1 axis.
胃癌（GC）是一种全球流行的胃肠道肿瘤。长链非编码RNA（lncRNAs）是一种新型转录本，已成为当前研究的热点；然而，大多数lncRNAs在胃癌进展中的功能仍不清楚。本研究的重点是阐明lncRNA CNALPTC1在胃癌中的作用和表达。
在胃癌细胞和组织中，采用定量实时聚合酶链反应（qRT-PCR）检测CNALPTC1的表达，并研究其表达与临床病理特征之间的联系。观察CNALPTC1抑制和上调对胃癌细胞生理行为的影响。此外，通过生物信息学分析和预测靶向CNALPTC1的微小RNA（miRNA）以及与miRNA相互作用的靶基因，研究其对胃癌细胞侵袭、增殖和迁移的影响。
在胃癌组织和细胞系中观察到CNALPTC1表达水平升高。分析表明，CNALPTC1基因沉默导致抑制，而CNALPTC1上调分别导致胃癌细胞侵袭、增殖和迁移的促进。此外，我们观察到CNALPTC1作为miR-6788-5p的分子海绵发挥作用，并且CNALPTC1的表达水平与miR-6788-5p呈负相关。此外，还发现miR-6788-5p的直接靶标是PAK1，其可以逆转miR-6788-5p的抑制功能。
我们的研究表明，CNALPTC1通过负调控miR-6788-5p/PAK1途径促进胃癌发展。通过对CNALPTC1/miR-6788-5p/PAK1轴进行靶向研究，可能会改善胃癌治疗。
