Abstract
BackgroundGastric cancer is a highly aggressive malignant tumor with heterogeneity and is still a global health problem. The present study aimed to investigate the role of Cyclin I-like (CCNI2) in the regulation of phenotype and tumorigenesis, as well as its underlying mechanisms.MethodThe expression profile of CCNI2 in gastric cancer was determined based on The Cancer Genome Atlas (TCGA) database and immunohistochemical staining. The effects of altered CCNI2 expression on the biological phenotypes such as proliferation, clone formation, apoptosis and migration of gastric cancer cell lines BGC-823 and SGC-7901 were investigated. Mice xenograft models were established to reveal the role of CCNI2 knockdown on tumorigenesis. The potential mechanism of CCNI2 regulating gastric cancer was preliminarily determined by RNA sequencing.ResultCCNI2 was abundantly expressed in gastric cancer and was positively correlated with pathological stage. Knockdown of CCNI2 slowed down the malignant progression of gastric cancer by inhibiting tumor cell proliferation, increasing the susceptibility to apoptosis and suppressing migration. Moreover, downregulation of CCNI2 attenuated the ability of gastric cancer cells to form tumors in mice. Additionally, there was an interaction between CCNI2 and transcription factor hepatoma-derived growth factor (HDGF) in SGC-7901 cells. Knockdown of CCNI2 alleviated the promoting effects of HDGF overexpression in gastric cancer cells.ConclusionsCCNI2 promoted the progression of human gastric cancer through HDGF, which drew further interest regarding its clinical application as a potential therapeutic target.
Highlights
Gastric cancer is a highly aggressive malignant tumor with heterogeneity and is still a global health problem
CCNI2 promoted the progression of human gastric cancer through hepatoma-derived growth factor (HDGF), which drew further interest regarding its clinical application as a potential therapeutic target
CCNI2 is abundantly expressed in gastric cancer Based on The Cancer Genome Atlas (TCGA) database of 407 gastric cancer samples for expression profile analysis, we found that the expression level of CCNI2 in tumors was significantly higher than that of normal samples (Fig. 1A)
Summary
Gastric cancer is a highly aggressive malignant tumor with heterogeneity and is still a global health problem. The present study aimed to investigate the role of Cyclin I-like (CCNI2) in the regulation of phenotype and tumorigenesis, as well as its underlying mechanisms. Cyclin I-like (CCNI2), a homologue of CCNI, is a novel CDK5 activator. It reported that cell cycle progression and proliferation were inhibited after knockdown of CCNI2 [16]. Lai et al, demonstrated that CCNI2 played a promoting role in the progression of colorectal cancer [17]. These studies point towards a potential promoting effect of CCNI2 on cancers that warrants further investigations
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