The inhibitory effects and mechanisms of rhamnogalacturonan I pectin from potato on HT-29 colon cancer cell proliferation and cell cycle progression

Background Aberrant proliferation of retinal pigment epithelial (RPE) cells under pathologic condition results in the occurrence of proliferative vitreoretinopathy (PVR). Icariin (ICA)-a flavonol glucoside-has been shown to inhibit proliferation of many cell types, but the effect on RPE cells is unknown. This study aimed to clarify the inhibitory effects of ICA on RPE cells against platelet-derived growth factor (PDGF)-BB-induced cell proliferation, and discuss the regulatory function of H19 in RPE cells. Methods MTS assay was conducted to determine the effects of ICA on cell proliferation. Flow cytometry analysis was performed to detect cell cycle progression. Quantitative real-time PCR and western blot assay were used to measure the expression patterns of genes in RPE cells. Results ICA significantly suppressed PDGF-BB-stimulated RPE cell proliferation in a concentration-dependent manner. Moreover, since administration of ICA induced cell cycle G0/G1 phase arrest, the anti-proliferative activity of ICA may be due to G0/G1 phase arrest in RPE cells. At molecular levels, cell cycle regulators cyclin D1, CDK4, CDK6, p21 and p53 were modulated in response to treatment with ICA. Most importantly, H19 was positively regulated by ICA and H19 depletion could reverse the inhibitory effects of ICA on cell cycle progression and proliferation in PDGF-BB-stimulated RPE cells. Further mechanical explorations showed that H19 knockdown resulted in alternative expressions levels of cyclin D1, CDK4, CDK6, p21 and p53 under ICA treatment. Conclusions Our findings revealed that ICA was an effective inhibitor of PDGF-BB-induced RPE cell proliferation through affecting the expression levels of cell cycle-associated factors, and highlighted the potential application of ICA in PVR therapy. H19 was described as a target regulatory gene of ICA whose disruption may contribute to excessive proliferation of RPE cells, suggesting that modulation of H19 expression may be a novel therapeutic approach to treat PVR.

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LncRNA EPIC1 Promotes Cancer Cell Proliferation and Inhibits Apoptosis in Gallbladder Cancer Interacting with lncRNA LET

10.21203/rs.3.rs-45031/v1 ◽

2020 ◽

Author(s):

Changbo Fu ◽

Lei Nie ◽

Tao Yin ◽

Xuan Xu ◽

weijun lu

Keyword(s):

Cell Cycle ◽

Cell Proliferation ◽

Gallbladder Cancer ◽

Cancer Cell ◽

Cell Cycle Progression ◽

Human Cancer ◽

Cancer Cell Proliferation ◽

Cycle Progression ◽

Tumor Tissues ◽

Proliferation And Apoptosis

Abstract Background: LncRNA EPIC1 is likely involved in human cancer by promoting cell cycle progression. Our study was carried out to investigate the involvement of EPIC1 in gallbladder cancer (GBC). Methods: Expression levels of EPIC1 in two types of tissues (GBC and paracancerous) and plasma were measured by performing qPCR. GBC-SD and SGC-996 cells were transfected with LET and EPIC1 expression vectors.Results: In the preset study we found that EPIC1 was upregulated in tumor tissues than in paracancerous tissues of GBC patients, and plasma levels of EPIC1 were significantly correlated with levels of EPIC1 in tumor tissues. LncRNA LET was downregulated in tumor tissues than in paracancerous tissues and was inversely correlated with EPIC1 in both tumor tissues and paracancerous tissues. Overexpression of EPIC1 led to downregulated LET, and LET overexpression also mediated the downregulation of EPIC1. EPIC1 led to accelerated GBC cell proliferation and inhibited apoptosis. Overexpression of LET played opposites roles. In addition, overexpression of LET also attenuated the effects of EPIC1 overexpression on cancer cell proliferation and apoptosis. Conclusion: Therefore, therefore, lncRNA EPIC1 may promote cancer cell proliferation and inhibit apoptosis in GBC by interacting with LET.

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