miR‐377‐5p inhibits lung cancer cell proliferation, invasion, and cell cycle progression by targeting AKT1 signaling

2018 ◽  
Vol 120 (5) ◽  
pp. 8120-8128 ◽  
Author(s):  
Han Wu ◽  
Hai Yan Liu ◽  
Wen Jie Liu ◽  
Yong Li Shi ◽  
Dawei Bao
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Cell Cycle Progression ◽  
Cancer Cell Proliferation ◽  
Lung Cancer Cell ◽  
Cycle Progression

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

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.

scholarly journals The LncRNA EPEL Promotes Lung Cancer Cell Proliferation Through E2F Target Activation

2018 ◽  
Vol 45 (3) ◽  
pp. 1270-1283 ◽  
Author(s):  
Seong-Min Park ◽  
Eun-Young Choi ◽  
Dong-Hyuck Bae ◽  
Hyun Ahm Sohn ◽  
Seon-Young Kim ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Cancer Patients ◽  
Cancer Cell ◽  
Target Genes ◽  
Cyclin B1 ◽  
Cancer Cell Proliferation ◽  
Lung Cancer Cell ◽  
Lung Cancer Patients

Background/Aims: Recent studies have revealed that many long non-coding RNAs (lncRNAs) play oncogenic or tumor-suppressive roles in various cancers. Lung cancer is the leading cause of cancer-related death worldwide, and many lung cancer patients frequently relapse after surgery, even those in the early stages. However, the oncogenic or tumor-suppressive roles and clinical implications of lncRNAs in lung cancer have not been fully elucidated. Methods: The association between an E2F-mediated cell proliferation enhancing lncRNA (EPEL) expression and lung cancer patient survival was accessed using public microarray data with clinical information. Cancer-related phenotypes were analyzed by the siRNA knockdown of EPEL in two lung cancer cell lines. Gene set analysis of gene expression data were performed to identify pathways regulated by EPEL. RNA immunoprecipitation, RT-qPCR, and ChIP assays were performed to explore the functions of selected target genes regulated by EPEL. Results: EPEL, known as LOC90768 and MGC45800, was associated with the relapse and survival of lung cancer patients and promoted lung cancer cell proliferation through the activation of E2F target genes. EPEL knockdown specifically down-regulated the expression of cell cycle-related E2F target genes, including Cyclin B1 (CCNB1), in lung cancer cells but not that of apoptosis- or metabolism-related E2F target genes. EPEL interacted with E2F1 and regulated the expression of the E2F target genes by changing the binding efficiency of E2F1 to the E2F target promoters. Moreover, the expression levels of EPEL and CCNB1 both alone and in combination were robust prognostic markers for lung cancer. Conclusions: Considering its specific effects on cell cycle-related E2F target genes and its significant association with the prognosis of lung cancer patients, we suggest that the transcriptional regulation of EPEL through E2F target genes is potentially a target for the development of novel therapeutic strategies for lung cancer patients.

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