miR-4319 Suppresses the Growth of Esophageal Squamous Cell Carcinoma Via Targeting NLRC5

2020 ◽  
Vol 13 (2) ◽  
pp. 144-149
Author(s):  
Xiao Hu ◽  
Min Wang ◽  
Lei Cao ◽  
Li Cong ◽  
Yujie Gao ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Squamous Cell Carcinoma ◽  
Cell Growth ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cancer Progression ◽  
Squamous Cell ◽  
Cell Cycle Progression ◽  
Luciferase Reporter ◽  
Cell Cycle Distribution

Background: The functions of microRNAs (miRNAs) in cancer progression have been recognized in recent years. However, the role of miR-4319 in esophageal squamous cell carcinoma (ESCC) remains unclear. Objective: We aimed to investigate the biological roles of miR-4319 in ESCC progression and the associated mechanisms. Methods: Real-time PCR was performed to examine the levels of miR-4319 in ESCC cell lines. The effects of miR-4319 and NOD-like receptor (NLR) family, caspase activation and recruitment domain (CARD) domain containing 5 (NLRC5) on cell proliferation and cell cycle progression were evaluated using MTT assay, colony formation and flow cytometry assays. Bioinformatics techniques and luciferase reporter assay were applied to validate NLRC5 as a miR-4319 target. Results: The miR-4319 expression was lower in ESCC cells than in the normal cell line. The expression of miR-4319 repressed cell growth and induced cell cycle arrest. NLRC5 was validated as a direct downstream target of miR-4319. Overexpression of NLRC5 potentiated the effects of miR-4319 on cell growth and cell cycle distribution. Conclusion: Our results demonstrated that miR-4319 might function as a tumor suppressor by targeting NLRC5 in ESCC.

scholarly journals MicroRNA-527 Induces Proliferation and Cell Cycle in Esophageal Squamous Cell Carcinoma Cells by Repressing PH Domain Leucine-Rich-Repeats Protein Phosphatase 2

Dose-Response ◽  
2020 ◽  
Vol 18 (2) ◽  
pp. 155932582092868 ◽  
Author(s):  
Qingjie Xian ◽  
Ronglei Zhao ◽  
Juanjuan Fu
Keyword(s):  
Cell Cycle ◽  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cancer Progression ◽  
Squamous Cell ◽  
Protein Phosphatase ◽  
Ph Domain ◽  
Gene Reporter Assay ◽  
Protein Phosphatase 2

Increasing evidence indicated that microRNAs served dominant roles in carcinogenesis and cancer progression by targeting potential downstream genes. In our study, we found that miR-527 was an upregulated expression in human esophageal squamous cell carcinoma (ESCC) cells and tissues. Furthermore, overexpression of miR-527 promoted cell proliferation and colony formation, enhanced anchorage-independent growth ability, and contributed to cell cycle. In addition, protein phosphatase 2 (PHLPP2) was identified as the direct downstream target gene of miR-527 and was confirmed by luciferase gene reporter assay. In summary, we concluded that miR-527 acted as an oncogenic microRNA in ESCC development by directly targeting PHLPP2 might be a novel therapeutic target for the treatment of ESCC.

scholarly journals Inhibited MicroRNA-301 Restrains Angiogenesis and Cell Growth in Esophageal Squamous Cell Carcinoma by Elevating PTEN

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Bin Wang ◽  
Peiyan Hua ◽  
Ruimin Wang ◽  
Jindong Li ◽  
Guangxin Zhang ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Growth ◽  
Esophageal Squamous Cell Carcinoma ◽  
Tumor Growth ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Cell Cycle Distribution ◽  
Pten Inhibition ◽  
The Impact

Abstract Objective Esophageal squamous cell carcinoma (ESCC) is featured by early metastasis and late diagnosis. MicroRNA-301 (miR-301) is known to participate in diverse cancers. Nevertheless, effects of miR-301 on ESCC remain unexplored. Thus, we aim to explore the role of miR-301 in ESCC progression. Methods Expression of miR-301 and phosphatase and tensin homologue (PTEN) in ESCC tissues and cell lines was assessed. Next, the screened cells were treated with altered miR-301 or PTEN oligonucleotide and plasmid, and then, the colony formation ability, cell viability, migration, invasion, cell cycle distribution and apoptosis of ESCC cells were assessed. Moreover, tumor growth and microvessel density (MVD) were also assessed, and the targeting relationship between miR-301 and PTEN was affirmed. Results MiR-301 was upregulated, and PTEN was downregulated in ESCC tissues and cells. KYSE30 cells and Eca109 cells were selected for functional assays. In KYSE30 cells, inhibited miR-301 or overexpressed PTEN suppressed cell malignant behaviors, and silenced PTEN eliminated the impact of miR-301 inhibition on ESCC progression. In Eca109 cells, miR-301 overexpression or PTEN inhibition promoted cell malignant behaviors, and PTEN overexpression reversed the effects of miR-301 elevation on ESCC progression. The in vivo assay revealed that miR-301 inhibition or PTEN overexpression repressed ESCC tumor growth and MVD, and miR-301 elevation or PTEN reduction had contrary effects. Moreover, PTEN was targeted by miR-301. Conclusion Taken together, results in our study revealed that miR-301 affected cell growth, metastasis and angiogenesis via regulating PTEN expression in ESCC.

Circ_DLG1 facilitates esophageal squamous cell carcinoma progression by mediating miR-338-3p/MAP3K9 axis via activating MAPK/ERK pathway

2020 ◽  
Author(s):  
Yixuan Yang ◽  
Bing Zhu ◽  
Zhaofeng Ning ◽  
Xiaodong Wang ◽  
Zhaoxia Li ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Mitogen Activated Protein Kinase ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Erk Pathway

Abstract Background: Esophageal squamous cell carcinoma (ESCC) is an aggressive malignancy with a high incidence and poor prognosis. The document of circular RNAs (circRNAs) is frequently associated with cancer development. This study intended to explore the functional mechanism of circ_DLG1 in ESCC.Methods: The expression of circ_DLG1, miR-338-3p and Mitogen-Activated Protein Kinase Kinase Kinase 9 (MAP3K9) was measured by quantitative real-time polymerase chain reaction (qRT-PCR). Cell cycle, proliferation, migration and invasion were performed for functional analysis using flow cytometry, 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) and transwell assay, respectively. The protein levels of MAP3K9, p38, phosphor p38 (p-p38), ERK1/2, phosphor ERK1/2 (p-ERK1/2) were detected by western blot. Bioinformatics tool for target prediction used the online tool starBase. Dual-luciferase reporter assay was performed to verify the target relationship. The animal experiments were performed to ascertain the role of circ_DLG1 in vivo.Results: The expression of circ_DLG1 was elevated in ESCC tissues, plasma and cells. Circ_DLG1 knockdown inhibited cell cycle, proliferation, migration and invasion. MAP3K9 was highly expressed in ESCC tissues and cells, and its overexpression rescued the effects of circ_DLG1 knockdown. MiR-338-3p was a link between circ_DLG1 and MAP3K9, and circ_DLG1 regulated the expression of MAP3K9 by targeting miR-338-3p. The MAPK/ERK pathway was involved in the circ_DLG1/miR-338-3p/MAP3K9 regulatory axis. Circ_DLG1 knockdown blocked the tumor growth in vivo by regulating miR-338-3p and MAP3K9.Conclusion: Circ_DLG1 contributed to the malignant progression of ESCC by mediating the miR-338-3p/MAP3K9 axis via activating the MAPK/ERK signaling pathway. This paper provided a novel action mode of circ_DLG1 in ESCC.

scholarly journals Circular RNA MYLK serves as an oncogene to promote cancer progression via microRNA-195/cyclin D1 axis in laryngeal squamous cell carcinoma

2019 ◽  
Vol 39 (9) ◽  
Author(s):  
Xiaohui Duan ◽  
Na Shen ◽  
Jie Chen ◽  
Jing Wang ◽  
Qinghua Zhu ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cyclin D1 ◽  
Cancer Progression ◽  
Squamous Cell ◽  
Cell Cycle Progression ◽  
Laryngeal Squamous Cell Carcinoma ◽  
Circular Rnas

Abstract Laryngeal squamous cell carcinoma (LSCC) is a common aggressive head and neck cancer. Circular RNAs (circRNAs) are implicated in numerous physiological and pathological processes, including tumorigenesis. The present study aimed to investigate the expression profile and biological role of circMYLK in LSCC. We found that circMYLK was highly expressed in LSCC tissues and cell lines. circMYLK overexpression promoted LSCC cell proliferation and G1/S cell cycle transition; whereas circMYLK knockdown had the contrary effects. Mechanistically, circMYLK can serve as a competing endogenous RNA for miR-195 to increase cyclin D1 expression in LSCC, and rescue experiments further showed that restoration of miR-195 could block the oncogenic role of circMYLK in LSCC. In conclusion, our findings indicate that the circMYLK/miR-195/cyclin D1 regulatory axis could affect the proliferation and cell cycle progression of LSCC cells, and may provide a novel therapeutic target for the treatment of LSCC.

scholarly journals miR-200b induces cell cycle arrest and represses cell growth in esophageal squamous cell carcinoma

2016 ◽  
Vol 37 (9) ◽  
pp. 858-869 ◽  
Author(s):  
Hai-Feng Zhang ◽  
Abdulraheem Alshareef ◽  
Chengsheng Wu ◽  
Ji-Wei Jiao ◽  
Poul H. Sorensen ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Squamous Cell Carcinoma ◽  
Cell Growth ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cell Cycle Arrest ◽  
Squamous Cell ◽  
Cycle Arrest

scholarly journals ZFPM2-AS1 facilitates cell growth in esophageal squamous cell carcinoma via up-regulating TRAF4

2020 ◽  
Vol 40 (4) ◽  
Author(s):  
Gaozhong Sun ◽  
Changhao Wu
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Growth ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Antisense Rna ◽  
Suppressive Effect ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Reporter Assays

Abstract Emerging evidence has confirmed that long noncoding RNAs (lncRNAs) are strongly involved in tumor initiation and development. LncRNA ZFPM2 antisense RNA 1 (ZFPM2-AS1) has been identified as a tumor facilitator in some cancers; nevertheless, its functional significance and regulatory mechanism remain greatly unclear in esophageal squamous cell carcinoma (ESCC). Here, we detected ZFPM2-AS1 expression in ESCC cell lines using qRT-PCR. ZFPM2-AS1 knockdown models were established for investigating the biological function of ZFPM2-AS1 in ESCC cells. The association between miR-3612 and ZFPM2-AS1 or TRAF4 was assessed by RNA pull-down and luciferase reporter assays. The present study indicated that ZFPM2-AS1 was significantly up-regulated in ESCC cells. Functional assays manifested that ZFPM2-AS1 knockdown restrained cell proliferation, migration and invasion, and facilitated cell apoptosis in ESCC. Mechanistically, ZFPM2-AS1 promoted ESCC cell growth and up-regulated TRAF4 to trigger NF-κB pathway by sequestering miR-3612. Besides, miR-3612 was confirmed to be a tumor inhibitor in ESCC. Through restoration experiments, we observed that TRAF4 overexpression could recover the suppressive effect of ZFPM2-AS1 on ESCC cell growth. Collectively, all the results suggested that ZFPM2-AS1 was an oncogene in ESCC cell growth by up-regulating TRAF4 and activating NF-κB pathway.

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