scholarly journals Increased expression of lncRNA FTH1P3 predicts a poor prognosis and promotes aggressive phenotypes of laryngeal squamous cell carcinoma

2019 ◽  
Vol 39 (6) ◽  
Author(s):  
Haozhan Yuan ◽  
Hong Jiang ◽  
Yanting Wang ◽  
Yameng Dong
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell ◽  
Cell Apoptosis ◽  
Poor Prognosis ◽  
Clinical Stage ◽  
Cell Cancer ◽  
Positive Lymph Node ◽  
Migration And Invasion ◽  
Advanced Clinical Stage ◽  
In Cells

AbstractLaryngeal squamous cell cancer (LSCC) is a highly aggressive malignancy in the head and neck region. Recent studies have shown that long noncoding RNAs (lncRNAs) are novel transcripts that play an important role in the progression of LSCC. However, the overall pathophysiological regulation of lncRNAs to LSCC is largely unknown. The present study aimed to determine the clinical significances of lncRNA ferritin heavy chain 1 pseudogene 3 (FTH1P3) and to identify its potential roles in LSCC. Quantitative real-time PCR (qRT-PCR) showed that FTH1P3 expression was significantly up-regulated in LSCC tissues than that in non-neoplastic tissues. High FTH1P3 expression was positively correlated with the poor differentiation, high T classification, positive lymph node metastasis, and advanced clinical stage. Overall survival analysis showed that high levels of FTH1P3 predicted a poor prognosis in LSCC patients. Moreover, elevated expression of FTH1P3 was found to increase LSCC cell proliferation, migration and invasion, and to inhibit cell apoptosis, Conversely, knockdown of FTH1P3 suppressed LSCC cell proliferation, migration and invasion, and induced cell apoptosis. In addition, overexpression of FTH1P3 resulted in an increase in cells in S phase and a decrease in cells in G0/G1 phase, whereas inhibition of FTH1P3 did the opposite effects. Taken together, these results suggested that increased expression of FTH1P3 predicts a poor prognosis and promotes aggressive phenotypes of LSCC by regulating cell proliferation, migration, invasion, apoptosis, and cell cycle, indicating FTH1P3 may serve as a promising therapeutic biomarker for the treatment of LSCC.

scholarly journals Circ_0072088 Promotes Proliferation, Migration, and Invasion of Esophageal Squamous Cell Cancer by Absorbing miR-377

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Na Fang ◽  
Yijun Shi ◽  
Yu Fan ◽  
Tao Long ◽  
Yongqian Shu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell ◽  
Noncoding Rna ◽  
Clinical Stage ◽  
Cell Cancer ◽  
Circular Rna ◽  
Vital Role ◽  
Migration And Invasion

Circular RNA (circRNA) is an endogenous noncoding RNA. Accumulative investigations have confirmed that circRNAs play a vital role in carcinogenesis and tumor progression. Herein, we examined the expression and mechanism of circ_0072088 in esophageal squamous cell carcinoma (ESCC). As a result, circ_0072088 was significantly overexpressed in ESCC tissues and cells, which was closely associated with tumor size, invasion depth, clinical stage, and lymph node metastasis of esophageal cancer. Nuclear and cytoplasmic separation as well as FISH assays showed that circ_0072088 was mainly localized in the cytoplasm of ESCC cells. RNase R treatment assay revealed that circ_0072088 was steadier than linear ZFR mRNA. circ_0072088 promoted ESCC cell proliferation, migration and invasion in vitro, and cell proliferation in vivo. Mechanistically, circ_0072088 upregulated VEGF gene expression by acting as the sponge of miRNA-377. In conclusion, circ_0072088 might be used as a diagnostic biomarker and therapeutic target for ESCC.

scholarly journals MiR-362-3p functions as a tumor suppressor through targeting MCM5 in cervical adenocarcinoma

2018 ◽  
Vol 38 (3) ◽  
Author(s):  
Dan Wang ◽  
Hongyan Wang ◽  
Yichun Li ◽  
Qian Li
Keyword(s):  
Cell Proliferation ◽  
Poor Prognosis ◽  
Histological Grade ◽  
Clinical Stage ◽  
Cervical Adenocarcinoma ◽  
Luciferase Reporter ◽  
Inverse Association ◽  
Advanced Clinical Stage ◽  
Adenocarcinoma Cell ◽  
Function Study

Our previous study suggested that minichromosome maintenance protein 5 (MCM5) overexpression was observed in cervical adenocarcinoma and closely associated with advanced clinical stage, more metastatic lymph nodes, present distant metastasis, low histological grade, and poor prognosis. Down-regulation of MCM5 inhibited cervical adenocarcinoma cell proliferation. The purpose of the present study is to search and confirm valuable microRNAs (miRNAs), which target MCM5 to modulate cervical adenocarcinoma cell proliferation. In our results, we found that levels of miR-362-3p expression were reduced in cervical adenocarcinoma tissues and cell lines. Moreover, 3′-UTR of MCM5 had binding site of miR-362-3p through analyzing Targetscan database and miRanda database, and there were an inverse association between miR-362-3p and MCM5 in cervical adenocarcinoma tissues. Furthermore, we verified miR-362-3p directly targeted to 3′-UTR of DCLK1 by luciferase reporter assay, and negatively regulated mRNA and protein expressions of MCM5 by qPCR and Western blot. Then, we conducted gain-of-function study and rescued-function study, and found that miR-362-3p served as a tumor suppressive miRNA to modulate cervical adenocarcinoma cell proliferation through regulating the functional target MCM5. Finally, we analyzed correlations between miR-362-3p expression and clinicopathological characteristics and observed that miR-362-3p low expression was associated with advanced clinical stage and poor prognosis. In conclusion, miR-362-3p is a tumor suppressive miRNA in cervical adenocarcinoma.

scholarly journals Downregulation of miR-1826 Indicates a Poor Prognosis for Osteosarcoma Patients and Regulates Tumor Cell Proliferation, Migration, and Invasion

2020 ◽  
Vol 2020 ◽  
pp. 1-6
Author(s):  
Peng Li ◽  
Lei Wei ◽  
Wenshuai Zhu
Keyword(s):  
Cell Proliferation ◽  
Cell Lines ◽  
Poor Prognosis ◽  
Cox Regression ◽  
Clinical Stage ◽  
Prognostic Significance ◽  
Prognostic Indicator ◽  
Migration And Invasion ◽  
Kaplan Meier ◽  
Low Levels

Background. Osteosarcoma (OS) is the most frequent bone tumor with high metastasis. This study is aimed at assessing the expression and prognostic significance of microRNA-1826 (miR-1826) in OS patients, as well as its biological function in tumor progression. Methods. Quantitative Real-Time PCR was employed to measure the expression of miR-1826 in OS tissues and cell lines. Kaplan-Meier survival analysis and Cox regression model were used to evaluate the prognostic value of miR-1826. CCK-8 and Transwell assay were conducted to investigate the effect of miR-1826 on OS cell proliferation, migration, and invasion. Results. miR-1826 expression was downregulated in OS tissues and cell lines and associated with OS patients’ clinical stage and distant metastasis. Low levels of miR-1826 were related with shorter survival time and determined as an independent prognostic indicator for the overall survival of OS patients. The overexpression of miR-1826 in OS cells led to inhibited cell proliferation, migration, and invasion. Conclusion. The decreased expression of miR-1826 predicts a poor prognosis in OS patients, and its overexpression inhibits OS cell proliferation, migration, and invasion. This newly identified miR-1826 provides a novel sight into the pathogenesis of OS and offers a candidate prognostic biomarker and therapeutic target for OS treatment.

Elevated O-GlcNAcylation Promotes Malignant Phenotypes of Hypopharyngeal Squamous Cell Carcinoma by Stabilizing Nrf2 through Regulation of the PI3K/Akt Pathway

2020 ◽  
Vol 20 (16) ◽  
pp. 1933-1942
Author(s):  
Wencheng Dai ◽  
Xiaoxia Jin ◽  
Bin Jiang ◽  
Weixian Chen ◽  
Zhenhua Ji ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Cell Migration ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Cell Apoptosis ◽  
Intracellular Signaling ◽  
Migration And Invasion ◽  
Related Factor ◽  
Hypopharyngeal Squamous Cell Carcinoma

Background and Purpose: O-GlcNAcylation is a significant protein posttranslational modification with O-linked β-N-acetylglucosamine (GlcNAc) for intracellular signaling. Elevated O-GlcNAcylation contributes to cell proliferation, cell migration, cell apoptosis and signal transduction in various cancers. However, the expression level and functional role of O-GlcNAcylation in Hypopharyngeal Squamous Cell Carcinoma (HSCC) is not clearly elucidated. Nuclear factor erythroid-2-related factor 2 (Nrf2) is a master transcriptional factor that has been found to be aberrantly activated in HSCC. Here, we provide a molecular rationale between O-GlcNAcylation and Nrf2 in HSCC patients. Methods:: The protein levels of O-GlcNAcylation and Nrf2 in HSCC tissues were detected by immunohistochemistry technique and western blot analysis. Then, O‐GlcNAcylation knockdown HSCC cells were applied in this study. Cell proliferation was detected by CCK8, colony-forming analysis, and cell cycle assays. Cell migration and invasion ability was evaluated by transwell assays. Cell apoptosis was measured by TUNEL analysis. Results: O-GlcNAcylation was obviously up-regulated in HSCC tissues, which correlated with tumor size and lymph node metastasis. In addition, the protein level of Nrf2 was found to positively correlate with the expression of O‐GlcNAcylation both in vivo and in vitro. Knockdown of O-GlcNAcylation significantly inhibited HSCC cell growth, suppressed cell migration, and promoted cell apoptosis, whereas overexpression of Nrf2 reversed these phenotypes. Mechanismly, the upregulation of O-GlcNAcylation promoted the phosphorylation of Akt, leading to the stabilization of Nrf2; this could be attenuated by inhibition of the PI3K/Akt signaling pathway. Conclusion: Here, we provide a molecular association between O-GlcNAcylation and Nrf2 in HSCC patients, thus providing valuable therapeutic targets for the disease.

scholarly journals LncRNA LINC00152 promotes laryngeal cancer progression by sponging miR-613

Open Medicine ◽  
2020 ◽  
Vol 15 (1) ◽  
pp. 240-248 ◽  
Author(s):  
Xuesong Zheng ◽  
Su Dong ◽  
Lele Sun ◽  
Jialu Xu ◽  
Jia Liu ◽  
...  
Keyword(s):  
Cancer Progression ◽  
Noncoding Rna ◽  
Molecular Mechanisms ◽  
Clinical Stage ◽  
Cell Cancer ◽  
Inhibitory Effect ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Advanced Clinical Stage ◽  
Normal Tissues

AbstractBackgroundLong noncoding RNA (lncRNA) LINC00152 (CYTOR) has been reported to be upregulated and to serve as a diagnostic biomarker in multiple types of cancers, including laryngeal squamous cell cancer (LSCC). However, the functional role and molecular mechanisms of LINC00152 in LSCC progression need to be further investigated.MethodsLINC00152 levels in LSCC and adjacent normal tissues were measured by quantitative real-time polymerase chain reaction (qRT-PCR). Gene knockdown of LINC00152 was achieved in LSCC cells by use of small interfering RNA (siRNA). Cell proliferation, apoptosis, migration and invasion were examined by a series of methods. The micoRNA (miRNA) interaction with LINC00152 was screened by starBase v2.0 and confirmed by luciferase reporter activity.ResultsLINC00152 levels in LSCC tissues were significantly higher than those in adjacent normal tissue, and patients with lymph node metastasis or an advanced clinical stage displayed higher LINC00152 expression. Moreover, siRNA-mediated LINC00152 knockdown significantly inhibited the proliferation, migration and invasion of LSCC cells and induced apoptosis in those cells. Mechanistically, LINC00152 functioned as a competing endogenous RNA (ceRNA) sponging miR-613. The inhibitory effect of LINC00152 knockdown on malignant behavior was abrogated by inhibiting miR-613.ConclusionLINC00152 exerts an oncogenic effect on the tumorigenesis of LSCC by sponging miR-613 and may serve as a potential target for treating LSCC.

scholarly journals Upregulation of miR-1269 Contributes to the Progression of Esophageal Squamous Cell Cancer Cells and Is Associated With Poor Prognosis

2021 ◽  
Vol 20 ◽  
pp. 153303382098585
Author(s):  
Xiuhui Bai ◽  
Qiang Wang ◽  
Xueqi Rui ◽  
Xiaohua Li ◽  
Xianming Wang
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell ◽  
Cox Regression ◽  
Cell Cancer ◽  
Prognostic Significance ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Control Group ◽  
Epithelial Cell Line ◽  
Cox Regression Analysis

Background: MicroRNA-1269 (miR-1269) has been identified upregulated in several cancers, as well as in esophageal cancer. In the present study, we investigated the clinical prognostic significance and potential functional role of miR-1269 in esophageal squamous cell carcinoma (ESCC). Methods: A total of 107 ESCC patients who underwent surgical resection were enrolled in this study. miR-1269 expression was measured using quantitative real-time PCR (qRT-PCR). Kaplan-Meier method and multivariate Cox regression analysis were used to explore the prognostic significance of miR-1269. CCK-8 assays and Transwell assays were used to investigate the effects of miR-1269 on cell proliferation, migration, and invasion. The direct association between miR-1269 and SOX6 was evaluated using a dual-luciferase reporter assay. Results: The expression of miR-1269 was significantly upregulated in ESCC tissues and cell lines compared with adjacent normal tissues and esophageal epithelial cell line, respectively. What’s more, the upregulation of miR-1269 was associated with positive lymph node metastasis and advanced TNM stage. ESCC patients with high miR-1269 expression had shorter overall survival than those with low miR-1269 expression levels. Compared with the control group, overexpression of miR-1269 promoted cell proliferation, migration, and invasion, while knockdown of miR-1269 inhibited cell proliferation, migration, and invasion. SOX6 was a direct target of miR-1269. Conclusion: These results suggest that miR-1269 plays an important role in the progression of ESCC by targeting SOX6 and may be a potential prognostic biomarker and the miR-1269/SOX6 axis may be a therapeutic target for the patient with ESCC.

Corilagin Inhibits Esophageal Squamous Cell Carcinoma by Inducing DNA Damage and Down-Regulation of RNF8

2019 ◽  
Vol 19 (8) ◽  
pp. 1021-1028 ◽  
Author(s):  
Fanghua Qiu ◽  
Lifang Liu ◽  
Yu Lin ◽  
Zetian Yang ◽  
Feng Qiu
Keyword(s):  
Cell Proliferation ◽  
Dna Damage ◽  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Cell Apoptosis ◽  
Cell Counting ◽  
Antitumor Effects

Background:Esophageal squamous cell carcinoma (ESCC), the most prevalent histologic subtype of esophageal cancer, is an aggressive malignancy with poor prognosis and a high incidence in the East. Corilagin, an active component present in Phyllanthus niruri L., has been shown to suppress tumor growth in various cancers. However, the effects of corilagin on ESCC and the mechanisms for its tumor suppressive function remain unknown.Methods:Cell proliferation was measured by Cell Counting Kit-8 assay and colony formation assays. Annexin V/PI double-staining was performed to assess cell apoptosis. Immunofluorescence staining and western blotting were used to evaluate the protein expression. A xenograft mice model was used to assess the in vivo antitumor effects of corilagin alone or in combination with cisplatin.Results:We for the first time showed that corilagin was effectively able to inhibit ESCC cell proliferation and induce cell apoptosis. Additionally, our results validated its antitumor effects in vivo using a xenograft mouse model. Mechanistically, we found that corilagin caused significant DNA damage in ESCC cells. We found that corilagin could significantly attenuate the expression of the E3 ubiquitin ligase RING finger protein 8 (RNF8) through ubiquitin-proteasome pathway, leading to the inability of DNA damage repair response and eventually causing cell apoptosis. Furthermore, we also showed that corilagin substantially enhanced the antitumor effects of chemotherapy drug cisplatin both in vitro and in vivo.Conclusion:Our results not only provided novel and previously unrecognized evidences for corilagin-induced tumor suppression through inducing DNA damage and targeting RNF8 in ESCC, but also highlighted that corilagin might serve as an adjunctive treatment to conventional chemotherapeutic drugs in ESCC patients.

scholarly journals Sevoflurane inhibits malignant progression of colorectal cancer via hsa_circ_0000231-mediated miR-622

2021 ◽  
Vol 28 (1) ◽  
Author(s):  
Jingpeng Wang ◽  
Shuyuan Li ◽  
Gaofeng Zhang ◽  
Huihua Han
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Volatile Anesthetic ◽  
Tumor Formation ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Circular Rnas

Abstract Background Sevoflurane (Sev), a commonly used volatile anesthetic, has been reported to inhibit the process of colorectal cancer (CRC). Circular RNAs (circRNAs) are revealed to participate in the pathogenesis of CRC. This study aims to reveal the mechanism of hsa_circ_0000231 in Sev-mediated CRC progression. Methods The expression of hsa_circ_0000231 and microRNA-622 (miR-622) was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Protein level was determined by western blot analysis. Cell proliferation was investigated by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), cell colony formation and DNA content quantitation assays. Cell apoptosis was detected by Annexin V-fluorescein isothiocyanate and propidium iodide double staining and caspase 3 activity assays. Cell migration and invasion were investigated by wound-healing and transwell invasion assays, respectively. The putative relationship between hsa_circ_0000231 and miR-622 was predicted by circular RNA Interactome online database, and identified by dual-luciferase reporter and RNA immunoprecipitation assays. The impacts of hsa_circ_0000231 on Sev-mediated tumor formation in vivo were presented by in vivo assay. Results Hsa_circ_0000231 expression was upregulated, while miR-622 was downregulated in CRC tissues and cells compared with control groups. Sev treatment decreased hsa_circ_0000231 expression, but increased miR-622 expression in CRC cells. Sev treatment suppressed cell proliferation, migration and invasion, and induced cell apoptosis. Hsa_circ_0000231 overexpression restored Sev-mediated CRC progression in vitro. Additionally, hsa_circ_0000231 acted as a sponge of miR-622, and miR-622 inhibitors reversed the impacts of hsa_circ_0000231 silencing on CRC process. Furthermore, Sev treatment inhibited tumor growth by regulating hsa_circ_0000231 in vivo. Conclusion Hsa_circ_0000231 attenuated Sev-aroused repression impacts on CRC development by sponging miR-622. This findings may provide an appropriate anesthetic protocol for CRC sufferers undergoing surgery.

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