scholarly journals CircRNA circ-ATAD1 suppresses the maturation of miR-168 to participate in colorectal cancer

2021 ◽  
Author(s):  
Li Cao ◽  
Peng Chen ◽  
Shang Zhao ◽  
Guanglong Dong
Keyword(s):  
Colorectal Cancer ◽  
Gastric Cancer ◽  
Cell Proliferation ◽  
Expression Vector ◽  
Tumor Tissue ◽  
Inhibitory Effects ◽  
Poor Survival ◽  
Tissue Samples

Abstract Background: CircRNA circ-ATAD1 has been characterized as an oncogenic circRNA in gastric cancer, while its role in colorectal cancer is This study was carried out to explore the role of circ-ATAD1 in colorectal cancer (CRC).Methods: Paired CRC and adjacent non-tumor tissue samples collected from 64 CRC patients were subjected to RNA extractions and RT-qPCRs to analyze the expression of circ-ATAD1, premature miR-168 and mature miR-168 in The effects of circ-ATAD1 overexpression on the maturation of miR-168 was analyzed by transfecting circ-ATAD1 expression vector into CRC cells, followed by determining the expression of premature miR-168 and mature miR-168 through RT-qPCR. The role of circ-ATAD1, premature miR-168 and mature miR-168 in regulating the proliferation of CRC cells was explored by CCK-8Results: In this study we found that circ-ATAD1 was upregulated in CRC and predicted poor survival. In addition, circ-ATAD1 was inversely correlated with mature miR-168, but not premature miR-168. In CRC cells, circ-ATAD1 overexpression decreased the expression of mature miR-168, but not premature miR-168. Moreover, circ-ATAD1 overexpression reduced the inhibitory effects of miR-168 overexpression on cell proliferation.Conclusions: Therefore, circ-ATAD1 is overexpressed in CRC and it may suppress the maturation of miR-168 to participate in CRC.

scholarly journals LncRNA SLC7A11-AS1 is Upregulated in Colorectal Cancer and Promotes the Proliferation of Cancer Cells by Suppressing the Maturation of miR-34a

2021 ◽  
Author(s):  
Peijiang Chang ◽  
Maosheng Wang
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cancer Biology ◽  
Prognostic Value ◽  
Inhibitory Effects ◽  
Poor Survival ◽  
Tumor Tissues ◽  
Tcga Dataset

Abstract Background: LncRNA SLC7A11-AS1 is recently characterized critical player in cancer biology. We analyzed TCGA dataset and observed the upregulation of SLC7A11-AS1 in colorectal cancer (CRC). We therefore analyzed the role of SLC7A11-AS1 in CRC. Methods: Paired CRC and non-tumor tissues were collected from 60 CRC patients and expression of SLC7A11-AS1 in tissues was determined by RT-qPCR. The 60 CRC patients were followed up for 5 years to analyze the prognostic value of SLC7A11-AS1 for CRC. Correlations were analyzed by linear regression. The effects of SLC7A11-AS1 overexpression on the expression of miR-34a precursor and mature miR-34a were analyzed by RT-qPCR. Cell proliferation was analyzed by CCK-8 assay.Result: SLC7A11-AS1 was upregulated in CRC and predicted poor survival. SLC7A11-AS1 and mature miR-34a were inversely correlated, while SLC7A11-AS1 was not significantly correlated with the precursor of miR-34a. In CRC cells, SLC7A11-AS1 overexpression resulted in the reduced level of mature miR-34a, but not miR-34a precursor. Moreover, SLC7A11-AS1 overexpression reduced the inhibitory effects of miR-34a overexpression on cell proliferation. Conclusion: SLC7A11-AS1 may promote the proliferation of cancer cells in CRC by suppressing the maturation of miR-34a.

scholarly journals Taraxasterol acetate targets RNF31 to inhibit RNF31/p53 axis-driven cell proliferation in colorectal cancer

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Chao-Tao Tang ◽  
Jing Yang ◽  
Zi-De Liu ◽  
Youxiang Chen ◽  
Chunyan Zeng
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Cell Growth ◽  
Cell Model ◽  
Tissue Samples ◽  
The Third ◽  
Common Cancer ◽  
A Cell ◽  
Growth Of Tumor

AbstractColorectal cancer (CRC) is the third most common cancer worldwide. Several studies have suggested that taraxasterol acetate (TA) can inhibit the growth of tumor cells. However, to date, it remains unclear how TA inhibits cell growth and how RNF31 functions as an oncogene. We examined the expression of RNF31 in CRC tissue samples via immunohistochemistry and elucidated the function of RNF31 in CRC cells by constructing a cell model with RNF31 depletion. A cycloheximide (CHX)-chase analysis and immunofluorescence assays were conducted to demonstrate that TA can promote RNF31 degradation by activating autophagy. We used the PharmMapper website to predict targets of TA and identified RNF31. CHX-chase experiments showed that TA could facilitate RNF31 degradation, which was inhibited by the administration of chloroquine. Immunofluorescence assays showed that RNF31 protein was colocalized with LC3I/II and p62, suggesting that TA promoted RNF31 degradation by activating autophagy. We also found that CRC patients with RNF31 overexpression had poorer survival than those with low RNF31 expression. The results of the CHX-chase experiment showed that depletion of RNF31 alleviated p53 degradation, which was inhibited by MG132. A series of co-immunoprecipitation (Co-IP) assays revealed that RNF31 interacts with p53 and promotes p53 ubiquitination and degradation. A Co-IP assay performed with a truncated RNF31 plasmid showed that the PUB domain interacts with p53. Moreover, the PUB domain is the key structure in the induction of p53 ubiquitination. Our findings reveal a key role of RNF31 in CRC cell growth and indicate a mechanism through which TA inhibits cell growth.

scholarly journals LINC 01436 is Overexpressed in Colorectal Cancer and Promotes Cancer Cell Proliferation by Suppressing the Maturation of Tumor Suppressive miR-466

2021 ◽  
Author(s):  
Hong Li ◽  
Wei Dong ◽  
Jie Hou ◽  
De He
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Precursor Cell ◽  
Cancer Cell Proliferation ◽  
Poor Survival ◽  
Follow Up Study ◽  
Prognostic Analysis

Abstract LINC 01436 (lncRNA) promotes lung and gastric two types of cancers. However, it is unclear that whether this lncRNA also participate in colorectal cancer (CRC). This study was therefore carried out to analyze the role of LINC 01436 in CRC. Expression of LINC 01436 in CRC patient tissues was analyzed by RT-qPCR and follow-up study was performed for prognostic analysis. Correlation between LINC 01436 and mature miR-466 or miR-466 precursor was analyzed by linear regression. Mature miR-466 and miR-466 precursor expression in CRC cells with the overexpression of LINC 01436 was studied by performing RT-qPCR. The proliferation of CRC cells was subjected to CCK-8 assay analysis. LINC 01436 was upregulated in CRC and predicted poor survival. LINC 01436 and mature miR-466 were inversely correlated, but LINC 01436 and miR-466 precursor were not correlated. In CRC cells, LINC 01436 mediated the downregulation of mature miR-466, but not miR-466 precursor. Cell proliferation analysis showed that LINC 01436 overexpression rescued cell proliferation reduced by miR-466. LINC 01436 is overexpressed in CRC and it may promote cancer cell proliferation by suppressing the maturation of miR-466.

CircRNA CircRIMS is Overexpressed in Esophageal Squamous Cell Carcinoma and Downregulate miR-613 through Methylation to Increase Cell Proliferation

2020 ◽  
Author(s):  
Haijun Wan ◽  
Bosi Yuan ◽  
Kang Jiang ◽  
Juan Wei ◽  
Xiaoyue Feng ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Prognostic Value ◽  
Proliferation Assay ◽  
Inhibitory Effects ◽  
Poor Survival ◽  
Brdu Assay

Abstract BackgroundEsophageal squamous cell carcinoma (ESCC) as the most common subtype of esophageal cancer accounts for about 95% of all cases. CircRNA CircRIMS has been characterized as an oncogenic circRNA in gastric cancer, while its role in other cancers is unknown. This study aimed to explore the role of CircRIMS in esophageal squamous cell carcinoma (ESCC). MethodsTissues collected from 60 ESCC patients were used in this study. The expression of CircRIMS and miR-613 were detected by RT-qPCRs. The 60 ESCC patients were followed up for 5 years to evaluate the prognostic value of CircRIMS for ESCC. The role of CircRIMS in regulating the expression of miR-613 and methylation was assess by overexpression experiments and RT-qPCRs. The role of CircRIMS and miR-613 in regulating cell proliferation was analyzed by BrdU assay. ResultsWe found that CircRIMS was overexpressed in ESCC and predicted poor survival. In addition, miR-613 was downregulated in ESCC and inversely correlated with CircRIMS. In ESCC cells, overexpression of CircRIMS decreased the expression levels of miR-613 and increased the methylation of miR-613 gene. Cell proliferation assay showed that overexpression of CircRIMS reduced the inhibitory effects of overexpression of miR-613 on cell proliferation. ConclusionsCircRIMS may downregulate miR-613 through methylation to increase cell proliferation in ESCC.

scholarly journals LncRNA DCST1-AS1 downregulates miR-29b through methylation in glioblastoma (GBM) to promote cancer cell proliferation

2020 ◽  
Author(s):  
Sheng Hu ◽  
Yiqun Yao ◽  
Xiao Hu ◽  
Yongjian Zhu
Keyword(s):  
Cell Proliferation ◽  
Mortality Rate ◽  
Cancer Cell ◽  
Reverse Transcription ◽  
Brain Cancer ◽  
Methylation Level ◽  
Cancer Cell Proliferation ◽  
Inhibitory Effects ◽  
Poor Survival

Abstract Background: Glioblastoma (GBM) is the most malignant form of brain cancer, owing to the high mortality rate. We in this study analyzed the role of DCST1-AS1 in glioblastoma (GBM).Methods: QuantiTect Reverse Transcription Kit (QIAGEN) was used, with RNA samples as template to synthesize cDNA. Results: It is observed that upregulation of DCST1-AS1 in GBM predicted poor survival. MiR-29b was downregulated in GBM and inversely correlated with the expression of DCST1-AS1. In GBM cells, DCST1-AS1 overexpression led to the downregulation of miR-29b and the increased methylation level of miR-29b gene. Cell proliferation analysis showed that DCST1-AS1 overexpression led to increased cell proliferation rate. Moreover, DCST1-AS1 overexpression significantly reversed the inhibitory effects of miR-29b on cancer cell proliferation. Conclusions: DCST1-AS1 may downregulate miR-29b through methylation in GBM to promote cancer cell proliferation.

scholarly journals Expression of miR-1290 and Its Target Genes THBS1 and DKK3 in Colorectal Cancer Patients

2021 ◽  
Author(s):  
Sima Nobari ◽  
Mohammad Hasan Soheilifar ◽  
Hoda Keshmiri Neghab ◽  
Farid Azizi Jalilian ◽  
Fatemeh Bahreini ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Target Genes ◽  
Tumor Tissue ◽  
Expression Level ◽  
Tissue Samples ◽  
Small Noncoding Rnas ◽  
Colorectal Cancer Patients ◽  
And Control ◽  
Control Study

Background: MicroRNAs (miRNAs) are small noncoding RNAs (containing approximately 22 nucleotides), which modulate and control the expression of target genes by binding them. MiRNAs play a crucial role in tumorigenesis. Thus, alterations in the expression level of miRNAs play a key role in the pathobiology of numerous cancers. In this research, the expression level of MicroRNA-1290 (miR1290) and its target genes THBS1 and DKK3 were evaluated in colorectal cancer (CRC) patients. Methods: This case-control study was carried out on 144 paraffin-embedded tissue samples of CRC and adjacent tissues from patients who referred to Imam Khomeini Hospital, Tehran, Iran. Total RNA was isolated from the tissue using Trizol reagent following the manufacturer’s instructions and then reverse transcribed to cDNA. The expression of miR-1290 and its target genes was measured by quantitative Real-Time PCR (qRT-PCR). Statistical analyses were performed using SPSS V.20 statistical software. Results: We present evidence that the miR-1290 expression in CRC tissues was significantly higher than in the normal margin, and its targets were downregulated in tumor tissue compared to the adjacent tissue. Conclusion: This study supports the essential role of miR-1290 and its contribution to CRC invasion and metastasis through targeting THBS1 and DKK3, as biomarkers for CRC diagnosis.

scholarly journals Diverse Expression of IL-32 in Diffuse and Intestinal Types of Gastric Cancer

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Mladen Pavlovic ◽  
Nevena Gajovic ◽  
Milena Jurisevic ◽  
Slobodanka Mitrovic ◽  
Gordana Radosavljevic ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Tumor Tissue ◽  
Prognostic Markers ◽  
Diffuse Type ◽  
Histological Differentiation ◽  
Tissue Samples ◽  
Advanced Stages ◽  
The Relationship ◽  
Grade Iii

Introduction. Gastric cancer (GC) represents one of the most common cancers worldwide, frequently diagnosed at advanced stages with poor prognosis, indicating on need for new diagnostic and prognostic markers. The aim of the study was to determine the expression of IL-32, proinflammatory and angiogenic mediators, in patients with diffuse and intestinal gastric cancer and the relationship with clinicopathological aspects. Material and Methods. The tissue samples of diffuse and intestinal types of tumor of 70 patients with gastric cancer were analyzed. Expression of IL-32, VEGF, IL-17, and CD31 was measured by immunohistochemistry. Results. IL-32 expression was significantly lower in tissue samples from patients with diffuse type of gastric cancer that is also a severe and more progressive form (TNM stages III and IV, poor histological differentiation, and higher nuclear grade III). Expression of IL-17 was also decreased in patients with diffuse type of gastric cancer. Microvascular density was diminished in diffuse type of gastric cancer. Conclusions. Downregulated expression of IL-32 in tumor tissue of patients with diffuse type of gastric cancer may implicate on its role in limiting ongoing proinflammatory and proangiogenic processes. This emphasizes on unrecognized role of IL-32 in biology of diffuse type of gastric cancer.

scholarly journals Atypical role of sprouty in p21 dependent inhibition of cell proliferation in colorectal cancer

2015 ◽  
Vol 55 (9) ◽  
pp. 1355-1368 ◽  
Author(s):  
Qiong Zhang ◽  
Katherine Shim ◽  
Kevin Wright ◽  
Alexander Jurkevich ◽  
Sharad Khare
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Dependent Inhibition

Knockdown of PGM1 Synergistically Enhances Anticancer Effects of Orlistat in Gastric Cancer Under Glucose Deprivation

2021 ◽  
Author(s):  
Bo Cao ◽  
Huan Deng ◽  
Hao Cui ◽  
Ruiyang Zhao ◽  
Hanghang Li ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Lipid Metabolism ◽  
Fatty Acid Synthase ◽  
Enrichment Analysis ◽  
Glucose Deprivation ◽  
Metabolic Reprogramming ◽  
The Cancer Genome Atlas

Abstract Background Phosphoglucomutase 1 (PGM1) acts as an important regulator in glucose metabolism. However, the role of PGM1 in gastric cancer (GC) remains unclear. This study aims to investigate the role of PGM1 and develop novel regimens based on metabolic reprogramming in GC. MethodsCorrelation and enrichment analysis of PGM1 was conducted based on The Cancer Genome Atlas database. Data derived from the Kaplan-Meier Plotter database were analyzed for correlations between PGM1 expression and survival time of GC patients. CCK-8, EdU, flow cytometry assays, generation of subcutaneous tumor and lung metastasis mouse models were used to determine growth and metastasis in vitro and in vivo. Cell glycolysis was detected by a battery of glycolytic indicators, including lactate, pyruvic acid, ATP production and glucose uptake. Fatty Acid Synthase (FASN) activity and detection of lipid regulators levels by western blot were used to reflect on the cell lipid metabolism. ResultsCorrelation and enrichment analysis suggested that PGM1 was closely associated with cell proliferation and metabolism. PGM1 was overexpressed in GC tissues and cell lines. High PGM1 expression served as an indicator of shorter survival for specific subpopulation of GC patients, which was also correlated with some clinicopathological features, including T stage and TNM stage. Under low glucose conditions, knockdown of PGM1 significantly suppressed cell proliferation and glycolysis levels, whereas lipid metabolism was enhanced. Orlistat, as a drug that was designed to inhibit FASN activity for obesity treatment, effectively induced apoptosis, suppressed FASN activity. However, orlistat conversely increased glycolytic levels in GC cells. Orlistat exhibited more significant inhibitive effects on GC progression after knockdown of PGM1 under glucose deprivation due to combination of glycolysis and lipid metabolism. ConclusionsDownregulation of PGM1 expression under glucose deprivation synergistically enhanced anti-cancer effects of orlistat. This combination application may serve as a novel strategy for GC treatment.

High Expression of sLex Associated with Poor Survival in Argentinian Colorectal Cancer Patients

2014 ◽  
Vol 29 (1) ◽  
pp. e30-e39 ◽  
Author(s):  
Ariel Zwenger ◽  
Martin Rabassa ◽  
Sandra Demichelis ◽  
Gabriel Grossman ◽  
Amada Segal-Eiras ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Lymph Nodes ◽  
Cancer Patients ◽  
Normal Mucosa ◽  
Poor Survival ◽  
Primary Tumors ◽  
Metastatic Lymph Nodes ◽  
Metastatic Lymph ◽  
Colorectal Cancer Patients

Aim Colorectal cancer (CRC) is one of the most prevalent malignancies in Argentina with 11,043 new cases and 6,596 deaths estimated to have occurred in 2008. The present study was developed to clarify the differential expression of MUC1, MUC2, sLex, and sLea in colorectal cancer patients and their relationship with survival and clinical and histological features. Methods Ninety primary tumor samples and 43 metastatic lymph nodes from CRC patients were studied; follow-up was documented. Twenty-six adenoma and 68 histological normal mucosa specimens were analyzed. An immunohistochemical approach was applied and statistical analysis was performed. Results In tumor samples, MUC1, sLea, and sLex were highly expressed (94%, 67%, and 91%, respectively); also, we found a significantly increased expression of the 3 antigens in primary tumors and metastatic lymph nodes compared with normal mucosa and adenomas. MUC2 was expressed in 52% of both normal mucosa and CRC samples; this reactivity significantly decreased in metastatic lymph nodes (p<0.05). A multiple comparison analysis showed that MUC1 and sLex discriminated among 3 groups: normal, adenoma, and CRC tissues. The increase of sLex expression showed an association with recurrence, and survival analysis showed that a high sLex staining was significantly associated with a poor survival. By multivariate analysis MUC1 inmunoreactivity correlated positively and significantly with tumor size, while MUC2 expression showed the opposite correlation. Conclusions The correlation of sLex overexpression in primary tumors and metastatic lymph nodes, the discrimination among the normal, adenoma, and CRC groups based on sLex expression, as well as its association with recurrence and survival, all suggest a prognostic role of sLex in Argentinian CRC patients.

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