scholarly journals LncRNA H19 as a Competing Endogenous RNA to Regulate AQP Expression in the Intestinal Barrier of IBS-D Patients

2021 ◽  
Vol 11 ◽  
Author(s):  
Guanqun Chao ◽  
Zhaojun Wang ◽  
Yi Yang ◽  
Shuo Zhang
Keyword(s):  
Intestinal Barrier ◽  
Control Group ◽  
Vector Group ◽  
Empty Vector ◽  
Non Coding Rna ◽  
Irritable Bowel ◽  
Long Non Coding Rna ◽  
Empty Vector Group

ObjectiveThe study aimed to investigate the role of Long non-coding RNA (LncRNA) H19 in the pathogenesis of Diarrhea Irritable Bowel Syndrome (IBS-D), and further to the regulatory effect of LncRNA H19 on AQP1, 3 in the intestinal mucosa of IBS-D patients, so as to seek a new way to elucidate the mechanism of IBS in clinic.MethodsThe levels of LncRNA H19, AQP1, and AQP3 were detected in colonic tissues of IBS-D patients, compared with that in healthy controls. Through RNA gene interference and activation methods, small activating RNA (saRNA) and small interfering (siRNA) were transfered into Caco-2 cells in vitro experiment, and sub-group for two control group, siH19 empty vector group, siH19 interference group, overexpression H19 vector group, and overexpression H19 empty vector group. Quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR) and Western blot were applied to evaluate the expression levels of LncRNA H19 and the amount of AQP1 and AQP3 protein expression, respectively.ResultsCompared with healthy volunteers, the levels of LncRNA H19, AQP1, and AQP3 in the colonic mucosa of IBS-D patients were significantly decreased (P < 0.05). The results in vitro transfection experiment revealed that the level of LncRNA H19 in the siH19 interference group was significantly declined (P < 0.05), while there was a remarkable increase in the overexpression H19 vector group (P < 0.05), compared with the corresponding control groups. The expression of AQP1 and AQP3 in Caco-2 cells was of positive correlation with the level of LncRNA H19.ConclusionThat the down-regulation of LncRNA H19 resulted in the expression changes of AQP1 and AQP3 may play an important role in the occurrence and development of IBS-D.

Lentiviral-Mediated Beclin-1 Overexpression Inhibits Cell Proliferation and Induces Autophagy of Human Esophageal Carcinoma Eca109 Cell Xenograft in Nude Mice

2020 ◽  
Vol 15 (1) ◽  
pp. 70-77
Author(s):  
Junhe Zhang ◽  
Weihua Dong
Keyword(s):  
Growth Rate ◽  
Cell Proliferation ◽  
Esophageal Carcinoma ◽  
Nude Mice ◽  
Beclin 1 ◽  
Control Group ◽  
Vector Group ◽  
Empty Vector ◽  
Empty Vector Group

Background: Esophageal carcinoma is one of the common malignant tumors in digestive tract. BECLIN-1 is a key gene that regulates autophagy, and its abnormal expression may be related with many human tumors. However, the mechanism of BECLIN-1 in esophageal carcinoma remains unknown. Objective: In this study, we explored the effect of BECLIN-1 overexpression on tumor growth in mice with esophageal carcinoma and its mechanism. Methods: Recombined lentiviral vector containing BECLIN-1 was used to transfect human esophageal carcinoma Eca109 cells and establish stable cell line. qRT-PCR was used to detect BECLIN-1 mRNA level in the transfected Eca109 cells, CCK-8 assay was used to detect cell proliferation. Beclin-1, P62 and LC3-II protein expression levels in Eca109 cells were detected using Western blot analysis. Subcutaneous xenograft nude mice model of human esophageal carcinoma was established, and the tumor growths in Beclin-1 group, control group and empty vector group were monitored. Beclin-1 protein expression in vivo was detected by immunohistochemistry. Results: Beclin-1 mRNA and protein were overexpressed in Eca109 cells. Compared with empty vector group, the growth rate of cells transfected with BECLIN-1 decreased significantly. Compared with the control group and empty vector group, the expression level of P62 protein in beclin-1 group was significantly decreased, while the expression level of LC3-II protein was significantly increased. The tumor growth rate in nude mice of Beclin-1 group was significantly lower than that of the control group and empty vector group, and Beclin-1 protein was mainly expressed in Beclin-1 group in vivo. Conclusion: BECLIN-1 can induce autophagy in esophageal carcinoma Eca109 cells, and it can significantly inhibit the growth of esophageal carcinoma.

scholarly journals SP1 induced Long non-coding RNA AGAP2-AS1 promotes cholangiocarcinoma proliferation via silencing of CDKN1A 

2020 ◽  
Author(s):  
Hao Ji ◽  
Juan Wang ◽  
Binbin Lu ◽  
Juan Li ◽  
Jing Zhou ◽  
...  
Keyword(s):  
Alternative Splicing ◽  
Molecular Mechanism ◽  
Cell Lines ◽  
Mrna Degradation ◽  
Biological Role ◽  
Non Coding Rna ◽  
Long Non Coding Rna ◽  
Regulate Gene

Abstract Background: LncRNA can regulate gene at various levels such as apparent genetics, alternative splicing, and regulation of mRNA degradation. However, the molecular mechanism of LncRNA in cholangiocarcinoma is still unclear. This deserves further exploration. Methods:We investigated the expression of AGAP2-AS1 in 32 CCA tissues and two CCA cell lines. We found a LncRNA AGAP2-AS1 which induced by SP1 has not been reported in CCA, and Knockdown and overexpression were used to investigate the biological role of AGAP2-AS1 in vitro. CHIP and RIP were performed to verify the putative targets of AGAP2-AS1. Results:AGAP2-AS1 was significantly upregulated in CCA tumor tissues.SP1 induced AGAP2-AS1 plays an important role in tumorigenesis. AGAP2-AS1 knockdown significantly inhibited proliferation and caused apoptosis in CCA cells. In addition, we demonstrated that AGAP2-AS1 promotes the proliferation of CCA. Conclusions: We conclude that the long non-coding RNA AGAP2-AS1 plays a role in promoting the proliferation of cholangiocarcinoma.

scholarly journals LncRNA STXBP5-AS1 suppresses stem cell-like properties of pancreatic cancer by epigenetically inhibiting neighboring androglobin gene expression

2020 ◽  
Vol 12 (1) ◽  
Author(s):  
Shi Chen ◽  
Long Huang ◽  
Ge Li ◽  
Funan Qiu ◽  
Yaodong Wang ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Stem Cell ◽  
Annexin V ◽  
Non Coding Rna ◽  
Rna Immunoprecipitation ◽  
Sphere Formation ◽  
Long Non Coding Rna

Abstract Previous studies suggest the tumor suppressor role of long non-coding RNA (lncRNA) STXBP5-AS1 in cervical and gastric cancer, but its expression pattern and functional mechanism are still elusive in pancreatic cancer (PC). Relative expression of STXBP5-AS1 in PC both in vivo and in vitro was analyzed by real-time PCR. IC50 of Gemcitabine was determined by the MTT assay. Cell proliferation in response to drug treatment was investigated by colony formation assay. Cell apoptosis was measured by both caspase-3 activity and Annexin V/PI staining. Cell invasion capacity was scored by the transwell assay in vitro, and lung metastasis was examined with the tail vein injection assay. Cell stemness was determined in vitro by sphere formation and marker profiling, respectively, and in vivo by limited dilution of xenograft tumor incidence. Subcellular localization of STXBP5-AS1 was analyzed with fractionation PCR. Association between STXBP5-AS1 and EZH2 was investigated by RNA-immunoprecipitation. The binding of EZH2 on ADGB promoter was analyzed by chromatin immunoprecipitation. The methylation was quantified by bisulfite sequencing. We showed downregulation of STXBP5-AS1 in PC associated with poor prognosis. Ectopic STXBP5-AS1 inhibited chemoresistance and metastasis of PC cells. In addition, STXBP5-AS1 compromised stemness of PC cells. Mechanistically, STXBP5-AS1 potently recruited EZH2 and epigenetically regulated neighboring ADGB transcription, which predominantly mediated the inhibitory effects of STXBP5-AS1 on stem cell-like properties of PC cells. Our study highlights the importance of the STXBP5-EZH2-ADGB axis in chemoresistance and stem cell-like properties of PC.

scholarly journals Long Non-Coding RNA GAS5 and Intestinal MMP2 and MMP9 Expression: A Translational Study in Pediatric Patients with IBD

2019 ◽  
Vol 20 (21) ◽  
pp. 5280 ◽  
Author(s):  
Marianna Lucafò ◽  
Letizia Pugnetti ◽  
Matteo Bramuzzo ◽  
Debora Curci ◽  
Alessia Di Silvestre ◽  
...  
Keyword(s):  
Pediatric Patients ◽  
Tissue Injury ◽  
Taqman Assay ◽  
Translational Study ◽  
Non Coding Rna ◽  
New Information ◽  
Mmp9 Expression ◽  
Long Non Coding Rna

Background: The long non-coding RNA (lncRNA) growth arrest–specific transcript 5 (GAS5) seems to be involved in the regulation of mediators of tissue injury, in particular matrix metalloproteinases (MMPs), implicated in the pathogenesis of inflammatory bowel disease (IBD). We investigated the role of GAS5 in regulating MMP2 and MMP9 expression in pediatric patients with IBD and in vitro. Methods: In total, 25 IBD patients were enrolled: For each patient paired inflamed and non-inflamed biopsies were collected. RNA was extracted and GAS5, MMP2, and MMP9 were quantified by TaqMan assay. The expression of GAS5 and MMPs was also determined in the human monocytic THP1 cells differentiated into macrophages and stimulated with lipopolysaccharide (LPS). The function of GAS5 was assessed by overexpressing the lncRNA and evaluating the MMPs levels. Results: Real-time PCR results demonstrated a downregulation of GAS5 and an upregulation of both MMPs in inflamed tissues. In vitro data confirmed the trend observed in patients for the three genes: The stimulation with LPS promoted a downregulation of GAS5 while an increase of MMPs was observed. Overexpression experiments showed that higher levels of GAS5 lead to a decrease of both enzymes. Conclusion: These results provide new information about the role of GAS5 in IBD: The lncRNA could mediate tissue damage by modulating the expression of MMPs.

scholarly journals Sp1 Induced Long Non-coding Rna Agap2-as1 Promotes Cholangiocarcinoma Proliferation via Silencing of Cdkn1a

2020 ◽  
Author(s):  
Hao Ji ◽  
Juan Wang ◽  
Binbin Lu ◽  
Juan Li ◽  
Jing Zhou ◽  
...  
Keyword(s):  
Alternative Splicing ◽  
Molecular Mechanism ◽  
Cell Lines ◽  
Biological Role ◽  
Non Coding Rna ◽  
Long Non Coding Rna ◽  
Regulate Gene

Abstract Background: LncRNA can regulate gene at various levels such as apparent genetics, alternative splicing, and regulation of mRNA degradation.However, the molecular mechanism of LncRNA in cholangiocarcinoma is still unclear.This deserves further exploration.Methods: We investigated the expression of AGAP2-AS1 in 32 CCA tissues and two CCA cell lines. We found a LncRNA AGAP2-AS1 which induced by SP1 has not been reported in cholangiocarcinoma and studied itKnockdown and overexpression were used to investigate the biological role of AGAP2-AS1 in vitro. CHIP and RIP were performed to verify the putative targets of AGAP2-AS1.Results: AGAP2-AS1 was significantly upregulated in 32 CCA tumor tissues.SP1 induced AGAP2-AS1 plays an important role in tumorigenesis.AGAP2-AS1 knockdown significantly inhibited proliferation and caused apoptosis in CCA cells. In addition, we demonstrated that AGAP2-AS1 acts as an oncogene in CCA.Conclusions: We conclude that the long non-coding RNA AGAP2-AS1 plays a role in promoting the proliferation of cholangiocarcinoma.

Expression of long non-coding RNAs ROR and MALAT1 in uterine fibroids

2021 ◽  
Vol 20 (4) ◽  
pp. 17-21
Author(s):  
S.A. Levakov ◽  
◽  
G.Ya. Azadova ◽  
A.E. Mamedova ◽  
Kh.R. Movtaeva ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Uterine Fibroids ◽  
Reproductive Age ◽  
Expression Level ◽  
Control Group ◽  
Tissue Samples ◽  
Non Coding Rna ◽  
Non Coding Rnas ◽  
Long Non Coding Rna

Objective. To study the expression level of long non-coding RNAs ROR and MALAT1 in tissue samples of uterine fibroids. Patients and methods. Samples of myomatous nodes and tissues of normal myometrium in 28 women of reproductive age were examined. The analysis of the expression of long non-coding RNAs was carried out using a real-time reverse-transcription polymerase chain reaction (RT-PCR) with specific primers. Results. There was a significant decrease in the expression level of long non-coding RNA ROR and an increase in the MALAT1 expression in tissue samples of uterine fibroids relative to the control group. Conclusion. The results obtained demonstrate a possible role of long non-coding RNAs in the development of uterine fibroids and correlate with the data which we obtained for patients with endometriosis. Detecting the expression level of long non-coding RNAs can improve the existing methods for diagnosing this disease. However, further research is required to determine the clinical significance of MALAT1 and ROR, and the molecular mechanisms underlying the action of these RNAs in uterine fibroid cells. Key words: long non-coding RNAs, uterine fibroids, myomectomy, lncROR, MALAT1

scholarly journals A KRAS-responsive long non-coding RNA controls microRNA processing

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Lei Shi ◽  
Peter Magee ◽  
Matteo Fassan ◽  
Sudhakar Sahoo ◽  
Hui Sun Leong ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Progression ◽  
Lung Tumorigenesis ◽  
Downstream Signaling ◽  
Non Coding Rna ◽  
Microrna Processing ◽  
Long Non Coding Rna

AbstractWild-type KRAS (KRASWT) amplification has been shown to be a secondary means of KRAS activation in cancer and associated with poor survival. Nevertheless, the precise role of KRASWT overexpression in lung cancer progression is largely unexplored. Here, we identify and characterize a KRAS-responsive lncRNA, KIMAT1 (ENSG00000228709) and show that it correlates with KRAS levels both in cell lines and in lung cancer specimens. Mechanistically, KIMAT1 is a MYC target and drives lung tumorigenesis by promoting the processing of oncogenic microRNAs (miRNAs) through DHX9 and NPM1 stabilization while halting the biogenesis of miRNAs with tumor suppressor function via MYC-dependent silencing of p21, a component of the Microprocessor Complex. KIMAT1 knockdown suppresses not only KRAS expression but also KRAS downstream signaling, thereby arresting lung cancer growth in vitro and in vivo. Taken together, this study uncovers a role for KIMAT1 in maintaining a positive feedback loop that sustains KRAS signaling during lung cancer progression and provides a proof of principle that interfering with KIMAT1 could be a strategy to hamper KRAS-induced tumorigenesis.

scholarly journals Role of the long non‑coding RNA HOTAIR/miR‑126 axis in an in vitro psoriasis model

2021 ◽  
Vol 21 (5) ◽  
Author(s):  
Weifeng Zha ◽  
Bo Guo ◽  
Shuyue Chen ◽  
Junwei Lu ◽  
Yunyun Shan
Keyword(s):  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals A Concise Review on the Role of CircPVT1 in Tumorigenesis, Drug Sensitivity, and Cancer Prognosis

2021 ◽  
Vol 11 ◽  
Author(s):  
Soudeh Ghafouri-Fard ◽  
Tayyebeh Khoshbakht ◽  
Mohammad Taheri ◽  
Elena Jamali
Keyword(s):  
Circular Rna ◽  
Cancer Prognosis ◽  
Genomic Locus ◽  
Non Coding Rna ◽  
Clinical Investigations ◽  
Cancer Types ◽  
Long Non Coding Rna

CircPVT1 (hsa_circ_0001821) is a cancer-related circular RNA (circRNA) that originated from a genomic locus on chromosome 8q24. This locus has been previously found to encode the oncogenic long non-coding RNA PVT1. Expression of this circRNA has been found to be upregulated in diverse neoplastic conditions. CircPVT1 acts as a sponge for miR-125a, miR-125b, miR-124-3p, miR-30a-5p, miR-205-5p, miR‐423‐5p, miR‐526b, miR-137, miR-145-5p, miR-497, miR-30d/e, miR-455-5p, miR-29a-3p, miR-204-5p, miR-149, miR-106a-5p, miR-377, miR-3666, miR-203, and miR-199a-5p. Moreover, it can regulate the activities of PI3K/AKT, Wnt5a/Ror2, E2F2, and HIF-1α. Upregulation of circPVT1 has been correlated with decreased survival of patients with different cancer types. In the current review, we explain the oncogenic impact of circPVT1 in different tissues based on evidence from in vitro, in vivo, and clinical investigations.

scholarly journals Long non-coding RNA PSMA3-AS1 enhances cell proliferation, migration and invasion by regulating miR-302a-3p/RAB22A in glioma

2020 ◽  
Vol 40 (9) ◽  
Author(s):  
Li-li Zhou ◽  
Meng Zhang ◽  
Yan-zhen Zhang ◽  
Mei-fen Sun
Keyword(s):  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Nude Mouse Model ◽  
Cell Behaviors ◽  
Non Coding Rna ◽  
The Central Nervous System ◽  
Long Non Coding Rna

Abstract Glioma is the most prevalent solid tumor in the central nervous system (CNS). Recently, it has been indicated that long non-coding RNAs (lncRNAs) substantially adjust the development of a variety of human cancers. In the present study, it was found and verified via microarray analysis that lncRNA PSMA3-AS1 exhibited a high expression in glioma tissues and cell lines. Then CCK-8, 5-Ethynyl-2′-deoxyuridine (EdU) staining, plate clone assay, Transwell assay, Western blotting and nude mouse model were adopted to verify PSMA3-AS1’s effects on glioma. Knockdown of PSMA3-AS1 inhibited the migration, proliferation and invasion of glioma cells in vivo and in vitro. Besides, PSMA3-AS1 bound to miR-302a-3p directly reduced the expression of miR-302a-3p, thus functioning as an endogenous sponge confirmed by luciferase reporter assay and bioinformatics analysis. PSMA3-AS1 knockdown remarkably enhanced the role of miR-302a-3p overexpression in cell behaviors in glioma. Moreover, these assays also confirmed that RAB22A was a target of miR-302a-3p. In this research, therefore, the PSMA3-AS1/miR-302a-3p/RAB22A pathway regulatory axis may be revealed in the pathogenesis of glioma, and PSMA3-AS1 can be used as an underlying target for the treatment and prognosis of glioma.

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