scholarly journals LncRNA PCNAP1 Promotes Hepatoma Cell Proliferation through Targeting miR-340-5p and is Associated with Patient Survival

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Miao He ◽  
Lingjing Hu ◽  
Ping Bai ◽  
Tingting Guo ◽  
Nan Liu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Noncoding Rna ◽  
Hepatoma Cell ◽  
Survival Rates ◽  
Poor Survival ◽  
Potential Therapeutic Target ◽  
Normal Tissues ◽  
Potential Biomarker ◽  
Underlying Mechanisms ◽  
Competitive Endogenous Rna

Hepatocellular carcinoma (HCC) is one of the most common malignancies and causes poor outcome. Dysregulation of long noncoding RNA (lncRNA) is involved in HCC. Upregulation of the lncRNA PCNAP1 has been reported to promote HBV-infectious HCC growth, but its clinical significance and underlying mechanisms in HCC development remain unclear. Here, we report that PCNAP1 expression is increased in both HBV-infectious and noninfectious HCC tissues compared with matched normal tissues, and its upregulation correlates with poor survival rates of HCC patients. Furthermore, we found that PCNAP1 promotes HCC cell proliferation through acting as a competitive endogenous RNA (ceRNA) to sponge miR-340-5p, which has been reported to directly inhibit ATF7 expression in HCC cells. Moreover, the PCNAP1/miR-340-5p/ATF7 signaling associates with the poor survival rates of HCC patients. Collectively, our findings suggest that the PCNAP1/miR-340-5p/ATF7 signaling may be a potential biomarker for the prognosis of HCC patients and a potential therapeutic target for HCC.

scholarly journals Upregulation of lnc-ZNF281 Inhibits the Progression of Glioma via the AKT/GSK-3β/β-Catenin Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Yu-Qin Deng ◽  
Gang-Yong Kong ◽  
Song Li ◽  
Fen Li ◽  
Si-Lu Wen
Keyword(s):  
Cell Proliferation ◽  
Signaling Pathway ◽  
Noncoding Rna ◽  
Glioma Cells ◽  
Normal Tissues ◽  
Glioma Cell Proliferation ◽  
Underlying Mechanisms ◽  
And Migration ◽  
Gsk 3Β ◽  
Proliferation And Migration

The purpose of this study is to elucidate the roles and potential underlying mechanisms of long noncoding RNA lnc-ZNF281 in glioma. We performed qRT-PCR to detect the expression levels of lnc-ZNF281 in glioma tissues. The effects of lnc-ZNF281 on the proliferative and migrative abilities of T98G and HS683 glioma cells were examined by cell proliferation assay, colony formation assay, wound-healing assay, and transwell assay. Also, the effects of lnc-ZNF281 on AKT/GSK-3β/β-catenin pathway were analyzed. The results showed that the expression of lnc-ZNF281 in glioma tissues was decreased compared with normal tissues. lnc-ZNF281 overexpression inhibited the proliferative and migrative abilities of glioma cells, while lnc-ZNF281 knockdown obtained the opposite findings. Besides, overexpression of lnc-ZNF281 in glioma cells inactivated the AKT/GSK-3β/β-catenin signaling pathway. Furthermore, β-catenin activation reversed the suppressive effects of lnc-ZNF281 on glioma cells. Taken together, lnc-ZNF281 inhibits glioma cell proliferation and migration via AKT/GSK-3β/β-catenin pathway and may serve as a potential target for glioma treatment.

scholarly journals Emerging impact of the long noncoding RNA MIR22HG on proliferation and apoptosis in multiple human cancers

2020 ◽  
Vol 39 (1) ◽  
Author(s):  
Le Zhang ◽  
Cuixia Li ◽  
Xiulan Su
Keyword(s):  
Chromatin Remodeling ◽  
Noncoding Rna ◽  
Potential Role ◽  
Immune Escape ◽  
Prognostic Biomarker ◽  
Cellular Processes ◽  
Proliferation And Apoptosis ◽  
Underlying Mechanisms ◽  
Competitive Endogenous Rna

AbstractAn increasing number of studies have shown that long noncoding RNAs (lncRNAs) play important roles in diverse cellular processes, including proliferation, apoptosis, migration, invasion, chromatin remodeling, metabolism and immune escape. Clinically, the expression of MIR22HG is increased in many human tumors (colorectal cancer, gastric cancer, hepatocellular carcinoma, lung cancer, and thyroid carcinoma), while in others (esophageal adenocarcinoma and glioblastoma), it is significantly decreased. Moreover, MIR22HG has been reported to function as a competitive endogenous RNA (ceRNA), be involved in signaling pathways, interact with proteins and interplay with miRNAs as a host gene to participate in tumorigenesis and tumor progression. In this review, we describe the biological functions of MIR22HG, reveal its underlying mechanisms for cancer regulation, and highlight the potential role of MIR22HG as a novel cancer prognostic biomarker and therapeutic target that can increase the efficacy of immunotherapy and targeted therapy for cancer treatment.

scholarly journals DCTPP1, an Oncogene Regulated by miR-378a-3p, Promotes Proliferation of Breast Cancer via DNA Repair Signaling Pathway

2021 ◽  
Vol 11 ◽  
Author(s):  
Ming Niu ◽  
Ming Shan ◽  
Yang Liu ◽  
Yanni Song ◽  
Ji-guang Han ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Dna Repair ◽  
Survival Rates ◽  
The Other ◽  
Poor Survival ◽  
Induced Apoptosis ◽  
Cell Growth And Proliferation

Breast cancer (BRCA) is one of the most deadly cancers worldwide, with poor survival rates that could be due to its high proliferation. Human all-alpha dCTP pyrophosphatase 1 (DCTPP1) is implicated in numerous diseases, including cancers. However, its role in BRCA is unclear. In this study, we used bioinformatic analyses of the ONCOMINE, UALCAN, and GEPIA databases to determine the expression pattern of DCTPP1 in BRCA. We found that elevated DCTPP1 levels correlate with poor BRCA prognosis. DCTPP1 silencing inhibited BRCA cell proliferation and induced apoptosis in vitro, as well as in vivo. Our data show that this tumorigenic effect depends on DNA repair signaling. Moreover, we found that DCTPP1 is directly modulated by miR-378a-3p, whose downregulation is linked to BRCA progression. Our results showed down-regulation of miR-378a-3p in BRCA. Upregulation of miR-378a-3p, on the other hand, can inhibit BRCA cell growth and proliferation. This study shows that reduced miR-378a-3p level enhances DCTPP1 expression in BRCA, which promotes proliferation by activating DNA repair signaling in BRCA.

scholarly journals Long Noncoding RNA LINC00958 Suppresses Apoptosis and Radiosensitivity of Colorectal Cancer Through Targeting miR-422a

2021 ◽  
Author(s):  
Hong Liang ◽  
Qiuyan Zhao ◽  
Zhonglin Zhu ◽  
Chao Zhang ◽  
Hui Zhang
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Noncoding Rna ◽  
Luciferase Reporter ◽  
Flow Cytometric ◽  
Potential Biomarker ◽  
Reporter Assays ◽  
Cancer Tissues

Abstract Background: Long non-coding RNAs (lncRNAs) have been elucidated to participate in the development and progression of various cancers. In this study, we aim to explore the underlying functions and mechanisms of LINC00958 in colorectal cancer. Methods: LINC00958 expression in colorectal cancer tissues was examined by qRT-PCR. The associations between LINC00958 expression with clinical characteristics and prognosis were evaluated. The biological functions of LINC00958 were detected by CCK-8, MTT, colony formation and Flow cytometric analyses. RNA-pull down, RIP and luciferase reporter assays were used to confirm the regulation of LINC00958 on miR-422a. Rescue experiments were performed to detect the effects of miR-422a on the roles of LINC00958. Results: LINC00958 was upregulated in colorectal cancer tissues and cell lines; high LINC00958 level was significantly associated with tumor differentiation, T stage and TNM stage, and also predicted poor prognosis. Cell experiments showed that LINC00958 promoted cell proliferation and suppressed apoptosis and the sensitivity of radiotherapy in vitro, and promoted cell growth in vivo. Bioinformatics analysis predicted the binding site of miR-422a on LINC00958. Mechanistically, RNA-pull down, RIP and luciferase reporter assays demonstrated that LINC00958 specially targeted miR-422a. In addition, we provided evidence that miR-422a suppressed MAPK1 expression through directly binding to the 3’-UTR of MAPK1, thereby inhibiting cell proliferation and enhancing apoptosis and the radiosensitivity. Furthermore, miR-422a rescued the roles of LINC00958 on promoting MAPK1 expression and cell proliferation and decreasing apoptosis and the radiosensitivity. Conclusions: LINC00958 promoted MAPK1 expression and cell proliferation and suppressed apoptosis and the radiosensitivity through targeting miR-422a, highlighting a potential biomarker for the prognosis and treatment of colorectal cancer.

scholarly journals Tumor Associated Macrophages: Origin, Recruitment, Phenotypic Diversity, and Targeting

2021 ◽  
Vol 11 ◽  
Author(s):  
Tetiana Hourani ◽  
James A. Holden ◽  
Wenyi Li ◽  
Jason C. Lenzo ◽  
Sara Hadjigol ◽  
...  
Keyword(s):  
Strong Influence ◽  
Phenotypic Diversity ◽  
Survival Rates ◽  
Cancer Therapeutics ◽  
Therapy Resistance ◽  
Tumor Associated Macrophages ◽  
Poor Survival ◽  
Potential Therapeutic Target ◽  
Detailed Review ◽  
Therapeutic Outcomes

The tumor microenvironment (TME) is known to have a strong influence on tumorigenesis, with various components being involved in tumor suppression and tumor growth. A protumorigenic TME is characterized by an increased infiltration of tumor associated macrophages (TAMs), where their presence is strongly associated with tumor progression, therapy resistance, and poor survival rates. This association between the increased TAMs and poor therapeutic outcomes are stemming an increasing interest in investigating TAMs as a potential therapeutic target in cancer treatment. Prominent mechanisms in targeting TAMs include: blocking recruitment, stimulating repolarization, and depletion methods. For enhancing targeting specificity multiple nanomaterials are currently being explored for the precise delivery of chemotherapeutic cargo, including the conjugation with TAM-targeting peptides. In this paper, we provide a focused literature review of macrophage biology in relation to their role in tumorigenesis. First, we discuss the origin, recruitment mechanisms, and phenotypic diversity of TAMs based on recent investigations in the literature. Then the paper provides a detailed review on the current methods of targeting TAMs, including the use of nanomaterials as novel cancer therapeutics.

scholarly journals Downregulated Expression of hsa_circ_0005556 in Gastric Cancer and Its Clinical Significance

2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
Liangwei Yang ◽  
Yu Yu ◽  
Xiuchong Yu ◽  
Jiaming Zhou ◽  
Zhiping Zhang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Roc Curve ◽  
Noncoding Rna ◽  
Operating Characteristic ◽  
Diagnostic Value ◽  
Circular Rnas ◽  
Normal Tissues ◽  
Potential Biomarker ◽  
Polymerase Chain

Background. Gastric cancer (GC) has a poor prognosis due to the lack of ideal tumor markers. Circular RNAs (circRNAs) are a novel type of noncoding RNA related to the occurrence of GC. Among our research, we investigated the role of hsa_circ_0005556 in GC. Materials and Methods. The expression of hsa_circ_0005556 of 100 paired GC tissues and adjacent normal tissues was detected using quantitative reverse transcription-polymerase chain reaction (qRT-PCR). A receiver operating characteristic (ROC) curve was established to evaluate the diagnostic value of hsa_circ_0005556. The correlation between the expression of hsa_circ_0005556 and corresponding clinicopathological characteristic was explored. Results. hsa_circ_0005556 was significantly downregulated in GC tissues contrasted with adjacent normal tissues (n=100, p<0.001). The areas under the ROC curve (AUC) of hsa_circ_0005556 were up to 0.773, while 64% sensitivity and 82% specificity, respectively. Moreover, its expression levels were significantly associated with differentiation (p=0.001), TNM stage (p=0.013), and lymphatic metastasis (p=0.039). GC patients of high hsa_circ_0005556 levels had a longer overall survival (OS) than those of the low group (p=0.047). Conclusion. hsa_circ_0005556 is a potential biomarker for GC, which may guide judgment of the indication of endoscopic treatment for early gastric cancer (EGC).

scholarly journals SPATS2, negatively regulated by miR-145-5p, promotes hepatocellular carcinoma progression through regulating cell cycle

2020 ◽  
Vol 11 (10) ◽  
Author(s):  
Gang Dong ◽  
Shanshan Zhang ◽  
Shen Shen ◽  
Lulu Sun ◽  
Xuemei Wang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
G1 Arrest ◽  
Poor Survival ◽  
Potential Therapeutic Target ◽  
Normal Tissues ◽  
Proliferation And Metastasis ◽  
And Function ◽  
Hcc Cells

Abstract Spermatogenesis associated serine rich 2 (SPATS2) has been reported to contribute to the tumorigenesis of multiple malignancies. The molecular function of SPATS2 in hepatocellular carcinoma (HCC) is still not fully understood. In this study, we aimed to investigate the expression pattern and function roles of SPATS2 in HCC. The regulation of SPATS2 expression was also explored. We found that SPATS2 was highly expressed in HCC tissues in comparison with that in adjacent normal tissues. High expression of SPATS2 was associated with vascular invasion, advanced TNM stages, tumor multiplicity, and poor survival. Functionally, SPATS2 was found to promote the proliferation and metastasis of HCC cells both in vitro and in vivo, while knockdown of SPATS2 enhanced apoptosis and G1 arrest of HCC cells in vitro. Mechanistically, bioinformatics analysis revealed that MiR-145-5p directly targeted SPATS2 and functional rescue experiments verified that MiR-145-5p overexpression could abolish the effect of SPATS2 on the regulation of HCC malignant phenotype. Taken together, our findings suggest that SPATS2 functions as an oncogene in HCC. The MiR-145-5p/SPATS2 axis provides a novel mechanism underlying HCC progression and may serve as a potential therapeutic target for HCC.

scholarly journals Overexpression of long intergenic noncoding RNA LINC00312 inhibits the invasion and migration of thyroid cancer cells by down-regulating microRNA-197-3p

2017 ◽  
Vol 37 (4) ◽  
Author(s):  
Kai Liu ◽  
Wen Huang ◽  
Dan-Qing Yan ◽  
Qing Luo ◽  
Xiang Min
Keyword(s):  
Cell Proliferation ◽  
Thyroid Cancer ◽  
Noncoding Rna ◽  
Luciferase Reporter ◽  
Luciferase Reporter Gene ◽  
Invasion And Migration ◽  
Normal Tissues ◽  
Gene Assay ◽  
Long Intergenic Noncoding Rna ◽  
And Migration

The study evaluated the ability of long intergenic noncoding RNA LINC00312 (LINC00312) to influence the proliferation, invasion, and migration of thyroid cancer (TC) cells by regulating miRNA-197-3p. TC tissues and adjacent normal tissues were collected from 211 TC patients. K1 (papillary TC), SW579 (squamous TC), and 8505C (anaplastic TC) cell lines were assigned into a blank, negative control (NC), LINC00312 overexpression, miR-197-3p inhibitors, and LINC00312 overexpression + miR-197-3p mimics group. The expression of LINC00312, miR-197-3p, and p120 were measured using quantitative real-time PCR (qRT-PCR) and Western blotting. Cell proliferation was assessed via CCK8 assay, cell invasion through the scratch test, and cell migration via Transwell assay. In comparison with adjacent normal tissues, the expression of LINC00312 is down-regulated and the expression of miR-197-3p is up-regulated in TC tissues. The dual luciferase reporter gene assay confirmed that P120 is a target of miR-197-3p. The expression of LINC00312 and p120 was higher in the LINC00312 overexpression group than in the blank and NV groups. However, the expression of miR-197-3p was lower in the LINC00312 overexpression group than in the blank and NC groups. The miR-197-3p inhibitors group had a higher expression of miR-197-3p, but a lower expression of p120 than the blank and NC groups. The LINC00312 overexpression and miR-197-3p inhibitor groups had reduced cell proliferation, invasion and migration than the blank and NC groups. These results indicate that a LINC00312 overexpression inhibits the proliferation, invasion, and migration of TC cells and that this can be achieved by down-regulating miR-197-3p.

scholarly journals UCA1, a long noncoding RNA, promotes the proliferation of CRC cells via p53/p21 signaling

2016 ◽  
Vol 11 (1) ◽  
pp. 206-210
Author(s):  
Shen Yi ◽  
Ying Xiao-jiang ◽  
Li Zhen-jun ◽  
Li Gang ◽  
Xue Wu-jin ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Noncoding Rna ◽  
Proliferation Rate ◽  
Cell Counting ◽  
Quantitative Real Time Pcr ◽  
Human Colorectal Cancer ◽  
Underlying Mechanisms ◽  
Hct116 Cells

AbstractObjectiveRecently, the role of long noncoding RNAs (lncRNAs) in human colorectal cancer (CRC) has been a subject of intense focus. We set out to determine the function of one lncRNA, termed urothelial carcinoma-associated 1 (UCA1) in CRC cell proliferation and its underlying mechanisms.MethodsQuantitative real-time PCR (qRT-PCR) was applied to detect the expression level of UCA1 in 50 pairs of CRC samples compared with non-tumor colon tissues. Cell growth was determined using the Cell Counting Kit-8 (CCK-8). Western blotting was carried out to analyze the related protein expression. Flow cytometry was done to evaluate cell apoptosis by UCA1 inhibition.ResultsWe found an increased expression of UCA1 in CRC samples. Knockdown of UCA1 in HCT116 cells induced a decrease in cell proliferation rate compared to control samples. This oncogenic activity may be enhanced through p53/ p21 signaling.ConclusionOur results supported the hypothesis that upregulation of UCA1 contributes to the unlimited proliferation rate of CRC cells, at least partially through the negative regulation of p53/p21 signaling pathway. Finally, we found that UCA1 merely influenced CRC cell apoptosis.

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