scholarly journals ALG3 Contributes to the Malignant Biological Properties of Oral Squamous Cell Carcinoma Cells Through Regulating CDK-Cyclin Pathway

2020 ◽  
Author(s):  
Peihong Shao ◽  
Chengshi Wei ◽  
Yun Wang
Keyword(s):  
Western Blot ◽  
Colony Formation ◽  
Enrichment Analysis ◽  
Biological Properties ◽  
The Cancer Genome Atlas ◽  
Cell Counting ◽  
Invasion And Migration ◽  
Elevated Expression ◽  
Cancer Genome Atlas ◽  
And Migration

Abstract Background: In this study, we planned to investigate the function and potential mechanisms of Alpha-1,3-mannosyltransferase (ALG3) in oral squamous cell carcinoma (OSCC). Methods: Data from The Cancer Genome Atlas (TCGA) was used to analyze ALG3 expression and its effect on the prognosis of patients with OSCC. Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis was applied to explore the signaling pathways related to ALG3. In OSCC cells, ALG3 expression was measured by qPCR and western blot. Cell counting kit-8, colony formation, and transwell assays were implemented to detect the effects of ALG3 on the malignant biological properties OSCC cells. The expression of key proteins related to CDK-Cyclin pathway was detected by western blot. Results: The expression of ALG3 in OSCC samples was higher than that of the control samples, and the increase of ALG3 expression was related to unfavorable prognosis of OSCC patients. Additionally, the elevated expression of ALG3 was associated with pathological stage, lymph node metastasis and primary lesion in OSCC patients. ALG3 depletion blocked the growth, colony formation, invasion and migration of OSCC cells, while over-expression ALG3 reversed these phenomena. Moreover, exhaustion of ALG3 resulted in decreased expression of MCM7, CCNB2, CDK1 and PCNA, while these phenomena were inversed after ALG3 up-regulation. Conclusions: The enhancement of ALG3 expression promoted the aggressive biological behaviors of OSCC cells probably by promoting CDK-Cyclin pathway.

scholarly journals miR-27b Targets HOXB8 to Inhibit Malignant Behaviors of Osteosarcoma

2019 ◽  
Vol 18 ◽  
pp. 153303381987079
Author(s):  
Yingyong Wu ◽  
Jinyun Peng
Keyword(s):  
Cell Proliferation ◽  
Western Blot ◽  
Cell Lines ◽  
Colony Formation ◽  
Cell Counting ◽  
Osteosarcoma Cell ◽  
Polymerase Chain ◽  
And Migration ◽  
Insight Into

MicroRNAs function as either tumor suppressor or oncogene in human cancers. This study aimed to explore the role of miR-27b in osteosarcoma. Expression of miR-27b or homeobox B8 in osteosarcoma cell lines was analyzed by quantitative real-time polymerase chain reaction and Western blot, respectively. Luciferase activity reporter assay and Western blot were conducted to explore the association between miR-27b and homeobox B8. Cell Counting Kit-8, colony formation assay, and wound-healing assay were performed to investigate the role of miR-27b or homeobox B8 on cell proliferation, colony formation, and cell migration. Expression of miR-27b was significantly reduced, while homeobox B8 was increased in osteosarcoma cell lines. In addition, homeobox B8 was validated as a direct target of homeobox B8. Moreover, miR-27b regulates osteosarcoma cell proliferation, colony formation, and migration through targeting homeobox B8. Taken together, our study provides novel insight into the progression of osteosarcoma, and the miR-27b–homeobox B8 axis identified may be developed as therapeutic targets against hepatocellular carcinoma in the future.

scholarly journals CircITGA7 Suppresses Gastric Cancer Progression Through miR-1471/MTDH Axis

2021 ◽  
Vol 9 ◽  
Author(s):  
Haifeng Jin ◽  
Zheng Wu ◽  
Bibo Tan ◽  
Zhen Liu ◽  
Binqian Zhang
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Progression ◽  
Enrichment Analysis ◽  
The Cancer Genome Atlas ◽  
Circular Rnas ◽  
Invasion And Migration ◽  
Suppressor Effect ◽  
And Migration

In recent years, there have been reports about the involvement of circular RNAs (circRNAs) in the pathogenesis of gastric cancer (GC), but the molecular mechanism in cell proliferation, invasion, and migration is still unclear. Based on The Cancer Genome Atlas (TCGA) database, we analyzed differentially expressed circRNAs between GC and non-tumor tissues. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analysis were used to clarify the functional role in GC. Here, we showed that circITGA7 was lowly expressed in GC tissues based on the TCGA database. In vitro, silencing the expression of circITGA7 increased cell proliferation and metastasis, whereas overexpression did the opposite. Mechanistically, miR-1471 has circITGA7 as a sponge, and miR-1471 has metadherin (MTDH) as a target gene. Consequently, functional analysis showed that the tumor suppressor effect of circITGA7 was the result of regulating the miR-1471/MTDH axis. Overall, the circITGA7/miR-1471/MTDH signaling pathway may play a crucial role in GC, providing a new potential mechanism involved in GC progression.

Silencing of miR-200a-3p Inhibits Proliferation, Invasion and Migration of Breast Cancer Cells by Targeting Ephrin-A5

2021 ◽  
Vol 11 (7) ◽  
pp. 1227-1235
Author(s):  
Yongmei Zhang ◽  
Huayi Zhang ◽  
Gang Guo
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cell Lines ◽  
The Cancer Genome Atlas ◽  
Luciferase Reporter Assay ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Reporter Assay ◽  
Invasion And Migration ◽  
And Migration

Increasing evidence suggests microRNAs (miRs/miRNAs) exert considerable functions in the pathogenesis of malignancies, including breast cancer (BC). The miR-200a-3p has previously been reported to promote tumorigenesis in different types of cancers. The present study aimed to investigate the potential role of and possible mechanisms of miR-200a-3p in BC. In this study miR-200a-3p and ephrin-A5 (EFNA5) expression in tissues of patients with BC was analyzed using The Cancer Genome Atlas (TCGA) database. And several BC cell lines were employed to determine the expression levels of miR-200a-3p and EFNA5. Then, miR-200a-3p expression was silenced by transfection with miR-200a-3p inhibitor. Cell proliferation was evaluated using a cell counting kit-8 kit and colony formation assay, whilst cell invasion and migration were detected using Transwell and wound healing assays, respectively. Then, the potential interaction between miR-200a-3p and EFNA5 was verified using luciferase reporter assay. Subsequently, rescue assays were conducted by co-transfection with miR-200a-3p inhibitor and short hairpin RNA (shRNA) targeted against EFNA5 (shRNA-EFNA5) to study the effects of TTN-AS1 and miR-211-5p on BC development. Results indicated that miR-200a-3p expression was significantly upregulated while EFNA5 was notably downregulated in BC tissues and cell lines. Cells transfected with miR-200a-3p inhibitor presented lower abilities of cell proliferation, invasion and migration. Moreover, the luciferase reporter assay confirmed that EFNA5 was a direct target of miR-200a-3p. And EFNA5 silencing reversed the inhibitory effects of miR-200a-3p inhibitor on proliferation, invasion and migration of BC cells. Taken together, these findings revealed that miR-200a-3p silencing inhibits proliferation, invasion and migration of BC cells by targeting EFNA5, which provides insights into the regulatory mechanism of BC and new strategies for developing therapeutic interventions for this disease.

scholarly journals HAVCR1 Affects the MEK/ERK Pathway in Gastric Adenocarcinomas and Influences Tumor Progression and Patient Outcome

2019 ◽  
Vol 2019 ◽  
pp. 1-10
Author(s):  
Ji Xue ◽  
Ying Li ◽  
Jianfeng Yi ◽  
Hong Jiang
Keyword(s):  
Colony Formation ◽  
Hepatitis A Virus ◽  
The Cancer Genome Atlas ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Loss Of Function ◽  
Reverse Transcription Pcr ◽  
Gastric Adenocarcinomas ◽  
Potential Biomarker ◽  
Cancer Genome Atlas

The hepatitis A virus cellular receptor 1 (HAVCR1) gene as a sensitive and specific biomarker has been reported in various diseases. Especially, HAVCR1 overexpression promotes the development and progression of several human cancers. Hence, we aimed to detect the effects of HAVCR1 on gastric adenocarcinoma (GAC). We first determined the expression of HAVCR1 in GAC tissues compared with normal gastric tissues based on the Cancer Genome Atlas (TCGA) database using bioinformatics analysis methods. Then, we assessed the biological function of HAVCR1 in GAC cells using quantitative real-time reverse transcription-PCR (qRT-PCR), western blot, cell counting kit-8- (CCK-) 8, colony formation assay, wound healing assay, and transwell assay. Our results showed that HAVCR1 expression was upregulated in GAC tissues and positively associated with poor survival. Loss-of-function analyses indicated that knockdown of HAVCR1 inhibited the proliferation, colony formation, migration, and invasion of GAC cells. Furthermore, reduction of HAVCR1 in GAC cells can decrease the expression of phosphorylated MEK/ERK. These findings suggested that HAVCR1 may represent a potential biomarker for GAC prognosis, as well as a novel therapeutic target for GAC treatment.

scholarly journals PIMREG, a Marker of Proliferation, Facilitates Aggressive Development of Cholangiocarcinoma Cells Partly Through Regulating Cell Cycle-Related Markers

2020 ◽  
Vol 19 ◽  
pp. 153303382097968
Author(s):  
Zhao-Ming Jiang ◽  
Hong-Bin Li ◽  
Shu-Guo Chen
Keyword(s):  
Cell Cycle ◽  
Western Blot ◽  
Cell Lines ◽  
Gene Set Enrichment Analysis ◽  
Cell Counting ◽  
Aberrant Expression ◽  
Gene Set ◽  
Invasion And Migration ◽  
The Public ◽  
And Migration

Background: Phosphatidylinositol binding clathrin assembly protein interacting mitotic regulator (PIMREG) is a protein associated with cell proliferation. Its aberrant expression was reported to be correlated with the development in multiple tumors. However, its role in cholangiocarcinoma (CAA) has not yet been evaluated in detail. Methods: Data were acquired from the public TCGA database for evaluating the expression pattern of PIMREG and assessing its clinical relevance as well as its correlation with overall survival. RBE and HUH28 cell lines were selected to perform loss- and gain-of-function of PIMREG assays respectively. Quantitative real-time PCR (RT-qPCR) and western blot analyses were used to measure the mRNA and protein levels of PIMREG. Cell Counting Kit-8, colony formation tests, and Transwell assays served to measure the effect of PIMREG on the proliferative, invasive and migratory capacities of CAA cells, appropriately. Gene set enrichment analysis (GSEA) was conducted to identify PIMREG associated gene set, which was further confirmed by western blot. Results: PIMREG was found to be highly expressed in CAA tissues and cell lines according to the public dataset and RT-qPCR analysis, and negatively related to the prognosis of patients with CAA. Moreover, knockdown of PIMREG suppressed and overexpression of PIMREG promoted the proliferation, invasion and migration of CAA cells. Furthermore, GSEA revealed that high PIMREG expression was positively associated with cell cycle signaling. And the next western blot analysis demonstrated that silencing PIMREG resulted in a reduction on the levels of p-CDK1, CCNE1, and CCNB1, whereas PIMREG overexpression led to an opposite result. Conclusion: The results suggested that PIMREG facilitates the growth, invasion and migration of CAA cells partly by regulating the cell cycle relative biomarkers, revealing that PIMREG may be a crucial molecule in the progression of CAA.

scholarly journals COL6A3 promotes cellular malignancy of osteosarcoma by activating the PI3K/AKT pathway

2020 ◽  
Vol 66 (6) ◽  
pp. 740-745
Author(s):  
Hong-Li Guo ◽  
Gang Chen ◽  
Ze-Long Song ◽  
Jia Sun ◽  
Xi-Hai Gao ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Colony Formation ◽  
Akt Signaling ◽  
Cell Counting ◽  
Akt Pathway ◽  
Akt Signaling Pathway ◽  
Invasion And Migration ◽  
Geo Dataset ◽  
And Migration

SUMMARY OBJECTIVE In this study, we aimed to investigate the role of COL6A3 on cell motility and the PI3K/AKT signaling pathway in osteosarcoma. METHODS The relative expression of COL6A3 was achieved from a GEO dataset in osteosarcoma tissue. siRNA technology was applied to decrease the COL6A3 expression in cells, and cell counting kit-8 (CCK-8) assay and colony formation analysis were used to examine the cell proliferation potential. Knockdown COL6A3 made the proliferation and colony formation abilities worse than the COL6A3 without interference. Likewise, in contrast to the si-con group, cell invasion and migration were inhibited in the si-COL6A3 group. Moreover, the western blot results suggested that the PI3K/AKT signaling pathway was manipulated by measuring the protein expression of the PI3K/AKT pathway-related markers, due to the COL6A3 inhibition. CONCLUSION COL6A3 plays a crucial role in modulating various aspects of the progression of osteosarcoma, which would provide a potentially effective treatment for osteosarcoma.

Effects and Mechanisms of Anlotinib and Dihydroartemisinin Combination Therapy in Ameliorating Malignant Biological Behavior of Gastric Cancer Cells

2020 ◽  
Vol 21 ◽  
Author(s):  
Qiong Luo ◽  
Suyun Zhang ◽  
Donghuan Zhang ◽  
Rui Feng ◽  
Nan Li ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Molecular Mechanisms ◽  
Chorioallantoic Membrane ◽  
Cell Counting ◽  
Biological Behavior ◽  
Gastric Cancer Cells ◽  
Invasion And Migration ◽  
Apoptosis Related Protein ◽  
And Migration

Background: Gastric cancer(GC) is currently one of the major malignancies that threatens human lives and health. Anlotinib is a novel small-molecule that inhibits angiogenesis to exert anti-tumor effects. However, the function in gastric cancer is incompletely understood. Objective: The aim of the present study was to investigate the anti-tumor effects and molecular mechanisms of anlotinib combined with dihydroartemisinin (DHA) in SGC7901 gastric cancer cells. Method: Different concentrations of anlotinib and DHA were used to treat SGC7901 gastric cancer cells, after which cell proliferation was measured. Drug interactions of anlotinib and DHA were analyzed by the Chou-Talalay method with CompuSyn software. proliferation, apoptosis, invasion, migration, and angiogenesis were measured using the cell counting kit-8 (CCK8) assay, flow cytometry, Transwell invasion assays, scratch assays, and chicken chorioallantoic membrane (CAM) assays. proliferation-associated protein (Ki67), apoptosis-related protein (Bcl-2), and vascular endothelial growth factor A (VEGF-A) were quantified by Western bloting. Results: The combination of 2.5 μmol/L of anlotinib and 5 of μmol/L DHA was highly synergistic in inhibiting cell growth, significantly increased the apoptosis rate and suppressed obviously the invasion and migration capability and angiogenesis of gastric cancer cells. In addition, the expression levels of Ki67, Bcl-2, and VEGF-A, as well as angiogenesis, were significantly decreased in the Combination of drugs compared with in control and either drug alone. Conclusion: The combination of anlotinib and DHA showed synergistic antitumor activity, suggesting their potential in treating patients with gastric cancer.

scholarly journals The roles and prognostic significance of ABI1-TSV-11 expression in patients with left-sided colorectal cancer

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yu Zhang ◽  
Zhaohui Zhong ◽  
Mei Li ◽  
Jingyi Chen ◽  
Tingru Lin ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Prognostic Significance ◽  
Growth Factor Receptor ◽  
The Cancer Genome Atlas ◽  
Actin Dynamics ◽  
Elevated Expression ◽  
Sw480 Cells ◽  
And Migration

AbstractAbnormally expressed and/or phosphorylated Abelson interactor 1 (ABI1) participates in the metastasis and progression of colorectal cancer (CRC). ABI1 presents as at least 12 transcript variants (TSVs) by mRNA alternative splicing, but it is unknown which of them is involved in CRC metastasis and prognosis. Here, we firstly identified ABI1-TSV-11 as a key TSV affecting the metastasis and prognosis of left-sided colorectal cancer (LsCC) and its elevated expression is related to lymph node metastasis and shorter overall survival (OS) in LsCC by analyzing data from The Cancer Genome Atlas and TSVdb. Secondly, ABI1-TSV-11 overexpression promoted LoVo and SW480 cells adhesion and migration in vitro, and accelerated LoVo and SW480 cells lung metastasis in vivo. Finally, mechanism investigations revealed that ABI1-isoform-11 interacted with epidermal growth factor receptor pathway substrate 8 (ESP8) and regulated actin dynamics to affect LoVo and SW480 cells biological behaviors. Taken together, our data demonstrated that ABI1-TSV-11 plays an oncogenic role in LsCC, it is an independent risk factor of prognosis and may be a potential molecular marker and therapeutic target in LsCC.

scholarly journals CSIG-03. RECONCILING TUMOR HETEROGENEITY IN GLIOBLASTOMA USING A PATHWAY-BASED APPROACH

2020 ◽  
Vol 22 (Supplement_2) ◽  
pp. ii28-ii28
Author(s):  
Alvaro Alvarado ◽  
Kaleab Tessema ◽  
Kunal Patel ◽  
Riki Kawaguchi ◽  
Richard Everson ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Patient Survival ◽  
Molecular Subtype ◽  
Gene List ◽  
Enrichment Analysis ◽  
Gene Set Enrichment Analysis ◽  
The Cancer Genome Atlas ◽  
Molecular Architecture ◽  
Survival Pathways ◽  
Cancer Genome Atlas

Abstract Despite efforts to gain a deeper understanding of its molecular architecture, glioblastoma (GBM) remains uniformly fatal. While genome-based molecular subtyping has revealed that GBMs may be parsed into several molecularly distinct categories, this insight has yielded little progress towards extending patient survival. In particular, the great phenotypic heterogeneity of GBM – both inter and intratumorally – has hindered therapeutic efforts. To this end, we interrogated tumor samples using a pathway-based approach to resolve tumoral heterogeneity. Gene set enrichment analysis (GSEA) was applied to gene expression data and used to provide an overview of each sample that can be compared to other samples by generating sample clusters based on overall patterns of enrichment. The Cancer Genome Atlas (TCGA) samples were clustered using the canonical and oncogenic signatures and in both cases the clustering was distinct from the molecular subtype previously reported and clusters were informative of patient survival. We also analyzed single cell RNA sequencing datasets and uniformly found two clusters of cells enriched for cell cycle regulation and survival pathways. We have validated our approach by generating gene lists from common elements found in the top contributing genesets for a particular cluster and testing the top targets in appropriate gliomasphere patient-derived lines. Samples enriched for cell cycle related genesets showed a decrease in sphere formation capacity when E2F1, out top target, was silenced and when treated with fulvestrant and calcitriol, which were identified as potential drugs targeting this genelist. Conversely, no changes were observed in samples not enriched for this gene list. Finally, we interrogated spatial heterogeneity and found higher enrichment of the proliferative signature in contrast enhancing compared with non-enhancing regions. Our studies relate inter- and intratumoral heterogeneity to critical cellular pathways dysregulated in GBM, with the ultimate goal of establishing a pipeline for patient- and tumor-specific precision medicine.

scholarly journals Long noncoding RNA LINC01291 promotes the aggressive properties of melanoma by functioning as a competing endogenous RNA for microRNA-625-5p and subsequently increasing IGF-1R expression

2021 ◽  
Author(s):  
Lijun Wu ◽  
Ke Li ◽  
Wei Lin ◽  
Jianjiang Liu ◽  
Qiang Qi ◽  
...  
Keyword(s):  
Colony Formation ◽  
Noncoding Rna ◽  
Melanoma Cells ◽  
The Cancer Genome Atlas ◽  
Cell Counting ◽  
Tumor Xenograft ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Competing Endogenous Rna ◽  
Melanoma Tumor

AbstractStudies have confirmed the relationship between dysregulated long noncoding RNAs and melanoma pathogenesis. However, the regulatory functions of long intergenic non-protein coding RNA 1291 (LINC01291) in melanoma remain unknown. Therefore, we evaluated LINC01291 expression in melanoma and explored its roles in regulating tumor behaviors. Further, the molecular events via which LINC01291 affects melanoma cells were investigated. LINC01291 expression in melanoma cells was analyzed using The Cancer Genome Atlas database and quantitative real-time polymerase chain reaction. Functional assays, including the Cell Counting Kit-8 assay, colony formation assay, flow cytometry, cell migration and invasion assays, and tumor xenograft models, were used to examine LINC01291’s role in melanoma cells. Additionally, bioinformatics analysis, RNA immunoprecipitation, luciferase reporter assay, and western blotting were conducted to determine the tumor-promoting mechanism of LINC01291. LINC01291 was upregulated in melanoma tissues and cell lines. Following LINC01291 knockdown, cell proliferation, colony formation, migration, and invasion were diminished, whereas apoptosis was enhanced and the cell cycle was arrested at G0/G1. In addition, loss of LINC01291 decreased the chemoresistance of melanoma cells to cisplatin. Furthermore, LINC01291 interference inhibited melanoma tumor growth in vivo. Mechanistically, LINC01291 functions as a competing endogenous RNA by sponging microRNA-625-5p (miR-625-5p) in melanoma cells and maintaining insulin-like growth factor 1 receptor (IGF-1R) expression. Rescue experiments revealed that the roles induced by LINC01291 depletion in melanoma cells could be reversed by suppressing miR-625-5p or overexpressing IGF-1R. Our study identified the LINC01291/miR-625-5p/IGF-1R competing endogenous RNA pathway in melanoma cells, which may represent a novel diagnostic biomarker and an effective therapeutic target for melanoma.

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