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1.
Exp Ther Med ; 23(3): 204, 2022 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-35126707

RESUMO

The melanoma antigen gene family A (MAGEA) family of proteins comprises of cancer-testis antigens that are highly expressed in a number of tumours but are minimally expressed in normal cells. Due to its expression characteristics, this protein family has become a popular target for anti-cancer drugs and immunotherapy research over recent years. Although, elevated expression levels of MAGEA6 has been found in different types of tumours, there remains to be insufficient information on the function of MAGEA6 and its associated gene regulation pathways. The present study used Transwell, Cell Counting Kit-8 and wound healing assays to analyse the effects of MAGEA6 on Eca109 cell invasion, migration and proliferation. The main functions and pathways involved in MAGEA6 were predicted by Illumina Hiseq screening for mutually regulated genes and core genes. Eca109 cell line with a high expression of MAGEA6 was a stable cell line obtained by transfection in the early stage, and this cell line was used in subsequent experiments. Transcriptome sequencing was performed on this cell line and the Eca109 cell line that normally expressed MAGEA6. It was revealed that a high expression of MAGEA6 conferred a significant stimulating effect on cell proliferation whilst also significantly increasing cell invasion and migration. Transcriptomic analysis identified 14 differentially expressed genes and 13 core regulatory genes closely associated with MAGEA6 expression regulation, such as methylsterol monooxygenase 1 (MSMO1). The present study suggest that MAGEA6 positively regulated MSMO1 expression, which may serve an oncogenic role in cells through this regulatory effect. Overall, this provided a novel route of investigation for an in-depth study of the regulatory function of MAGEA6.

2.
J Med Virol ; 2020 Jan 09.
Artigo em Inglês | MEDLINE | ID: mdl-31916268

RESUMO

Human papillomavirus (HPV) infection was associated with some carcinomas, especially malignant tumors in upper digestive tract, upper respiratory tract, and genitourinary system. The mechanism of the viral transformation of normal cells is still not very clear. To investigate the tumorigenesis of epithelial cells, E6/E7-induced malignant transformation model cells were used for expression profiling analysis by performing RNA expression microarray detection. Bioinformatics analysis was applied to investigate the cellular process changes along with the E6/E7 expression in SHEE cells. The differentially expressed genes were further grouped and uploaded for Search Tool for the Retrieval of Interacting Genes analysis. The protein-protein interaction results were visualized. The hub genes and their first-neighbors genes were selected, followed by gene ontology and Kyoto Encyclopedia of Genes and Genomes pathway analysis. The obtained results demonstrated that tumor-related biological processes began to emerge during the carcinogenesis process from 48th passage to 76th passage of SHEE cells after E6/E7 expression. Ten hub genes were identified and analyzed during the E6/E7-induced tumorigenesis. This study explores the gene expression network in the progressive transformation of immortalized esophageal epithelial cells induced by E6/E7 expression. Understanding the biological processes and hub genes that first appear during the transformation will provide some clues to the mechanism of E6/E7-induced carcinogenesis of esophageal epithelial cells.

3.
Exp Ther Med ; 18(3): 1816-1822, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31410142

RESUMO

Esophageal carcinoma (EC) is the sixth most deadly of all cancers. It is among the most malignant cancers due to its highly aggressive nature and low survival rate. The incidence of EC is high in Asia, particularly in Southern areas including China, Iran and Japan. There is a large body of evidence to suggest an association between the melanoma antigen gene (MAGE) family and the initiation of cancer; however, there is no clear evidence to suggest an association between EC and MAGE. Discovery of the chemical and physiological processes relevant to the occurrence of EC is vital for clinicians to diagnose and treat this highly aggressive cancer. The present study focused on the association of EC with the expression of MAGE family member A6 (MAGEA6) at the mRNA and protein levels using gene chip, reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and immunohistochemistry. The expression of MAGEA6 in human esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EAC) tissue samples were compared with those in paracancerous tissue. The result of the gene chip assay revealed that as the generation grew, there was a significant increase in MAGEA6 transcription in the esophageal epithelial cell line, SHEE Different ESC cell lines also exhibited a significantly higher transcription of MAGEA6 compared with the HaCaT cell line, as determined via reverse transcription-quantitative PCR. An higher positive rate of MAGEA6 expression in ESCC and EAC tissues was also revealed when compared with paracancerous tissues, as determined via immunohistochemistry. The results indicated that MAGEA6 is highly transcribed and expressed in the development of EC and may therefore serve as a novel biomarker for the diagnosis or treatment of EC.

4.
Anticancer Drugs ; 30(1): 38-45, 2019 01.
Artigo em Inglês | MEDLINE | ID: mdl-30134284

RESUMO

Dysregulation of miR-203-3p and miR-21-5p has been identified in esophageal cancer (EC). The restoration of miR-203-3p and reduction of miR-21-5p were able to cause tumor suppression. Here, co-transfection of miR-203-3p mimics and miR-21-5p inhibitors led to an extraordinary increased expression of miR-203-3p and synergistically inhibited proliferation, migration, and invasion in EC cells. Moreover, we found that Ran GTPase (Ran) was dramatically inhibited in EC cells treated with the co-transfection of miR-203-3p mimics and miR-21-5p inhibitors. Finally, in-vivo studies showed that overexpression of miR-203-3p, combined with the suppression of miR-21-5p, significantly co-inhibited growth of tumors. The obtained data suggested that the development of miRNA-based combination therapeutics represents a promising cancer treatment strategy.


Assuntos
Neoplasias Esofágicas/terapia , Carcinoma de Células Escamosas do Esôfago/terapia , MicroRNAs/administração & dosagem , MicroRNAs/antagonistas & inibidores , Animais , Apoptose/genética , Materiais Biomiméticos/administração & dosagem , Ciclo Celular/genética , Movimento Celular/genética , Sinergismo Farmacológico , Neoplasias Esofágicas/genética , Neoplasias Esofágicas/patologia , Carcinoma de Células Escamosas do Esôfago/genética , Carcinoma de Células Escamosas do Esôfago/patologia , Feminino , Humanos , Camundongos Endogâmicos BALB C , Camundongos Nus , MicroRNAs/genética , Invasividade Neoplásica , Distribuição Aleatória , Transfecção/métodos , Ensaios Antitumorais Modelo de Xenoenxerto , Proteína ran de Ligação ao GTP/antagonistas & inibidores , Proteína ran de Ligação ao GTP/biossíntese , Proteína ran de Ligação ao GTP/genética
5.
J Cancer ; 9(22): 4242-4249, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30519325

RESUMO

Esophageal cancer is one of the leading malignancies globally and long non-coding RNAs (lncRNAs) have been proved to have an important role in different malignancies including esophageal cancer. However their role in disease progression is still not clear. The objective of the study was to investigate the expression and role of LINC01234 in progression of esophageal cancer cells. LncRNA LINC01234 was found to be upregulated in esophageal cancer cells by chip sequencing. The expression level of LINC01234 was detected from different esophageal cancer cell lines by qRT-PCR. After this, the LINC01234 knockdown effects on cell proliferation, migration, invasion, and apoptosis were evaluated by cell proliferation assay, wound healing assay, invasion assay, and flow cytometric analysis in vitro. Expression of lncRNA LINC01234 was found to be markedly upregulated in the CEC2 cell line. Furthermore, cell proliferation, migration and invasion were significantly (P < 0.05) suppressed as compared to negative control while apoptotic rate was also found increased as a result of the knockdown of LINC01234. Significantly upregulated expression of LINC01234 in CEC2 cells and downregulated expression after knockdown is observed. The impact of LINC01234 knockdown on cell migration, invasion, proliferation and apoptosis indicated that LINC01234 may represent a new marker and a potential therapeutic target for esophageal cancer.

6.
Gastroenterol Res Pract ; 2018: 2028986, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-29853858

RESUMO

Objective: The incidence of the upper gastrointestinal tumor has increased rapidly during recent decades. The relationship between local water pollution and the tumor is still not much clear, so this study was conducted to further investigate the local water pollution and its influence on the malignant cell transformation. Prevalence of human papillomavirus (HPV) in local esophageal cancer (EC) patients was also analyzed in Shenqiu County for the first time. Methods: Two-step cell transformation was used to study different sources of water in the malignant cell transformation, and the existence of 3-methylcholanthrene (3-MC) in water was analyzed from the river and shallow and deep wells. HPV DNA in tissue samples of EC patients was detected by polymerase chain reaction (PCR) and HPV diagnostic kit. Results: The river water has higher cytotoxicity than the shallow well water and induced significant cell malignant transformation, while deep well water has not shown the malignant cell transformation. In Huaihe River water, the 3-MC concentration was found higher than shallow and deep wells. An HPV infection rate was found high in patients with esophageal cancer. Conclusion: Long-term consumption of polluted water can induce malignant cell transformation, and the presence of HPV may be an important cause of cancer.

7.
J Pak Med Assoc ; 67(10): 1512-1516, 2017 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-28955066

RESUMO

OBJECTIVE: To elucidate the genetic risk and role of alpha-synuclein gene in the pathogenesis of Parkinson's disease in Pakistani population. METHODS: This case-control study was conducted at Institute of Biomedical and Genetic Engineering (IBGE), Islamabad from May 2013 to May 2016, and comprised patients with Parkinson's disease and their ethnically-matched healthy controls. Allele-specific polymerase chain reaction was used for screening of three pathogenic single nucleotide polymorphisms in alpha-synuclein gene. Moreover, 20% samples were randomly selected for bidirectional Sanger sequencing to confirm the results. SPSS 13 was used for data analysis. RESULTS: Of the 374 participants, 174(46.5%) were patients and 200(53.5%) were controls. The mean age for the onset of the disease was 55±13 years. No polymorphism was observed for rs104893875(G>A), rs104893877(G>A) and rs104893878(C>G) in alpha-synuclein gene in samples of patients and controls. CONCLUSIONS: Alpha-synuclein gene mutations might not be relevant to all the populations in causing Parkinson's disease.


Assuntos
Doença de Parkinson/epidemiologia , Doença de Parkinson/genética , Polimorfismo de Nucleotídeo Único/genética , alfa-Sinucleína/genética , Adulto , Idoso , Estudos de Casos e Controles , Humanos , Pessoa de Meia-Idade , Paquistão/epidemiologia , Reação em Cadeia da Polimerase
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