scholarly journals Transcriptome Analysis Identified Elevated Expression of Bone Gamma-carboxyglutamic acid-containing Protein (BGLAP) in Human Cervical Cancer Tissues

2018 ◽  
Vol 11 (2) ◽  
pp. 1119-1126
Author(s):  
Anjali Devi S. Bettadapura ◽  
Vijay K. Munivenkatappa ◽  
Subba Rao V. Madhunapantula
Keyword(s):  
Cervical Cancer ◽  
Transcriptome Analysis ◽  
Carboxyglutamic Acid ◽  
Elevated Expression ◽  
Cancer Tissues ◽  
Human Cervical Cancer

ANXA2 is a potential marker for the diagnosis of human cervical cancer

2021 ◽  
Vol 15 (1) ◽  
pp. 57-67
Author(s):  
Zhe Wang ◽  
Chenhao Jiang ◽  
Lijuan Pang ◽  
Wei Jia ◽  
Chengyan Wang ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Membranes ◽  
Bioinformatics Analysis ◽  
High Specificity ◽  
Invasion And Migration ◽  
Potential Marker ◽  
Specificity And Sensitivity ◽  
And Migration ◽  
Cancer Tissues ◽  
Human Cervical Cancer

Aim: The aim is to study ANXA2 biomarkers for early diagnosis of cervical cancer. Materials & methods: The study used bioinformatics analysis and experimental verification of ANXA2 expression in cervical cancer. Results: ANXA2 expression was higher in cancer tissues than in non-cancer tissues (p = 0.002). ANXA2 was expressed in cell membranes of non-cancer tissues, whereas in cancer tissues it was expressed in both the cell membranes and the cytoplasm. Moreover, ANXA2 expression was more pronounced in squamous cell carcinomas. ANXA2 expression decreased overall survival of patients, and the data suggested that protein expression was associated with invasion and migration of tumors. Conclusion: ANXA2 has high specificity and sensitivity as a detection marker for cervical cancer and can assist in the diagnosis of cervical cancer.

scholarly journals Expression and significance of FOXM1 in human cervical cancer: A tissue micro-array study

2011 ◽  
Vol 34 (1) ◽  
pp. 1 ◽  
Author(s):  
Ping Guan ◽  
Hong Chen ◽  
Hua-Ju Li ◽  
Jie Duan ◽  
Jing-Yi Chen
Keyword(s):  
Cervical Cancer ◽  
Lymph Node ◽  
Lymph Node Status ◽  
Tissue Micro Array ◽  
Nuclear Expression ◽  
Node Status ◽  
Foxm1 Protein ◽  
Cancer Tissues ◽  
Pathological Stages ◽  
Human Cervical Cancer

Objective: This study was designed to investigate the expression and significance of the Forkhead Box M1 (FOXM1) transcription factor in human cervical cancer. Methods: The expression of FOXM1 protein was assessed in tissue microarrays containing 102 cervical cancer tissues by the Streptavidin–Peroxidase (SP) immunohistochemitry technique. The relationship between FOXM1 protein and clinico-pathological features (pathological stages, pathological types, TNM stage) was analyzed. Results: FOXM1 protein was located in the cytoplasma and/or nucleus. The overall expression of FOXM1 in the cytoplasm and nucleus was not associated with T stages (P=0.217) or lymph node status (P=0.313). The nuclear expression of FOXM1 protein was not associated with T stage (P=0.508) or lymph node status (P=0.345). Elevated translocation and activity of FOXM1 were discovered with a secondary analysis that showed that the differences of the nuclear expression of FOXM1, among different pathological stages, were statistically significant (P < 0.05). The nuclear expression of FOXM1 in low differential cervical cancer tissues was significantly higher than in high differential cervical cancer tissues (P < 0.05). Conclusion: The overexpression of FOXM1 protein in cervical cancer maybe associated with the progression of cervical cancer, and could be a potentially novel tumor marker useful for diagnosis and therapy of cervical cancer.

scholarly journals MicroRNA-425 induces apoptosis and suppresses migration and invasion of human cervical cancer cells by targeting RAB2B

2021 ◽  
Vol 35 ◽  
pp. 205873842110161
Author(s):  
Yue Tian ◽  
Ying Luo ◽  
Jing Wang
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Migration And Invasion ◽  
Cervical Cancer Cells ◽  
Induction Of Apoptosis ◽  
Cancer Tissues ◽  
Human Cervical Cancer

Dysregulation of microRNA-425 (miR-425) has been reported in several human cancers. However, the role of miR-425 in human cervical cancer via modulation of RAB2B expression is still unclear. This study was therefore designed to examine the expression and decipher the role of miR-425 in cervical cancer. The qRT-PCR was used for expression analysis. MTT and EdU assays were used for the determination of cell viability and proliferation, respectively. Annexin V/PI staining was used to detect apoptosis. Wound healing and transwell assays were used to monitor cell migration and invasion. Western blotting was used for protein expression analysis. The in vivo study was performed in xenografted mice model. The results of the present study revealed miR-425 to be significantly ( P = 0.032) down-regulated in cervical cancer tissues and cell lines. Additionally, low expression of miR-425 was associated with significantly ( P = 0.035) lower survival rate of the cervical cancer patients. Overexpression of miR-425 resulted in significant ( P = 0.024) decline of cervical cancer cell proliferation via induction of apoptosis. The induction of apoptosis was associated with up-regulation of Bax and down-regulation of Bcl-2. Besides, the migration and invasion of cancer cells significantly ( P < 0.01) decreased under miR-425 overexpression. Additionally, miR-425 could inhibit the growth of xenografted tumors in vivo. In silico analysis and dual luciferase assay revealed RAB2B as the direct target of miR-425 in cervical cancer. RAB2B was found to be significantly ( P < 0.05) up-regulated in cervical cancer tissues and cell lines and miR-425 overexpression suppressed the expression of RAB2B. Additionally, silencing of RAB2B could suppress the growth of cervical cancer cells but its overexpression could rescue the tumor-suppressive effects of miR-425. Taken together, the results revealed the tumor-suppressive roe of miR-425 and point towards its therapeutic potential in the management of cervical cancer.

Artepillin C Induces Selective Oxidative Stress and Inhibits Migration and Invasion in a Comprehensive Panel of Human Cervical Cancer Cell Lines

2019 ◽  
Vol 18 (12) ◽  
pp. 1750-1760 ◽  
Author(s):  
Raquel P. Souza ◽  
Patrícia S. Bonfim-Mendonça ◽  
Gabrielle M.Z.F. Damke ◽  
Analine R.B. de-Assis Carvalho ◽  
Bianca A. Ratti ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cervical Cancer ◽  
Cell Lines ◽  
Migration And Invasion ◽  
Epithelial Cell Line ◽  
Cellular Viability ◽  
Hpv 16 ◽  
Anticancer Properties ◽  
Artepillin C ◽  
Human Cervical Cancer

Background: Artepillin C (3,5-diprenyl-4-hydroxycinnamic acid) is the main bioactive component of Brazilian green propolis, and possesses, among other things, anticancer properties. However, to the best of our knowledge, there are no studies of artepillin C in cervical cancer. Method: To explore a new therapeutic candidate for cervical cancer, we have evaluated the effects of artepillin C on cellular viability in a comprehensive panel of human cervical cancer-derived cell lines including HeLa (human papillomavirus/HPV 18-positive), SiHa (HPV 16-positive), CaSki (HPV 16- and 18-positive) and C33A (HPV-negative) cells compared to a spontaneously immortalized human epithelial cell line (HaCaT). Results: Our results demonstrated that artepillin C had a selective effect on cellular viability and could induce apoptosis possibly by intrinsic pathway, likely a result of oxidative stress, in all cancer-derived cell lines but not in HaCaT. Additionally, artepillin C was able to inhibit the migration and invasion of cancer cells. Conclusion: Thus, artepillin C appears to be a promising new candidate as an anticancer drug for cervical cancer induced by different HPV types.

SUV39H1-Mediated DNMT1 is Participated in the Epigenetic Regulation of Smad3 in Cervical Cancer

2020 ◽  
Vol 20 ◽  
Author(s):  
Li Zhang ◽  
Sijuan Tian ◽  
Minyi Zhao ◽  
Ting Yang ◽  
Shimin Quan ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Lines ◽  
Epigenetic Regulation ◽  
Promoter Region ◽  
Methylation Status ◽  
Regulation Mechanism ◽  
Methylation Specific Pcr ◽  
Specific Pcr ◽  
Immune Factor ◽  
Cancer Tissues

Background: Smad3 is a pivotal intracellular mediator for participating in the activation of multiple immune signal pathway. Objective: The epigenetic regulation mechanism of the positive immune factor Smad3 in cervical cancer remains unknown. Therefore, the epigenetic regulation on Smad3 is investigated in this study. Methods: The methylation status of SMAD3 was detected by Methylation-specific PCR (MS-PCR) and Quantitative Methylation-specific PCR (MS-qPCR) in cervical cancer tissues and cell lines. The underlying molecular mechanisms of SUV39H1-DNMT1-Smad3 regulation was elucidated using cervical cancer cell lines containing siRNA or/and overexpression system. Confirmation of the regulation of DNMT1 by SUV39H1 used Chromatin immunoprecipitation-qPCR (ChIP-qPCR). The statistical methods used for comparing samples between groups were paired t tests and one-way ANOVAs. Results: H3K9me3 protein which regulated by SUV39H1 directly interacts with the DNMT1 promoter region to regulate its expression in cervical cancer cells, resulting in the reduce expression of the downstream target gene DNMT1. In addition, DNMT1 mediates the epigenetic modulation of the SMAD3 gene by directly binding to its promoter region. The depletion of DNMT1 effectively restores the expression of Smad3 in vitro. Moreover, in an in vivo assay, the expression profile of SUV39H1-DNMT1 was found to correlate with Smad3 expression in accordance with the expression at the cellular level. Notably, the promoter region of SMAD3 was hypermethylated in cervical cancer tissues, and this hypermethylation inhibits the subsequent gene expression. Conclusion: These results indicate that SUV39H1-DNMT1 is a crucial Smad3 regulatory axis in cervical cancer. SUV39H1-DNMT1 axis may provide a potential therapeutic target for the treatment of cervical cancer.

Genistein Induces Alterations of Epigenetic Modulatory Signatures in Human Cervical Cancer Cells

2018 ◽  
Vol 18 (3) ◽  
pp. 412-421 ◽  
Author(s):  
Madhumitha Kedhari Sundaram ◽  
Mohammad Zeeshan Ansari ◽  
Abdullah Al Mutery ◽  
Maryam Ashraf ◽  
Reem Nasab ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
In Silico ◽  
Tumour Suppressor Genes ◽  
Dietary Polyphenols ◽  
In Silico Studies ◽  
Genistein Treatment ◽  
Cervical Cancer Cells ◽  
Human Cervical Cancer Cells ◽  
Human Cervical Cancer

Introduction: Epidemiological studies indicate that diet rich in fruits and vegetables is associated with decreased cancer risk thereby indicating that dietary polyphenols can be potential chemo-preventive agents. The reversible nature of epigenetic modifications makes them a favorable target for cancer prevention. Polyphenols have been shown to reverse aberrant epigenetic patterns by targeting the regulatory enzymes, DNA methyltransferases (DNMTs) and histone deacetylases (HDACs). In vitro and in silico studies of DNMTs and HDACs were planned to examine genistein’s role as a natural epigenetic modifier in human cervical cancer cells, HeLa. Methods: Expression of the tumour suppressor genes (TSGs) [MGMT, RARβ, p21, E-cadherin, DAPK1] as well the methylation status of their promoters were examined alongwith the activity levels of DNMT and HDAC enzymes after treatment with genistein. Expression of DNMTs and HDACs was also studied. In-silico studies were performed to determine the interaction of genistein with DNMTs and HDACs. Results: Genistein treatment significantly reduced the expression and enzymatic activity of both DNMTs and HDACs in a time-dependent way. Molecular modeling data suggest that genistein can interact with various members of DNMT and HDAC families and support genistein mediated inhibition of their activity. Timedependent exposure of genistein reversed the promoter region methylation of the TSGs and re-established their expression. Conclusions: In this study, we find that genistein is able to reinstate the expression of the TSGs studied by inhibiting the action of DNMTs and HDACs. This shows that genistein could be an important arsenal in the development of epigenetic based cancer therapy.

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