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 (-)-Epigallocatechin-3-Gallate Induces Apoptosis and Inhibits Invasion and Migration of Human Cervical Cancer Cells

2012 ◽  
Vol 13 (9) ◽  
pp. 4815-4822 ◽  
Author(s):  
Chhavi Sharma ◽  
Qurrat El-Ain Nusri ◽  
Salema Begum ◽  
Elham Javed ◽  
Tahir A. Rizvi ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Invasion And Migration ◽  
Cervical Cancer Cells ◽  
And Migration ◽  
Human Cervical Cancer Cells ◽  
Human Cervical Cancer

scholarly journals Elevated MYO10 Predicts Poor Prognosis and its Deletion Hampers Proliferation and Migration Potentials of Cells Through Rewiring PI3K/Akt Signaling in Cervical Cancer

2020 ◽  
Vol 19 ◽  
pp. 153303382093677
Author(s):  
Jian-Hui He ◽  
Jian-Guo Chen ◽  
Bin Zhang ◽  
Jing Chen ◽  
Ke-Li You ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Messenger Rna ◽  
Poor Prognosis ◽  
Akt Signaling ◽  
The Cancer Genome Atlas ◽  
Migration And Invasion ◽  
Invasion And Migration ◽  
And Migration ◽  
Cancer Tissues

MYO10, recognized as an important regulator of cytoskeleton remodeling, has been reported to be associated with tumorigenesis. However, its functional implication in cervical cancer and potential mechanism still remain to be undetermined currently. MYO10 level in cervical cancer tissues was analyzed by using data retrieved from The Cancer Genome Atlas and ONCOMINE databases. Messenger RNA and protein expression levels were determined by quantitative real-time polymerase chain reaction and Western blotting. Small-interfering RNA and overexpressing plasmid were used for MYO10 silencing and overexpression, and cell proliferation was analyzed by CCK-8. Transwell assays were performed to investigate the ability of cell migration and invasion. MYO10 was upregulated in cervical cancer tissues and cells when compared to normal controls, and survival analysis showed patients with high MYO10 expression had worse overall survival. Moreover, knockdown/overexpression of MYO10 significantly inhibited/enhanced the proliferation, invasion, and migration capabilities of cervical cells transfected with siRNAs/overexpressing plasmid. Additionally, MYO10 silencing inhibited PI3K/Akt signaling pathway by decreasing the phosphorylation status of PI3K and AKT. Data from the present study indicated that MYO10 were overexpressed in patients with cervical cancer and positively linked with poor prognosis. Experimental results suggested that MYO10 induced a significant encouraging effect in cervical cancer cell proliferation, invasion, and migration, linked with involvement of PI3K/Akt signaling. Collectively, these results emphasize a novel role for MYO10 overexpression in cervical cancer and provide a potent therapeutic strategy against cervical cancer.

Interleukin-6 Promotes Cervical Cancer Development Through Janus Kinase 2/Signal Transducer and Activator of Transcription 6 Signaling Pathway

2021 ◽  
Vol 11 (1) ◽  
pp. 76-83
Author(s):  
Jie Zhang ◽  
Xiuwu Tang ◽  
Zhixing Jin ◽  
Hong Zhang
Keyword(s):  
Cervical Cancer ◽  
Signaling Pathway ◽  
Janus Kinase ◽  
Invasion And Migration ◽  
Normal Tissues ◽  
In Vivo Experiments ◽  
And Migration ◽  
Cervical Cancer Development ◽  
Cancer Tissues

Interleukin (IL)-6 regulates several cellular processes such as proliferation, differentiation and immune regulation. The pathogenesis of cervical cancer is closely related to abnormal secretion and regulation of cytokines. IL-6 in the pathogenesis of cervical cancer was investigated in the present study. In our work, we collected cervical cancer tissues and adjacent normal tissues first and then established mouse model of cervical cancer for following assays. Immunohistochemistry and Western blot analysis were performed to detect IL-6, JAK3 and STAT6 and qRT-PCR determined VEGF, MMP-2, MMP-9 and others in adjacent tissues and cancer tissues. MTT was used to detect the capability of proliferation, invasion and migration. Chromatin immunoprecipitation was employed to verify the binding of STAT6 to IL-6. The effect of STAT6 inhibitors, AS1517499 on JAK3/STAT6 axis was also detected through in vivo experiments. Except IL-6, the related proteins were upregulated in cervical cancer tissues. IL-6 (25–100 ng/mL) accelerated the growth of Hela cells. IL-6 improved cell migratory and invasive ability when recombinant IL-6 promoted phosphory-lation and JAK3/STAT6. The activity of IL-6 in Hela was mediated by JAK3/STAT6 signaling pathway as AS1517499 inhibited IL-6-induced JAK3/STAT6 phosphorylation and STAT6 bound to the IL-6 promoter. STAT6 inhibitors significantly suppressed tumor growth and reduced p-STAT3 level. IL-6 contributes to cervical cancer through JAK3/STAT6 signaling which could be a cornerstone of subsequent anti-cervical cancer treatment.

scholarly journals MiR-188-3p and miR-133b Suppress Cell Proliferation in Human Hepatocellular Carcinoma via Post-Transcriptional Suppression of NDRG1

2021 ◽  
Vol 20 ◽  
pp. 153303382110330
Author(s):  
Zhenzhao Luo ◽  
Yue Fan ◽  
Xianchang Liu ◽  
Shuiyi Liu ◽  
Xiaoyu Kong ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Cell Migration ◽  
Cell Growth ◽  
Suppressive Effect ◽  
Luciferase Reporter ◽  
Invasion And Migration ◽  
And Migration ◽  
Cancer Tissues ◽  
Suppress Cell Proliferation

Background: Previous studies reported that N-myc downstream-regulated gene 1 (NDRG1) was upregulated in various cancer tissues and decreased expression of miR-188-3p and miR-133b could suppress cell proliferation, metastasis, and invasion and induce apoptosis of cancer cells. However, the molecular mechanism of NRDG1 involved in hepatocellular carcinoma (HCC) tumorigenesis is still unknown. Methods: The expressions of miR-188-3p, miR-133b, and NRDG1 in HCC tissues and cells were quantified by qRT-PCR and Western blot. MTT assay and transwell invasion assay were performed to evaluate cell growth and cell migration, respectively. Luciferase reporter assay were performed to determine whether miR-188-3p and miR-133b could directly bind to NRDG1 in HCC cells. Results: The results showed that NRDG1 was upregulated and these 2 microRNAs were downregulated in HCC tissues. NRDG1 was negatively correlated with miR-188-3p and miR-133b in HCC tissues. MiR-188-3p and miR-133b were demonstrated to directly bind to 3′UTR of NRDG1 and inhibit its expression. Upregulation of miR-188-3p and miR-133b reduced NRDG1 expression in hepatocellular carcinoma cell lines, which consequently inhibited cell growth and cell migration. Conclusions: Our finding suggested that miR-188-3p and miR-133b exert a suppressive effect on hepatocellular carcinoma proliferation, invasion, and migration through downregulation of NDRG1.

scholarly journals RNA-sequencing identified miR-3681 as a negative regulator in the proliferation and migration of cervical cancer cells via the posttranscriptional suppression of HGFR

RSC Advances ◽  
2019 ◽  
Vol 9 (39) ◽  
pp. 22376-22383 ◽  
Author(s):  
Fan Shi ◽  
Yingbing Zhang ◽  
Juan Wang ◽  
Jin Su ◽  
Zi Liu ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Rna Sequencing ◽  
Negative Regulator ◽  
Tumor Tissues ◽  
Differentially Expressed Mirnas ◽  
Cervical Cancer Cells ◽  
And Migration ◽  
Cancer Tissues ◽  
Proliferation And Migration

In this study, RNA-sequencing was used to investigate the differentially expressed miRNAs between cervical cancer tissues and matched adjacent non-tumor tissues.

miR-340 Inhibits the Development of Hepatocellular Carcinoma by Down-Regulating Akt Signaling Pathway

2021 ◽  
Vol 11 (9) ◽  
pp. 1785-1791
Author(s):  
Tangpeng Xu ◽  
Changli Ruan ◽  
Xu Bin ◽  
Mengxue Hu
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Pathological Grade ◽  
Akt Signaling Pathway ◽  
Invasion And Migration ◽  
Proliferation Ability ◽  
And Migration ◽  
Cancer Tissues

Hepatocellular carcinoma (HCC) is a serious threat to human health. miR-340 participates in HCC pathogenesis, but its specific mechanism is not completely clear. Therefore, our study assessed the mechanism by how miR-340 involves in HCC. The cancer tissues and paracancerous tissues of HCC patients were collected. miR-340 mimics/NC and Akt siRNA were transfected into HepG2 cells followed by analysis of miR-304 and EMT-related molecules expression by Real-time PCR, cell invasion and migration by Transwell assay, cell proliferation ability by CCK8 assay as well as p-Akt and p-mTOR level by Western blot. miR-340 in HCC tissues was significantly downregulated compared to adjacent tissues (P <0.001). With increased pathological grade, miR-340 expression was decreased gradually. p-Akt and p-mTOR in HCC tissues was significantly upregulated and elevated gradually with increased pathological grade. p-Akt and p-mTOR was negatively associated with miR-340 (P <0.001). After overexpression of miR-340, HepG2 cell proliferation, invasion, migration and epithelialization were significantly inhibited, and p-Akt and p-mTOR was reduced. When Akt expression was interfered with siRNA, cell proliferation and epithelialization was further inhibited. miR-340 inhibits the development of hepatocellular carcinoma through Akt signaling pathway.

scholarly journals The Long Non-Coding RNA XIST Interacted with MiR-124 to Modulate Bladder Cancer Growth, Invasion and Migration by Targeting Androgen Receptor (AR)

2017 ◽  
Vol 43 (1) ◽  
pp. 405-418 ◽  
Author(s):  
Yaoyao Xiong ◽  
Long Wang ◽  
Yuan Li ◽  
Minfeng Chen ◽  
Wei He ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Androgen Receptor ◽  
Cancer Cells ◽  
Cancer Growth ◽  
Invasion And Migration ◽  
Non Coding Rna ◽  
Bladder Cancer Cells ◽  
And Migration ◽  
Cancer Tissues ◽  
Long Non Coding Rna

Backgrounds/Aims: Long non-coding RNA (lncRNA) X-inactive specific transcript (XIST) is involved in the progression of several tumors. The interaction between lncRNA and miRNA or miRNA’s target genes is reported to play crucial roles in malignancy. In addition, Androgen receptor (AR) is considered to be involved in bladder cancer progression. In this study, we investigated the role of XIST in human bladder cancer and its interaction with miR-124 and AR. Methods: XIST and AR expression was detected in bladder tumor samples and cell lines. Effects of XIST and AR on bladder cancer cells growth, invasion and migration were analyzed. Bioinformatic analysis and luciferase assays were used to identify the interaction among XIST, AR and miR-124. The correlations of miR-124 with XIST and AR in bladder cancer samples were statistically analyzed. Results: XIST and AR were upregulated in bladder cancer tissues and positively correlated. Higher XIST and AR expression were related to poorer TNM stage of bladder cancer. XIST knockdown reduced bladder cancer cells’ proliferation, invasion and migration. While this inhibitory effect could be partially restored by AR overexpression. XIST inhibited miR-124 expression by directly targeting. Moreover, miR-124 could bind to the 3’UTR of AR to regulate its expression. MiR-124 inhibition partially restored the XIST knockdown-induced reduction of AR, c-myc, p27, MMP13 and MMP9 expression. In bladder cancer tissues, miR-124 level was inversely correlated with the expression of XIST and AR, respectively. Conclusion: These findings indicated that XIST might be an oncogenic lncRNA that promoted the bladder cancer growth, invasion and migration via miR-124 dependent AR regulation.

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