scholarly journals Sonophoresis Enhanced Transdermal Delivery of Cisplatin in the Xenografted Tumor Model of Cervical Cancer

2020 ◽  
Vol Volume 13 ◽  
pp. 889-902
Author(s):  
Shanshan Ma ◽  
Chang Liu ◽  
Bo Li ◽  
Tingting Zhang ◽  
Li Jiang ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Transdermal Delivery ◽  
Tumor Model ◽  
Xenografted Tumor

Long Non-Coding RNA ARAP1-AS1 Facilitates the Progression of Cervical Cancer by Regulating miR-149-3p and POU2F2

Pathobiology ◽  
2021 ◽  
pp. 1-12
Author(s):  
Ling Zhou ◽  
Xiao-li Xu
Keyword(s):  
Cervical Cancer ◽  
Tumor Model ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Non Coding Rna ◽  
Injection Model ◽  
Rna Immunoprecipitation ◽  
Long Non Coding Rna

<b><i>Background:</i></b> Emerging research has demonstrated that long non-coding RNAs (lncRNAs) attach great importance to the progression of cervical cancer (CC). LncRNA ARAP1-AS1 was involved in the development of several cancers; however, its role in CC is far from being elucidated. <b><i>Methods:</i></b> Real-time PCR (RT-PCR) was employed to detect ARAP1-AS1 and miR-149-3p expression in CC samples. CC cell lines (HeLa and C33A cells) were regarded as the cell models. The biological effect of ARAP1-AS1 on cancer cells was measured using CCK-8 assay, colony formation assay, flow cytometry, Transwell assay and wound healing assay in vitro, and subcutaneous xenotransplanted tumor model and tail vein injection model in vivo. Furthermore, interactions between ARAP1-AS1 and miR-149-3p, miR-149-3p and POU class 2 homeobox 2 (POU2F2) were determined by bioinformatics analysis, qRT-PCR, Western blot, luciferase reporter and RNA immunoprecipitation assay, respectively. <b><i>Results:</i></b> The expression of ARAP1-AS1 was enhanced in CC samples, while miR-149-3p was markedly suppressed. Additionally, ARAP1-AS1 overexpression enhanced the viability, migration, and invasion of CC cells. ARAP1-AS1 downregulated miR-149-3p via sponging it. ARAP1-AS1 and miR-149-3p exhibited a negative correlation in CC samples. On the other hand, ARAP1-AS1 enhanced the expression of POU2F2, which was validated as a target gene of miR-149-3p. <b><i>Conclusion:</i></b> ARAP1-AS1 was abnormally upregulated in CC tissues and indirectly modulated the POU2F2 expression via reducing miR-149-3p expression. Our study identified a novel axis, ARAP1-AS1/miR-149-3p/POU2F2, in CC tumorigenesis.

scholarly journals Crocetin Downregulates the Proinflammatory Cytokines in Methylcholanthrene-Induced Rodent Tumor Model and Inhibits COX-2 Expression in Cervical Cancer Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-5 ◽  
Author(s):  
Bing Chen ◽  
Zhao-Hui Hou ◽  
Zhe Dong ◽  
Chun-Dong Li
Keyword(s):  
Cervical Cancer ◽  
Interleukin 1 ◽  
Mrna Level ◽  
Tumor Model ◽  
Uterine Cervical Cancer ◽  
Polymorphonuclear Cells ◽  
Cervical Cancer Cells ◽  
Cox 2 ◽  
Oxide Synthase ◽  
Necrosis Factor

The effect of crocetin (C20H24O4) on methylcholanthrene- (MCA-) induced uterine cervical cancer in mice was studied in this paper. After the mice were treated orally with crocetin, maleic dialdehyde (MDA), polymorphonuclear cells (PMN), interleukin-1β(IL-1β), and tumor necrosis factor-α(TNF-α) were examined by ELISA or immunohistochemistry. The inducible nitric oxide synthase (iNOS) activation inHeLacells was analyzed using fluorescence microscopy for light microscopic examination. The MCA mice showed a significant increase in plasma MDA, PMN, IL-1β, TNF-α, and nitrates levels. At the same time, the mRNA level of COX-2 inHeLacells was also significantly increased. These changes were attenuated by crocetin supplementation in the MCA mice. Crocetin supplementation in the MCA mice also showed protection against cervical cancer. These results suggest that crocetin may act as a chemopreventive and an anti-inflammatory agent.

scholarly journals MicroRNA-373-3p inhibits the growth of cervical cancer by targeting AKT1 both in vitro and in vivo

2021 ◽  
Author(s):  
Min-Min Yu ◽  
Gen-ju Wang ◽  
Kai-Hua Wu ◽  
Song-Lin Xue ◽  
Li- Li Ju ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Tumor Model ◽  
Cell Counting ◽  
Over Expression ◽  
Cervical Carcinoma Cell Line ◽  
Cervical Cancer Cells ◽  
Mrna And Protein Expression

Objective: In this study, we aimed to investigate the function of microRNA-373-3p (miR-373-3p) in the pathogenesis of cervical cancer. Methods: Human and mouse cervical cancer cell lines were transfected with miR-373-3p mimic and inhibitor. Cell proliferation and viability were evaluated with Cell Counting Kit-8 (CCK-8) assay and Lactate Dehydrogenase (LDH) assay, respectively. The AKT1-targeting role of miR-373-3p was analyzed by qPCR and Western blot. Finally, a mouse xenograft cervical tumor model was adopted to study the in vivo effect of miR-373-3p on tumor growth and the expression of AKT1. Results: Over-expression of miR-373-3p significantly reduced the proliferation of cervical carcinoma cell line in vitro. In addition, miR-373-3p overexpression also inhibited cervical cancer growth in tumor-bearing mice. Mechanistically, we found that AKT1 gene can be targeted by miR-373-3p. MiR-373-3p mimic decreased the mRNA and protein expression of AKT1, while the miR-373-3p inhibitor increased the level of AKT1 in cervical cancer cells. AKT1 overexpression rescued the proliferation of cervical cancer cells transfected with miR-373-3p. Conclusion: MiR-373-3p can serve as a novel anti-tumor microRNA in cervical cancer by targeting AKT1.

scholarly journals Lysosomal dysfunction and autophagy blockade contribute to autophagy-related cancer suppressing peptide-induced cytotoxic death of cervical cancer cells through the AMPK/mTOR pathway

2020 ◽  
Vol 39 (1) ◽  
Author(s):  
Yang Yang ◽  
Qi Wang ◽  
Dongjian Song ◽  
Ruirui Zen ◽  
Lei Zhang ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Nude Mice ◽  
Tumor Model ◽  
Autophagic Flux ◽  
Factor Deficiency ◽  
Cervical Cancer Cells ◽  
Intracellular Process ◽  
Related Proteins

Abstract Background Autophagy is an intracellular process through which intracellular components are recycled in response to nutrient or growth factor deficiency to maintain homeostasis. We identified the peptide autophagy-related cancer-suppressing peptide (ARCSP), a potential antitumor peptide that disrupts intracellular homeostasis by blocking autophagic flux and causes cytotoxic death. Methods The proliferative ability of ARCSP-treated cervical cancer cells was examined by the CCK8, EdU, and colony formation assays. The TUNEL assay was used to detect apoptosis. Mitochondrial function was evaluated based on the mitochondrial membrane potential. Autophagic flux was detected by immunofluorescence and confocal microscopy. The autophagy-related proteins AMPK, Raptor, mTOR, p62, LC3B, atg7, Rab7, LAMP1, LAMP2, and cathepsin D were detected by Immunoblotting. The antitumor effect of ARCSP was explored in vivo by establishing a transplant tumor model in nude mice. Results The results demonstrated that ARCSP induced cell death and inhibited proliferation. ARCSP induced AMPK/mTOR activation, resulting in the accumulation of the proteins LC3B, p62 and Atg7. ARCSP also blocked autophagosome-lysosome fusion by inhibiting endosomal maturation and increasing the lysosomal pH. The accumulation of nonfused autophagosomes exacerbated cytotoxic death, whereas knocking down Atg7 reversed the cytotoxic death induced by ARCSP. ARCSP-treated cells exhibited increased cytotoxic death after cotreatment with an autophagy inhibitor (Chloroquine CQ). Furthermore, the tumors of ARCSP-treated nude mice were significantly smaller than those of untreated mice. Conclusions Our findings demonstrate that ARCSP, a novel lethal nonfused autophagosome inducer, might cause mitochondrial dysfunction and autophagy-related cytotoxic death and is thus a prospective agent for cancer therapy.

scholarly journals Circ-CCDC66 Upregulates REXO1 Expression to Aggravate Cervical Cancer Progression Via Restraining miR-452-5p

2020 ◽  
Author(s):  
Yun Zhang ◽  
Xing Li ◽  
Jun Zhang ◽  
Lin Mao
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cancer Progression ◽  
Tumor Model ◽  
Tumor Stage ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Cell Fractionation ◽  
Real Time Quantitative Pcr ◽  
Cancer Tumor

Abstract BackgroundCervical cancer is one most common cancer types among females around the world. CircRNAs have been revealed to participate in multiple biological functions, and are involved in many diseases’ progression. In current study, we aimed to elucidate whether circ-CCDC66 participates cervical cancer progression. MethodsReal-time quantitative PCR (RT-qPCR) was conducted to measure the expression of circ-CCDC66, miR-452-5p, and REXO1 mRNA. Cell fractionation assay and RNA fluorescence in situ hybridization (FISH) were performed to locate circ-CCDC66 in cells. Cell proliferation ability was detected using cell account kit 8 (CCK-8). TRANSWELL assay was applied to evaluate cell migration or invasion ability. Bioinformatics analysis, biotinylated RNA pull-down, RNA immunoprecipitation, and dual-luciferase reporter assays were conducted to assess the association between miR-452 and circ-CCDC66 or REXO1. Western blot was applied to measure the protein expression of REXO1. Animal tumor model was used to assess the effect of circ-CCDC66 in vivo.ResultsCirc-CCDC66 was upregulated in cervical cancer tumor tissues, and correlated with tumor stage and tumor size. Downregulation of circ-CCDC66 inhibited cervical cancer cell proliferation, migration, and invasion. Circ-CCDC66 was an efficient molecular sponge for miR-452-5p, and negatively regulated miR-452-5p expression. MiR-452 directly targeted REXO1. The effects of circ-CCDC66 on cervical cancer cells were functioned through miR-452-5p/REXO1 axis. In animal experiment, downregulation of circ-CCDC66 was found to suppress tumor growth in vivo.ConclusionOur results demonstrated the effects of circ-CCDC66/miR-452-5p/REXO1 axis in cervical cancer progression, we might provide a novel therapeutic target for cervical cancer.

Baicalein exerts antitumor effect in cervical cancer

2021 ◽  
Vol 11 (8) ◽  
pp. 1347-1353
Author(s):  
Yuhui Luo ◽  
Mingyan Wang ◽  
Li Zhang ◽  
Weining Jia ◽  
Erzhe Wengu ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Solid Tumor ◽  
Antitumor Effect ◽  
Tumor Volume ◽  
Tumor Model ◽  
Ascites Tumor ◽  
Tumor Tissues ◽  
Solid Tumor Model

The work verified that baicalein (BCN) inhibited the appearance and progress of cervical cancer in vitro and in vivo. MTT and CCK-8 methods were used to detect the toxicity of BCN to C33A cells and the number of C33A cells, respectively. For in vivo assays, a solid tumor model of cervical cancer and ascites tumor model was successfully established. The body weight, tumor volume and weight, survival time, and ascites volume were recorded. The anti-tumor ratio and increasing rate of life span were computed. H&E staining was performed to examine the liver tissues, kidney tissues, and tumor tissues. BCN inhibits the proliferation of human cervical cancer cell line C33A and induces apoptosis. The results from in vivo assays showed that BCN suppressed tumor growth and progression with decreased tumor volume and weight in a solid tumor model. BCN significantly induced cell apoptosis in solid tumor tissues. BCN also reduced ascites volume, prolonged survival time, and increased life extension rate in the ascites tumor model. These findings indicated that BCN exerted an antitumor effect against cervical cancer both in vitro and in vivo. According to the results, BCN might act as an important antitumor agent against cervical cancer.

scholarly journals Co-Administration of Anti-Angiogenic Peptide and DNA Vaccine in Cervical Cancer Tumor Model

2017 ◽  
Vol 10 (3) ◽  
Author(s):  
Parisa Saadat ◽  
Hoorieh Soleimanjahi ◽  
Seyed Mohsen Asghari ◽  
Maryam Fazeli ◽  
Hadi Razavinikoo ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Dna Vaccine ◽  
Tumor Model ◽  
Cancer Tumor

scholarly journals The augment of regulatory T cells undermines the efficacy of anti-PD-L1 treatment in cervical cancer

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Fengying Xu ◽  
Fengying Zhang ◽  
Qian Wang ◽  
Ying Xu ◽  
Shuifang Xu ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
T Cells ◽  
Regulatory T Cells ◽  
Checkpoint Inhibitors ◽  
Tumor Model ◽  
Clinical Samples ◽  
Tumor Growth Rate ◽  
Cervical Tumor ◽  
Great Expectation ◽  
Tumor Types

Abstract Background Immune checkpoint inhibitors have aroused great expectation of tumor eradication. However, the effect of anti-PD-L1 treatment for cervical cancer is unsatisfactory and the underlying antagonist to anti-PD-L1 efficacy is remained to be studied. Here, we investigated the anti-tumor effect of anti-PD-L1 treatment in cervical tumor model and identified the antagonist to the therapeutic efficacy of anti-PD-L1 treatment. Results We found that PD-L1 exhibited a moderate expression in both cervical tumor cell lines and clinical samples compared to other tumor types and the para-tumor tissue respectively. Interestingly, our results showed that the anti-PD-L1 treated mice were dichotomously divided into responsive and unresponsive group after five cycles of anti-PD-L1 treatment although all the mice had the same genome background. In addition, the unresponsive tumors showed less tumor necrosis area and higher immunosuppression activity induced by regulatory T cells (Tregs) population than the responsive ones. Furthermore, we found that anti-PD-L1 treatment autonomously upregulated Tregs proliferation and frequency in multiple immune organs, and, most importantly, Tregs depletion significantly depressed the tumor growth rate and tumor weight compared with either anti-PD-L1 or anti-CD25 treatment alone. Finally, we observed that the upregulating effector CD8+ T cell is associated with the better therapeutic effect of anti-PD-L1 therapy post Tregs depletion. Conclusions Anti-PD-L1 treatment upregulates Tregs frequency and proliferation in tumor model, and the depletion of Tregs may be a useful adjuvant strategy for anti-PD-L1 therapy of cervical cancer.

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