scholarly journals Qualitative and Quantitative Analysis of Tumor Cell Invasion Using Au Clusters

Nanomaterials ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 145
Author(s):  
Xiangchun Zhang ◽  
Qinqin Zheng ◽  
Ziqi Wang ◽  
Chao Xu ◽  
Haolei Han ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Quantitative Analysis ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Tumor Invasion ◽  
Inductively Coupled Plasma ◽  
Optical Microscope ◽  
Au Clusters ◽  
Icp Ms ◽  
Cervical Cancer Cells

Tumor invasion/metastasis is still the major cause of death in cancer patients. Membrane type-1 matrix metalloproteinase (MT1-MMP) is directly related to tumor invasion/metastasis. To accurately and quickly distinguish the risk of invasion/metastasis of primary tumor cells, it is urgent to develop a simple and precise quantitative method to distinguish the expression level of MT1-MMP. In this work, we have constructed red fluorescent Au clusters with peroxidase-like properties that could specifically bind to MT1-MMP on human cervical cancer cells. After MT1-MMP was labelled with Au clusters, we could visually see red fluorescence of MT1-MMP on cervical cancer cells via fluorescence microscopy and catalytic color imaging using an ordinary optical microscope. The constructed Au clusters contained 26 Au atoms; thus, the amount of MT1-MMP on cervical cancer cells could be accurately quantified using inductively coupled plasma mass spectrometry (ICP-MS). More importantly, the invasion/metastasis capabilities of the cervical cancer Siha, Caski and Hela cells with different MT1-MMP amounts could be accurately distinguished by fluorescence/catalysis qualitative imaging and ICP-MS quantitative analysis. This method of qualitative/quantitative analysis of tumor-associated proteins on cancer cells has great potential for accurately diagnosing aggressive tumor cells and assessment of their invasion/metastasis risk.

scholarly journals CLDN1 expression in cervical cancer cells is related to tumor invasion and metastasis

Oncotarget ◽  
2016 ◽  
Vol 7 (52) ◽  
pp. 87449-87461 ◽  
Author(s):  
Wei-na Zhang ◽  
Wei Li ◽  
Xiao-li Wang ◽  
Zheng Hu ◽  
Da Zhu ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Tumor Invasion ◽  
Invasion And Metastasis ◽  
Cervical Cancer Cells

scholarly journals Impact of Poly (Styrene–Acrylic Acid) Latex Nanoparticles on Colorectal and Cervical Cancer Cells

Polymers ◽  
2021 ◽  
Vol 13 (13) ◽  
pp. 2025
Author(s):  
Munther Alomari ◽  
Arwa Almahasheer ◽  
Balasamy Rabindran Jermy ◽  
Amal A. Al-Dossary ◽  
Hiba Bahmdan ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Cervical Cancer ◽  
Acrylic Acid ◽  
Cancer Cells ◽  
Drug Loading ◽  
Optical Microscope ◽  
Polymerization Process ◽  
Latex Particles ◽  
Cervical Cancer Cells ◽  
The Impact

Polymer nanoparticles are a promising approach for cancer treatment and detection, due to their biocompatibility, biodegradability, targeting capabilities, capacity for drug loading and long blood circulation time. This study aims to evaluate the impact of poly (styrene–acrylic acid) latex particles on colorectal and cervical cancer cells for anti-tumor efficiency. Latex particles were synthesized by a surfactant-free radical emulsion polymerization process and the obtained polymer particles were characterized in terms of size, size distribution, morphology using scanning electron microscopy (SEM) and transmission electron microscopy (TEM), and electrokinetic property (i.e., zeta potential). Human colorectal and cervical cancer, and normal cell lines, were then treated with different concentrations of poly (styrene–acrylic acid) latex particles. The cell morphology changes were pointed out using an optical microscope and the nanoparticles’ (NPs) cell cytotoxicity was evaluated using MTT assay. The obtained results showed that poly (styrene–acrylic acid) latex particles are effective against colorectal and cervical cancer cells if treated with an appropriate particle concentration for 48 h. In addition, it showed that normal cells are the least affected by this treatment. This indicates that these NPs are safe as a drug delivery carrier when used at a low concentration.

scholarly journals Expression of the long noncoding RNA DINO in HPV positive cervical cancer cells reactivates the dormant TP53 tumor suppressor through ATM/CHK2 signaling

2020 ◽  
Author(s):  
Surendra Sharma ◽  
Karl Munger
Keyword(s):  
Cervical Cancer ◽  
Tumor Suppressor ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Wild Type ◽  
Hpv E6 ◽  
Cervical Cancer Cells ◽  
Transcriptional Target

ABSTRACTTumor cells overcome the cytostatic and cytotoxic restraints of TP53 tumor suppressor signaling through a variety of mechanisms. High-risk human papillomavirus (HPV) positive tumor cells retain wild type TP53 because the HPV E6/UBE3A ubiquitin ligase complex targets TP53 for proteasomal degradation. While restoration of TP53 in tumor cells holds great promise for cancer therapy, attempts to functionally restore the dormant TP53 tumor suppressor in HPV positive cancer cells by inhibiting the HPV E6/UBE3A ubiquitin ligase complex have not yet been successful. The Damage Induced long noncoding RNA, DINO, (DINOL) is a TP53 transcriptional target that has been reported to bind to and stabilize TP53, thereby amplifying TP53 signaling. We show that HPV positive cervical carcinoma cells contain low levels of DINO because of HPV E6/UBE3A mediated TP53 degradation. Acute DINO expression overrides HPV16 E6/UBE3A mediated TP53 degradation, causing TP53 stabilization and increased expression of TP53 transcriptional target genes. This causes a marked sensitization to chemotherapy agents and renders cells vulnerable to metabolic stress. Acute DINO expression in HPV positive cervical cancer cells induces hallmarks of DNA damage response signaling and TP53 activation involves ATM/CHK2 signaling. DINO upregulation in response to DNA damage is independent of ATM/CHK2 and can occur in cancer cells that express mutant TP53.IMPORTANCEFunctional restoration of the TP53 tumor suppressor holds great promise for anti-cancer therapy. Current strategies are focused on modulating TP53 regulatory proteins. Long noncoding RNAs (lncRNAs) have emerged as important regulators of TP53 as well as modulators of downstream tumor suppressive transcriptional responses. Unlike many other cancer types, human papillomavirus (HPV) positive cancer cells retain wild type TP53 that is rendered dysfunctional by the viral E6 protein. We show that acute expression of the Damage Induced long Noncoding RNA, DINO, a known TP53 transcriptional target and functional modulator, causes TP53 reactivation in HPV positive cervical cancer cells. This causes increased vulnerability to standard chemotherapeutics as well as biguanide compounds that cause metabolic stress. Hence, strategies that target DINO may be useful for restoring TP53 tumor suppressor activity in HPV positive cancers and other tumor types that retain wild type TP53.

scholarly journals Pentoxifylline Sensitizes Cisplatin-Resistant Human Cervical Cancer Cells to Cisplatin Treatment: Involvement of Mitochondrial and NF-Kappa B Pathways

2020 ◽  
Vol 10 ◽  
Author(s):  
Alejandro Bravo-Cuellar ◽  
Pablo Cesar Ortiz-Lazareno ◽  
Erick Sierra-Díaz ◽  
Fabiola Solorzano-Ibarra ◽  
Anibal Samael Méndez-Clemente ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Public Health Problem ◽  
Major Public Health Problem ◽  
Nf Kappa B ◽  
Apoptotic Protein ◽  
Cervical Cancer Cells ◽  
Parp 1

BackgroundCervical cancer continues to be a major public health problem worldwide, and Cisplatin is used as first-line chemotherapy for this cancer; however, malignant cells exposed to CISplatin (CIS) become insensitive to the effects of this drug. PenToXifylline (PTX) is a xanthine that sensitizes several types of tumor cells to apoptosis induced by antitumor drugs, such as Adriamycin, Carboplatin, and CIS. The effects of PTX on tumor cells have been related to the disruption of the NF-κB pathway, thus preventing the activation of cell survival mechanisms such as the expression of anti-apoptotic genes, the secretion of proinflammatory interleukins, and growth factors.ObjectiveIn this work, we studied the antitumor proprieties of PTX in human SiHa cervical carcinoma cells resistant to CIS.Materials and MethodsSiHa and HeLa cervical cancer cells and their CIS-resistant derived cell lines (SiHaCIS-R and HeLaCIS-R, respectively) were used as in-vitro models. We studied the effects of PTX alone or in combination with CIS on cell viability, apoptosis, caspase-3, caspase-8, and caspase-9 activity, cleaved PARP-1, anti-apoptotic protein (Bcl-2 and Bcl-xL) levels, p65 phosphorylation, cadmium chloride (CdCl2) sensitivity, Platinum (Pt) accumulation, and glutathione (GSH) levels, as well as on the gene expression of GSH and drug transporters (influx and efflux).ResultsPTX sensitized SiHaCIS-R cells to the effects of CIS by inducing apoptosis, caspase activation, and PARP-1 cleavage. PTX treatment also decreased p65 phosphorylation, increased Pt levels, depleted GSH, and downregulated the expression of the ATP7A, ATP7B, GSR, and MGST1 genes.ConclusionPTX reverses the acquired phenotype of CIS resistance close to the sensitivity of parental SiHa cells.

Effect on humoral and cellular immunity and on apoptosis in CIN2, CIN3, and HPV16+ cervical cancer of therapeutic divalent genetic vaccination with CMV replicon system (CRS) delivering HPV16 recombinantly mutated E6 and E7 viral oncogenes targeting p53 and Rb, respectively

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. 3062-3062
Author(s):  
J. Giannios ◽  
J. Peristeris ◽  
N. Alexandropoulos ◽  
T. Kononas ◽  
P. Ginopoulos
Keyword(s):  
Cervical Cancer ◽  
Immune Responses ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Binding Sites ◽  
Injection System ◽  
Cellular Immune Responses ◽  
Cervical Cancer Cells ◽  
E6 And E7 ◽  
Cellular Immune

3062 Background: Prophylactic vaccines have no therapeutic capacity for all the women who are already infected with HPV16 and have developed cervical intraepithelial neoplasia (CIN) or cervical cancer. Approximately 300 million women with CIN and cervical cancer will require therapy in the next decades. Thus, there is a great demand for a therapeutic HPV vaccine. Methods: We developed a cytomegalovirus (CMV) replicon system (CRS) for delivery of the HPV16 recombinantly mutated E6 and E7 genes replacing part of the CMV genome for the HPV genes, which were genetically altered to block binding sites for p53 and Rb.The replicon-vectors infected and co-transfected CIN and cervical cancer cells in animal models derived from HPV16(+) CIN, and cervical Ca cells obtained from patients. The genetic vaccine was administered subcutaneously (SC) with a needless injection system. Results: After vaccination,the viral E6 oncogene did not degrade apoptotic p53, and it blocked activation of telomerase. This induced apoptosis and DNA repair in CIN and cervical cancer cells. Furthermore, the E7 viral oncogene did not degrade the retinoblastoma oncogene (Rb) protein releasing transcription factor E2F. This vaccination led to scheduled cell cycle entry, genetic stability, and mortalization of tumor cells. Humoral and cellular immune responses were exhibited, which led to irreversible D2 apoptotic stage of PCD type I leading to a bystander killing effect of CIN, and cervical cancer cells. BrdU and MTT analysis exhibited inhibition of DNA synthesis and metabolic activity of vaccinated tumor cells compared to controls. Conclusions: This genetic divalent vaccine coding for E6 and E7 mutations designed to prevent p53 and Rb binding sites activated humoral and cellular immune responses leading to apoptosis of CIN and cervical cancer cells. It is up to translational medicine to bring this therapeutic vaccine into the clinic for patients with CIN2, CIN3, and cervical cancer patients. No significant financial relationships to disclose.

scholarly journals LncRNA OIP5-AS1 Regulates the Warburg Effect Through miR-124-5p/IDH2/HIF-1α Pathway in Cervical Cancer

2021 ◽  
Vol 9 ◽  
Author(s):  
Li Li ◽  
Yan Ma ◽  
Kamalibaike Maerkeya ◽  
Davuti Reyanguly ◽  
Lili Han
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Warburg Effect ◽  
Hypoxia Inducible Factor ◽  
Hypoxic Condition ◽  
Cervical Cancer Cells ◽  
The Warburg Effect

Hypoxia reprogrammed glucose metabolism affects the Warburg effect of tumor cells, but the mechanism is still unclear. Long-chain non-coding RNA (lncRNA) has been found by many studies to be involved in the Warburg effect of tumor cells under hypoxic condition. Herein, we find that lncRNA OIP5-AS1 is up-regulated in cervical cancer tissues and predicts poor 5-years overall survival in cervical cancer patients, and it promotes cell proliferation of cervical cancer cells in vitro and in vivo. Moreover, OIP5-AS1 is a hypoxia-responsive lncRNA and is essential for hypoxia-enhanced glycolysis which is IDH2 or hypoxia inducible factor-1α (HIF-1α) dependent. In cervical cancer cells, OIP5-AS1 promotes IDH2 expression by inhibiting miR-124-5p, and IDH2 promotes the Warburg effect of cervical under hypoxic condition through regulating HIF-1α expression. In conclusion, hypoxia induced OIP5-AS1 promotes the Warburg effect through miR-124-5p/IDH2/HIF-1α pathway in cervical cancer.

scholarly journals The IFN-γ-IDO1-Kynureine Pathway-Induced Autophagy in Cervical Cancer Cell Promotes Phagocytosis of Macrophage

2020 ◽  
Author(s):  
Shao-Liang Yang ◽  
Hai-Xia Tan ◽  
Tian-Tian Niu ◽  
Yu-Kai Liu ◽  
Chun-Jie Gu ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Cancer Cell ◽  
Cervical Cancer Cell ◽  
Tryptophan Depletion ◽  
Siha Cells ◽  
Cervical Cancer Cells ◽  
Ido1 Expression ◽  
Ifn Γ

Abstract Bachground: Cervical cancer is a common malignant disease in female patients accompanied by active autophagy in tumor cells. However, much remains unknown about the regulatory factors of autophagy and its effect on immune response.Methods: Autophagy in HeLa and SiHa cells treated with IFN-γ, tryptophan depletion, kynurenine, and epacadostat was detected by western blot and autophagy detection kit. After co-cultured with pre-treated HeLa and SiHa cells, U937 was detected by flow cytometry to analyze the CD80, CD86, CD163, CD206 expression and the phagocytosis. Results: IFN-γ could significantly increase the autophagy level of HeLa and SiHa cells by promoting the indoleamine-2,3-dioxygenase-1 (IDO1) expression. HeLa and SiHa cells treated with recombinant human IFN-γ could significantly increase the phagocytosis and CD80, CD86 expression of U937, and this effect was associated with the autophagy in tumor cells. IFN-γ treatment and IDO1 overexpression promote tryptophan depletion and kynurenine accumulation in cervical cancer cells, and the latter was proved to be more potent in inducing autophagy of cervical cancer cells and promoting phagocytosis of macrophage. In vivo, IDO1 overexpression could significantly restrict the tumor growth in C57 mice, and the phagocytosis of macrophage was enhanced.Conclusions: IFN-γ promotes the autophagy of cervical cancer cell possibly through IDO1 expression and kynurenine metabolism, and further promotes macrophage phagocytosis in cervical cancer.

Water-soluble amphiphilic ruthenium(ii) polypyridyl complexes as potential light-activated therapeutic agents

2020 ◽  
Vol 56 (65) ◽  
pp. 9332-9335
Author(s):  
Sandra Estalayo-Adrián ◽  
Salvador Blasco ◽  
Sandra A. Bright ◽  
Gavin J. McManus ◽  
Guillermo Orellana ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Cellular Uptake ◽  
Therapeutic Agents ◽  
Water Soluble ◽  
Polypyridyl Complexes ◽  
Cervical Cancer Cells

Two new water-soluble amphiphilic Ru(ii) polypyridyl complexes were synthesised and their photophysical and photobiological properties evaluated; both complexes showed a rapid cellular uptake and phototoxicity against HeLa cervical cancer cells.

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