Selective mediation of ovarian cancer SKOV3 cells death by pristine carbon quantum dots/Cu2O composite through targeting matrix metalloproteinases, angiogenic cytokines and cytoskeleton

AbstractIt was shown that some nanomaterials may have anticancer properties, but lack of selectivity is one of challenges, let alone selective suppression of cancer growth by regulating the cellular microenvironment. Herein, we demonstrated for the first time that carbon quantum dots/Cu2O composite (CQDs/Cu2O) selectively inhibited ovarian cancer SKOV3 cells by targeting cellular microenvironment, such as matrix metalloproteinases, angiogenic cytokines and cytoskeleton. The result was showed CQDs/Cu2O possessed anticancer properties against SKOV3 cells with IC50 = 0.85 μg mL−1, which was approximately threefold lower than other tested cancer cells and approximately 12-fold lower than normal cells. Compared with popular anticancer drugs, the IC50 of CQDs/Cu2O was approximately 114-fold and 75-fold lower than the IC50 of commercial artesunate (ART) and oxaliplatin (OXA). Furthermore, CQDs/Cu2O possessed the ability to decrease the expression of MMP-2/9 and induced alterations in the cytoskeleton of SKOV3 cells by disruption of F-actin. It also exhibited stronger antiangiogenic effects than commercial antiangiogenic inhibitor (SU5416) through down-regulating the expression of VEGFR2. In addition, CQDs/Cu2O has a vital function on transcriptional regulation of multiple genes in SKOV3 cells, where 495 genes were up-regulated and 756 genes were down-regulated. It is worth noting that CQDs/Cu2O also regulated angiogenesis-related genes in SKOV3 cells, such as Maspin and TSP1 gene, to suppress angiogenesis. Therefore, CQDs/Cu2O selectively mediated of ovarian cancer SKOV3 cells death mainly through decreasing the expression of MMP-2, MMP-9, F-actin, and VEGFR2, meanwhile CQDs/Cu2O caused apoptosis of SKOV3 via S phase cell cycle arrest. These findings reveal a new application for the use of CQDs/Cu2O composite as potential therapeutic interventions in ovarian cancer SKOV3 cells.

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Selective Mediation of Ovarian Cancer Cell Death by Pristine Carbon Quantum Dots/Cu2O Composite Through Targeting Matrix Metalloproteinases, Angiogenic Cytokines and Cytoskeleton

10.21203/rs.3.rs-123605/v1 ◽

2020 ◽

Author(s):

Daomei Chen ◽

Bin Li ◽

Minfang Nie ◽

Yepeng Yang ◽

Xie Congjia ◽

...

Keyword(s):

Ovarian Cancer ◽

Quantum Dots ◽

Matrix Metalloproteinases ◽

Carbon Quantum Dots ◽

Phase Cell ◽

Ovarian Cancer Cells ◽

Cellular Microenvironment ◽

Anticancer Properties ◽

Skov3 Cells ◽

Angiogenic Cytokines

Abstract It was shown that some nanomaterials may have anticancer properties, but lack of selectivity is one of challenges, let alone selective suppression of cancer growth by regulating the cellular microenvironment. Herein, we demonstrated for the first time that carbon quantum dots/Cu2O composite (CQDs/Cu2O) selectively inhibited ovarian cancer SKOV3 cells by targeting cellular microenvironment, such as matrix metalloproteinases, angiogenic cytokines and cytoskeleton. The result was showed CQDs/Cu2O possessed anticancer properties against SKOV3 cells with IC50 = 0.85 μg mL−1, which was approximately 3-fold lower than that in normal mouse embryonic fibroblasts BABL-3T3 cells. Compared with popular anticancer drugs, the IC50 of CQDs/Cu2O was approximately 114-fold and 75-fold lower than the IC50 of commercial artesunate (ART) and oxaliplatin (OXA). Furthermore, CQDs/Cu2O possessed the ability to decrease the expression of MMP-2/9 and induced alterations in the cytoskeleton of SKOV3 cells by disruption of F-actin. It also exhibited stronger antiangiogenic effects than commercial antiangiogenic inhibitor (SU5416) through down-regulating the expression of VEGFR2. In addition, CQDs/Cu2O has a vital function on transcriptional regulation of multiple genes in SKOV3 cells, where 495 genes were up-regulated and 756 genes were down-regulated. It is worth noting that CQDs/Cu2O also regulated angiogenesis-related genes in SKOV3 cells, such as Maspin and TSP1 gene, to suppress angiogenesis. Therefore, CQDs/Cu2O selectively mediated of ovarian cancer cells death mainly through decreasing the expression of MMP-2, MMP-9, F-actin, and VEGFR2, meanwhile CQDs/Cu2O caused apoptosis of SKOV3 via S phase cell cycle arrest. These findings reveal a new application for the use of CQDs/Cu2O composite as potential therapeutic interventions in ovarian cancer.

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S-Phase Cell Cycle Arrest, Apoptosis, and Molecular Mechanisms of Aplasia Ras homolog Member I–Induced Human Ovarian Cancer SKOV3 Cell Lines

International Journal of Gynecological Cancer ◽

10.1097/igc.0000000000000105 ◽

2014 ◽

Vol 24 (4) ◽

pp. 629-634 ◽

Cited By ~ 10

Author(s):

Qiaoying Zhu ◽

Jianming Hu ◽

Huijuan Meng ◽

Yufei Shen ◽

Jinhua Zhou ◽

...

Keyword(s):

Cell Cycle ◽

Ovarian Cancer ◽

Molecular Mechanisms ◽

Significant Inhibition ◽

S Phase ◽

Phase Cell ◽

Cell Cycle Distribution ◽

Human Ovarian Cancer ◽

Skov3 Cell ◽

Skov3 Cells

ObjectiveAplasia Ras homolog member I (ARHI) is associated with human ovarian cancer (HOC) growth and proliferation; however, the mechanisms are unclear. The purpose of this study was to investigateARHIeffects in HOC SKOV3 cells.MethodsWe transfected SKOV3 cells with PIRES2-EGFP-ARHI and measured growth inhibition rates, cell cycle distribution, apoptosis rates, and expression of P-STAT3 (phosphorylated signal transduction and activators of transcription 3) and P-ERK (phosphorylated extracellular signal regulated protein kinase).ResultsOur data showed significant inhibition of growth, significantly increased S-phase arrest and apoptosis rates, and reduction of P-STAT3 and P-ERK1/2 expression levels.ConclusionsWe propose the mechanism may involveARHI-induced phosphorylation of ERK1/2 and STAT3 protein kinases, thereby blocking proliferation signaling pathways, to induce HOC SKOV3 apoptosis.

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Cancer antigen 125 assessment using carbon quantum dots for optical biosensing for the early diagnosis of ovarian cancer

RSC Advances ◽

10.1039/d1ra05121k ◽

2021 ◽

Vol 11 (49) ◽

pp. 31047-31057

Author(s):

Walaa E. Omer ◽

Mostafa F. Abdelbar ◽

Nesma M. El-Kemary ◽

Naoki Fukata ◽

Maged A. El-Kemary

Keyword(s):

Ovarian Cancer ◽

Quantum Dots ◽

Early Diagnosis ◽

Carbon Quantum Dots ◽

Biological Molecules ◽

Cancer Antigen 125 ◽

Cancer Antigen ◽

Optical Biosensing

Fluorometric quantification of biological molecules is a key feature used in many biosensing studies.

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Astaxanthin Combine with Human Serum Albumin to Abrogate Cell Proliferation, Migration, and Drug-resistant in Human Ovarian Carcinoma SKOV3 Cells

Anti-Cancer Agents in Medicinal Chemistry ◽

10.2174/1871520619666190225123003 ◽

2019 ◽

Vol 19 (6) ◽

pp. 792-801 ◽

Cited By ~ 7

Author(s):

Xiu-Zhen Su ◽

Ran Chen ◽

Cai-Bing Wang ◽

Xi-Lin Ouyang ◽

Yan Jiang ◽

...

Keyword(s):

Cell Cycle ◽

Ovarian Cancer ◽

Cell Proliferation ◽

Human Serum Albumin ◽

Serum Albumin ◽

Human Serum ◽

Phase Cell ◽

Drug Resistant ◽

Skov3 Cells ◽

Induced Apoptosis

Background: Astaxanthin (AST) shows a large range of beneficial effects together with anti-cancer and antioxidation properties. Human Serum Albumin (HSA) is the most abundant protein in blood plasma which plays the role of a depot and transport protein for many exogenous compounds. However, whether HSA could enhance AST-induced cytotoxic effects in human ovarian cancer cells has not been examined to date. Objective: This study aims to explore the anticancer effect and the molecular mechanism of AST combine with HSA induced cytotoxicity in ovarian cancer SKOV3 cells. Methods: The ovarian cancer SKOV3 cells were treated by AST combined with HSA to study the effects of cell proliferation, cell morphology, cell cycle arrest, related protein expression, nuclear transfer, cell migration, and drug-resistant. Results: Our data confirmed that AST+HSA treatment enhanced the anticancer effects of AST, arrested G1 phase cell cycle and induced apoptosis in SKOV3 cells. AST+HSA induced apoptosis via mitochondrial apoptotic pathways was related to the increased ratio of Bcl-2/Bax and activation of caspase-3. Besides, exposure of cells to AST+HSA triggered the inactivation of NF-κB and activation p53 and MAPKs signaling pathways. Furthermore, AST+HSA significantly overcome the drug-resistant and inhibited the migration of SKOV3 cells. Conclusion: AST combined treatment with HSA considerably inhibited NF-κB expression and translocation to nucleus, thereby improving the AST-induced cytotoxic effect on SKOV3 cells. These findings may provide rationale to combine AST with HSA for the treatment of ovarian cancer.

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Carbon Quantum Dots : Synthesis and Optronics Applications

10.24001/icsesd2017.25 ◽

2017 ◽

Author(s):

Swati S. Soley

Keyword(s):

Quantum Dots ◽

Carbon Quantum Dots

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LUMINESCENT DETERMINATION OF SUGAR IN NATURAL HONEY

Izvestia Ufimskogo Nauchnogo Tsentra RAN ◽

10.31040/2222-8349-2020-0-4-29-32 ◽

2020 ◽

Vol 0 (4) ◽

pp. 29-32

Author(s):

B.M. GAREEV ◽

◽

A.M. ABDRAKHMANOV ◽

G.L. SHARIPOV ◽

◽

...

Keyword(s):

Quantum Dots ◽

Laboratory Test ◽

Aqueous Solutions ◽

Analytical Method ◽

Sugar Content ◽

Carbon Quantum Dots ◽

Photoluminescence Intensity ◽

Sucrose Content ◽

Natural Honey

The photoluminescence of carbon quantum dots synthesized from natural honey and mixtures of honey and sugar has been studied. An increase in the sugar content leads to a decrease in the photoluminescence intensity without changing the shape of the luminescence spectrum of these quantum dots aqueous solutions, which is associated with a decrease in the yield of their synthesis in the sugar presence. The discovered effect can be used to detect sugar in honey. When examining five different market samples of flower honey using this method, two of them showed a significant decrease in the photoluminescence intensity. A laboratory test for compliance with GOST 19792-2017 Standard requirements established an excess of the sucrose content in these samples. Luminescent determination of sugar in honey does not require complicated equipment and can be used to develop a new analytical method for determining the sugar content in counterfeit natural honey.

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