scholarly journals An Assessment of InP/ZnS as Potential Anti-Cancer Therapy: Quantum Dot Treatment Increases Apoptosis in HeLa Cells

2021 ◽  
Vol 2 (1) ◽  
pp. 16-32
Author(s):  
Victoria Davenport ◽  
Cullen Horstmann ◽  
Rishi Patel ◽  
Qihua Wu ◽  
Kyoungtae Kim
Keyword(s):  
Cell Viability ◽  
Hela Cells ◽  
Fluorescent Imaging ◽  
Oxygen Species ◽  
Transcriptome Profile ◽  
Xtt Assay ◽  
Anti Cancer ◽  
Cervical Cancer Cells ◽  
Nitrogen Radicals ◽  
Ic50 Concentration

InP/ZnS quantum dots (QDs) are an emerging option in QD technologies for uses of fluorescent imaging as well as targeted drug and anticancer therapies based on their customizable properties. In this study we explored effects of InP/ZnS when treated with HeLa cervical cancer cells. We employed XTT viability assays, reactive oxygen species (ROS) analysis, and apoptosis analysis to better understand cytotoxicity extents at different concentrations of InP/ZnS. In addition, we compared the transcriptome profile from the QD-treated HeLa cells with that of untreated HeLa cells to identify changes to the transcriptome in response to the QD. RT-qPCR assay was performed to confirm the findings of transcriptome analysis, and the QD mode of action was illustrated. Our study determined both IC50 concentration of 69 µg/mL and MIC concentration of 167 µg/mL of InP/ZnS. It was observed via XTT assay that cell viability was decreased significantly at the MIC. Production of superoxide, measured by ROS assay with flow cytometry, was decreased, whereas levels of nitrogen radicals increased. Using analysis of apoptosis, we found that induced cell death in the QD-treated samples was shown to be significantly increased when compared to untreated cells. We conclude InP/ZnS QD to decrease cell viability by inducing stress via ROS levels, apoptosis induction, and alteration of transcriptome.

The Antitumor Efficiency of Zinc Finger Nuclease Combined with Cisplatin and Trichostatin A in Cervical Cancer Cells

2020 ◽  
Vol 20 (17) ◽  
pp. 2125-2135
Author(s):  
Ci Ren ◽  
Chun Gao ◽  
Xiaomin Li ◽  
Jinfeng Xiong ◽  
Hui Shen ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Zinc Finger ◽  
Hela Cells ◽  
Colony Formation ◽  
Trichostatin A ◽  
Combined Therapy ◽  
Hpv E7 ◽  
Anti Cancer ◽  
Cervical Cancer Cells

Background: Persistent infection with the high-risk of human papillomavirus (HR-HPVs) is the primary etiological factor of cervical cancer; HR-HPVs express oncoproteins E6 and E7, both of which play key roles in the progression of cervical carcinogenesis. Zinc Finger Nucleases (ZFNs) targeting HPV E7 induce specific shear of the E7 gene, weakening the malignant biological effects, hence showing great potential for clinical transformation. Objective: Our aim was to develop a new comprehensive therapy for better clinical application of ZFNs. We here explored the anti-cancer efficiency of HPV targeted ZFNs combined with a platinum-based antineoplastic drug Cisplatin (DDP) and an HDAC inhibitor Trichostatin A (TSA). Methods: SiHa and HeLa cells were exposed to different concentrations of DDP and TSA; the appropriate concentrations for the following experiments were screened according to cell apoptosis. Then cells were grouped for combined or separate treatments; apoptosis, cell viability and proliferation ability were measured by flow cytometry detection, CCK-8 assays and colony formation assays. The xenograft experiments were also performed to determine the anti-cancer effects of the combined therapy. In addition, the HPV E7 and RB1 expressions were measured by western blot analysis. Results: Results showed that the combined therapy induced about two times more apoptosis than that of ZFNs alone in SiHa and HeLa cells, and much more inhibition of cell viability than either of the separate treatment. The colony formation ability was inhibited more than 80% by the co-treatment, the protein expression of HPV16/18E7 was down regulated and that of RB1 was elevated. In addition, the xenografts experiment showed a synergistic effect between DDP and TSA together with ZFNs. Conclusion: Our results demonstrated that ZFNs combined with DDP or TSA functioned effectively in cervical cancer cells, and it provided novel ideas for the prevention and treatment of HPV-related cervical malignancies.

scholarly journals Physcion Induces Potential Anticancer Effects in Cervical Cancer Cells

Cells ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 2029
Author(s):  
Wojciech Trybus ◽  
Teodora Król ◽  
Ewa Trybus ◽  
Anna Stachurska
Keyword(s):  
Electron Microscopy ◽  
Reactive Oxygen Species ◽  
Cell Cycle ◽  
Cervical Cancer ◽  
Protein Expression ◽  
Cell Viability ◽  
Cancer Cells ◽  
Oxygen Species ◽  
Test Compound ◽  
Cervical Cancer Cells

Background: The extent of morphological and ultrastructural changes in HeLa cells was assessed by optical, fluorescence and electron microscopy after exposure to various concentrations of physcion, taking into account the biological properties of the test compound. Methods: Cell viability was assessed by MTT assay, while the cell cycle, LC3 expression, apoptosis, change of mitochondrial potential, Bcl-2 protein expression level and the level of reactive oxygen species were analyzed by flow cytometry. Results: As a result of physcion encumbrance, concentration-dependent inhibition of HeLa cell viability and the G0/G1 phase of the cell cycle was observed. Activation of the lysosomal system was also revealed, which was expressed by an increased number of lysosomes, autophage vacuoles and increased expression of the LC3 protein, a marker of the autophagy process. Transmission electron microscopy and fluorescence microscopy showed that physcion induced clear changes in cervical cancer cells, especially in the structure of the nucleus and mitochondria, which correlated with the production of reactive oxygen species by the test compound and indicated the induction of the oxidative process. At the same time, the pro-apoptotic effect of physcion was demonstrated, and this mechanism was dependent on the activation of caspases 3/7 and the reduction in Bcl-2 protein expression. Conclusion: The obtained results indicate an antitumor mechanism of action of physcion, based on the induction of oxidative stress, autophagy and apoptosis.

scholarly journals miR-4319 Reduces Tumorigenicity of Cervical Cancer Cells by Targeting TUFT1

2021 ◽  
Author(s):  
Lijun Zheng ◽  
Qiongzhen Ren ◽  
Weipei Zhu ◽  
Xiaomin Tao ◽  
Liangsheng Guo
Keyword(s):  
Cell Viability ◽  
Cell Apoptosis ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Tumor Suppressor Function ◽  
Over Expression ◽  
Anti Cancer ◽  
Cervical Cancer Cells ◽  
Direct Target ◽  
Dual Luciferase Reporter Assay

Abstract Background: In the present study, a new tumor suppressor function of miR-4319 was disclosed in CC. Methods: Up-regulation of miR-4319 suppressed cell viability, proliferation, migration, invasion, and induced cell apoptosis in CC cells were measured by cell transfection, CCK-8, colony formation, EdU, flow cytometer, wound healing, transwell migration and invasion and western blot assays. Moreover, Tuftelin 1 (TUFT1) was verified as a direct target of miR-4319 by binding its 3’-UTR, confirmed by dual-luciferase reporter assay. Result: The expression of miR-4319 was obviously decreased in clinical CC tissues and CC cell lines.TUFT1 was remarkably increased in clinical CC tissues and CC cell lines, and was negatively associated with miR-4319 expression. Furthermore, over-expression of TUFT1 partially restored the effects of miR-4319 mimic on cell viability, proliferation, migration, invasion, and cell apoptosis in CC cells. Conclusion: miR-4319 played an anti-cancer role in the occurrence and development of CC, which might be achieved by targeting TUFT1.

scholarly journals ANTICANCER EFFECTS OF RETINOIC ACID IN CERVICAL CANCER CELLS

2019 ◽  
Vol 81 (2) ◽  
Author(s):  
Sugania Malar Chinapayan ◽  
Praseetha Prabhakaran
Keyword(s):  
Cervical Cancer ◽  
Stem Cell ◽  
Retinoic Acid ◽  
Cell Viability ◽  
Cancer Cells ◽  
Hela Cells ◽  
Stem Cell Markers ◽  
Anticancer Effect ◽  
Cervical Cancer Cells ◽  
Differentiation Marker

Cervical cancer is a leading cause of cancer-related death in women, and it is known to have a poor prognosis. This is because, patients develop progressive or recurrent tumours after primary treatment, and the major reason for tumour recurrence is the presence of cancer stem cells (CSCs). It is known that retinoic acid (RA) has potential therapeutic effects on cervical cancer. However, the possible mode of action of RA in cervical cancer cells, and its relation to CSCs remains elusive. The aim of this research was to determine the anticancer effect of RA in cervical cancer cells (HeLa). HeLa cells were treated by various concentrations of RA ranging from 5-50µM to determine the effect of RA on cell viability, and cell proliferation. Both experiments were carried out using Celltiter-glo 2.0 assay and CyQuant NF assay, respectively. Apoptosis activity was determined using Caspase-Glo 3/7 assay. Immunofluorescent staining was conducted to detect the expression of differentiation marker (pan-keratin), and stem cell markers (CD133 and SSEA4) on untreated and treated HeLa cells with 10µM of RA. The findings showed that RA reduced cell viability and proliferation in a dose-dependent manner by 12-83% and 22-86%, respectively. However, a change in caspase3/7 activity between untreated, and 10µM RA-treated Hela cells were not detected indicating absence of apoptotic activity. The study also revealed that expression of differentiation marker (pan-keratin) was up-regulated, while expressions of stem cell markers (CD133 and SSEA4) were down-regulated. In addition, morphology of HeLa cells displayed a more differentiated phenotype that is less proliferative upon RA treatment. These findings suggest that RA showed its anticancer effect on cervical cancer cells by exhibiting cytotoxicity, inhibiting proliferation capacity, and inducing differentiation of cervical cancer cells. This finding shows that retinoic acid may potentially serve as a potent targeted therapy for cervical cancer and other cancers possessing CSCs within its tumors.  

scholarly journals Reactive Oxygen Species-Sensitive Nanophotosensitizers of Methoxy Poly(ethylene glycol)-Chlorin e6/Phenyl Boronic Acid Pinacol Ester Conjugates Having Diselenide Linkages for Photodynamic Therapy of Cervical Cancer Cells

Materials ◽  
2021 ◽  
Vol 15 (1) ◽  
pp. 138
Author(s):  
Ju-Il Yang ◽  
Hye-Lim Lee ◽  
Seon-Hee Choi ◽  
Jungsoo Kim ◽  
Young-Bob Yu ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Hela Cells ◽  
Light Irradiation ◽  
Oxygen Species ◽  
H2o2 Concentration ◽  
Poly Ethylene Glycol ◽  
Tumor Tissues ◽  
Cervical Cancer Cells ◽  
Poly Ethylene

The aim of this study is to fabricate nanophotosensitizers composed of methoxy poly(ethylene glycol) (mPEG), chlorin e6 (Ce6), and phenylboronic acid pinacol ester (PBAP) with diselenide linkages for reactive oxygen species (ROS)-sensitive photodynamic therapy (PDT) of cervical cancer cells. To fabricate nanophotosensitizers, Ce6 was conjugated with mPEG via selenocystamine linkage and then remaining carboxylic acid groups of Ce6 was attached to PBAP (mPEGseseCe6PBAP conjugates). Nanophotosensitizers of mPEGseseCe6PBAP conjugates were prepared by dialysis method. In transmission electron microscope (TEM) observation, nanophotosensitizers of mPEGseseCe6PBAP conjugates have spherical shapes and their diameters were less than 150 nm. The average diameter of mPEGseseCe6PBAP nanophotosensitizers was 92.7 ± 9.6 nm in particle size analysis. When H2O2 was added to the nanophotosensitizer solution, nanophotosensitizers were sensitively disintegrated according to the H2O2 concentration and then changed from monomodal distribution to multimodal distribution in particle size distribution. Furthermore, Ce6 release from nanophotosensitizers also increased according to the H2O2 concentration. When H2O2 was added to cell culture of HeLa human cervical cancer cells, intracellular Ce6 uptake of nanophotosensitizers were gradually increased according to the H2O2 concentration, indicating that nanophotosensitizers showed ROS-sensitive delivery of Ce6 against cancer cells.As well as free Ce6, nanophotosensitizers in the absence of light irradiation have low intrinsic cytotoxicity against RAW264.7 cells and HeLa cells. However, nanophotosensitizers induced cell death dose-dependently under light irradiation. Especially, nanophotosensitizers showed significantly higher ROS generation and phototoxicity against HeLa cells in vitro. When nanophotosensitizers were intravenously administered to animal tumor xenograft model of HeLa cells, tumor tissues revealed stronger fluorescence intensity than other tissues by light irradiation while absence of light irradiation induced relatively lower fluorescence intensity in tumor tissues, indicating that nanophotosensitizers have sensitivity against oxidative stress in tumor tissues. We suggest that nanophotosensitizers of mPEGseseCe6PBAP conjugates are promising vehicle for PDT of cervical cancer cells.

126 POTENTIAL EFFECTS OF ENGINEERED STEM CELLS TRANSDUCED WITH THERAPEUTIC GENES AGAINST HeLa HUMAN CERVICAL CANCER CELLS VIA A SELECTIVE TUMOR TROPISM CAUSED BY VASCULAR ENDOTHELIAL GROWTH FACTOR

2014 ◽  
Vol 26 (1) ◽  
pp. 177
Author(s):  
B.-R. Yi ◽  
S. U. Kim ◽  
K.-C. Choi
Keyword(s):  
Cervical Cancer ◽  
Stem Cells ◽  
Cell Viability ◽  
Cancer Cells ◽  
Real Time ◽  
Hela Cells ◽  
Real Time Pcr ◽  
Migration Assay ◽  
Cervical Cancer Cells ◽  
Human Cervical Cancer

According to the World Health Organization, cancer of cervix uteri is the second most common cancer among women worldwide. Recently, cervical cancer still remains a significant public health problem for women despite the development of the human papilloma virus vaccine. The aim of the present study was to investigate the therapeutic efficacy of genetically engineered stem cells (GESTEC) expressing bacterial cytosine deaminase (CD), human interferon-β (IFN-b) gene, or both against HeLa human cervical cancer and the migration factors of the GESTEC toward the cancer cells. A continuously dividing immortalized cell line of neural stem cells (NSC) from a single clone of human fetal brain, HB1.F3, was developed by introducing v-myc. The further introduction of these NSC with bacterial CD and human IFN-b resulted in the generation of HB1.F3.CD and HB1.F3.CD.IFN-b cells. The anticancer effect of these GESTEC was examined in a co-culture with HeLa cells using MTT assay to measure cell viability. A transwell migration assay was performed to assess the migration capability of the stem cells to cervical cancer cells. Next, several chemoattractant ligands and their receptors related to a selective migration of the stem cells towards HeLa cells were determined by real-time PCR. The cell viability of HeLa cells was decreased in response to 5-fluorocytosine (5-FC), a prodrug, indicating that 5-fluorouracil (5-FU), a toxic metabolite, was converted from 5-FC by the CD gene and it caused the cell death in a co-culture system. When IFN-b was additionally expressed with the CD gene by these GESTEC, the anticancer activity was significantly increased. In the migration assay, the GESTEC selectively migrated to HeLa cells. As results of real-time PCR, chemoattractant ligands such as MCP-1, SCF, and VEGF were expressed in HeLa cells, and several receptors such as uPAR, VEGFR2, and c-kit were produced by the GESTEC. These GESTEC transduced with the CD gene and IFN-b may provide the potential of a novel gene therapy for anti-cervical cancer treatments via their selective tumour tropism derived from VEGF and VEGFR2 expressions between HeLa cells and the GESTEC. This work was supported by a grant from the Next-Generation BioGreen 21 Program (No. PJ009599), Rural Development Administration, Republic of Korea.

scholarly journals The anti-cancer potency of photodynamic therapy of a novel chlorin derivative Amidochlorin p6 (ACP)

RSC Advances ◽  
2017 ◽  
Vol 7 (65) ◽  
pp. 40873-40880 ◽  
Author(s):  
Hongyue Zhang ◽  
Wenting Li ◽  
Guanghui Tan ◽  
Guohua Ding ◽  
Zhiqiang Wang ◽  
...  
Keyword(s):  
Cell Death ◽  
Photodynamic Therapy ◽  
Cell Viability ◽  
Hela Cells ◽  
Anti Cancer ◽  
Chlorin Derivative

Amidochlorin p6 (ACP) was uptaken by HeLa cells, showing excellent phototoxicity (the cell viability was 21% at a concentration of 8 μmol L−1), resulting in cell death.

scholarly journals Inhibition of Uncoupling Protein 2 Enhances the Radiosensitivity of Cervical Cancer Cells by Promoting the Production of Reactive Oxygen Species

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Cui Hua Liu ◽  
Zhe Hao Huang ◽  
Xin Yu Dong ◽  
Xin Qiang Zhang ◽  
Yuan Hang Li ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Cycle ◽  
Cervical Cancer ◽  
Hela Cells ◽  
Uncoupling Protein ◽  
Structure And Function ◽  
Oxygen Species ◽  
Mitochondrial Structure ◽  
Cervical Cancer Cells ◽  
And Function

Objective. The mechanism of enhanced radiosensitivity induced by mitochondrial uncoupling protein UCP2 was investigated in HeLa cells to provide a theoretical basis as a novel target for cervical cancer treatment. Methods. HeLa cells were irradiated with 4 Gy X-radiation at 1.0 Gy/min. The expression of UCP2 mRNA and protein was assayed by real-time quantitative polymerase chain reaction and western blotting. UCP2 siRNA and negative control siRNA fragments were constructed and transfected into HeLa cells 24 h after irradiation. The effect of UCP2 silencing and irradiation on HeLa cells was determined by colony formation, CCK-8 cell viability, γH2AX immunofluorescence assay of DNA damage, Annexin V-FITC/PI apoptosis assay, and propidium iodide cell cycle assay. The effects on mitochondrial structure and function were investigated with fluorescent probes including dichlorodihydrofluorescein diacetate (DCFH-DA) assay of reactive oxygen species (ROS), rhodamine 123, and MitoTracker Green assay of mitochondrial structure and function. Results. Irradiation upregulated UCP2 expression, and UCP2 knockdown decreased the survival of irradiated HeLa cells. UCP2 silencing sensitized HeLa cells to irradiation-induced DNA damage and led to increased apoptosis, cell cycle arrest in G2/M, and increased mitochondrial ROS. Increased radiosensitivity was associated with an activation of P53, decreased Bcl-2, Bcl-xl, cyclin B, CDC2, Ku70, and Rad51 expression, and increased Apaf-1, cytochrome c, caspase-3, and caspase-9 expression. Conclusions. UCP2 inhibition augmented the radiosensitivity of cervical cancer cells, and it may be a potential target of radiotherapy of advanced cervical cancer.

scholarly journals [ARTICLE WITHDRAWN] Overexpression of MicroRNA-34a-5p Inhibits Proliferation and Promotes Apoptosis of Human Cervical Cancer Cells by Downregulation of Bcl-2

2018 ◽  
Vol 26 (6) ◽  
pp. 977-985 ◽  
Author(s):  
Xiufen Wang ◽  
Yucui Xie ◽  
Jing Wang
Keyword(s):  
Cervical Cancer ◽  
Cell Viability ◽  
Cancer Cells ◽  
Hela Cells ◽  
Cell Apoptosis ◽  
Migration And Invasion ◽  
Direct Target Gene ◽  
Cervical Cancer Cells ◽  
Mrna And Protein Expression ◽  
Human Cervical Cancer Cells

Aberrant expressions of microRNAs (miRNAs) are involved in the development and progression of various types of cancers. In this study, we investigated the roles of miR-34a-5p in the proliferation, migration, invasion, and apoptosis of cervical cancer cells (HeLa cells). We found that overexpression of miR-34a-5p significantly inhibited the viability, migration, and invasion of HeLa cells, but promoted cell apoptosis. Suppression of miR-34a-5p showed opposite effects. The mRNA and protein expression levels of Bcl-2 in HeLa cells were increased by miR-34a-5p suppression but decreased by miR-34a-5p overexpression. Bcl-2 was a direct target gene of miR-34a-5p, which participated in the effects of miR-34a-5p on HeLa cell viability, migration, invasion, and apoptosis. Suppression of miR-34a-5p promoted the viability, migration, and invasion of HeLa cells by increasing the expression of Bcl-2. Moreover, overexpression of Bcl-2 significantly promoted cell viability, migration, and invasion and had no influence on cell apoptosis. Suppression of Bcl-2 showed the opposite effects, with an increase in apoptosis. Overexpression of Bcl-2 activated the PI3K/AKT and JAK/STAT pathways in cervical cancer cells. Suppression of Bcl-2 inactivated the PI3K/AKT and JAK/STAT pathways in cervical cancer cells.

Sign in / Sign up

Export Citation Format

Share Document