Effect of Superparamagnetic DMSO@γ-Fe2O3 Combined with Carmustine on Cervical Cancer

2021 ◽  
Vol 21 (12) ◽  
pp. 6196-6204
Author(s):  
Shu Wen ◽  
Weiping Xing ◽  
Lingxue Gao ◽  
Shuping Zhao
Keyword(s):  
Cervical Cancer ◽  
Toxic Effect ◽  
Cancer Cells ◽  
Colorimetric Method ◽  
Inhibitory Effect ◽  
Magnetic Nanomaterials ◽  
Combined Chemotherapy ◽  
Killing Effect ◽  
Cervical Cancer Cells

This study aimed to investigate the effects of DMSO@γ-Fe2O3 nanomagnetic fluid thermotherapy combined with the chemotherapy drug carmustine on cervical cancer cells under a certain intensity of alternating magnetic field. And the role of Mir-590-3P in the development and progression of cervical cancer. The optimal thermotherapy concentration of γ-Fe2O3 nanomaterials on cervical cancer cells was determined by in vitro heating. In addition, the MTT colorimetric method was used to evaluate the toxic effect of γ-Fe2O3 magnetic nanoparticles on cervical cancer cells, and the optimal therapeutic concentration of carbachol on cervical cancer cells was optimized (0.015 g · L−1). The cervical cancer cells were divided into control, γ-Fe2O3 hyperthermia, chemotherapy, and DMSO@γ-Fe2O3 combined chemotherapy groups. After 2 h exposure to hypothermic conditions, flow cytometry was used to assess cell apoptosis for each group. The heating effect of the γ-Fe2O3 magnetic nanomaterials was apparent. When the concentration of γ-Fe2O3 was ≥6 g· L−1, the temperature rise above 41 °C. γ-Fe2O3 is non-toxic to cervical cancer cells and has good biocompatibility. Taking the drug concentration of IC25 as the working concentration of this study, the working concentration of carmustine was 0.015 g · L−1. Both the 41 °C heat treatment and chemotherapy alone had a killing effect on glioma and cervical cancer cells (P < 0.05). Additionally, the combined inhibitory effect of DMSO@γ-Fe2O3 nanomagnetic fluid thermotherapy and drugs at this temperature was significantly stronger than that of thermotherapy and chemotherapy alone (P < 0.05). For the control, gamma-Fe2O3 hyperthermia, chemotherapy, and DMSO@γ-Fe2O3 combined chemotherapy groups, the apoptosis rates of the cervical cancer cells were 1.4%, 18.6%, 24.12%, and 38.97%, respectively. DMSO@γ-Fe2O3 nanomagnetic fluid thermotherapy combined with the chemotherapeutic drug carmustine exerted a noticeable toxic effect on the cervical cancer cells, and DMSO@γ-Fe2O3 significantly enhanced the killing effect of carmustine on cervical cancer cells.

scholarly journals Oncolytic Vaccinia Virus Harboring Aphrocallistes vastus Lectin Inhibits the Growth of Cervical Cancer Cells Hela S3

Marine Drugs ◽  
2021 ◽  
Vol 19 (10) ◽  
pp. 532
Author(s):  
Jiajun Ni ◽  
Hualin Feng ◽  
Xiang Xu ◽  
Tingting Liu ◽  
Ting Ye ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Vaccinia Virus ◽  
Cancer Cells ◽  
Inhibitory Effect ◽  
Genes Encoding ◽  
Cervical Cancer Cells ◽  
Hela S3 ◽  
Hela S3 Cells

Aphrocallistes vastus lectin (AVL) is a C-type marine lectin produced by sponges. Our previous study demonstrated that genes encoding AVL enhanced the cytotoxic effect of oncolytic vaccinia virus (oncoVV) in a variety of cancer cells. In this study, the inhibitory effect of oncoVV-AVL on Hela S3 cervical cancer cells, a cell line with spheroidizing ability, was explored. The results showed that oncoVV-AVL could inhibit Hela S3 cells growth both in vivo and in vitro. Further investigation revealed that AVL increased the virus replication, promote the expression of OASL protein and stimulated the activation of Raf in Hela S3 cells. This study may provide insight into a novel way for the utilization of lection AVL.

scholarly journals Shikonin Inhibits The Proliferation of Cervical Cancer Cells Via FAK/AKT/GSK3β Signalling

2021 ◽  
Author(s):  
Ziyan Xu ◽  
Liru Huang ◽  
Tiantian Zhang ◽  
Yuwei Liu ◽  
Mei Gong ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Biological Activities ◽  
Inhibitory Effect ◽  
Dependent Manner ◽  
Inhibitory Effects ◽  
Cervical Cancer Cells ◽  
And Migration

Abstract Cervical cancer is one of the most common female cancers worldwide, and it is one of the most lethal malignancies of the female reproductive system. Shikonin, a natural pigment of theophyllin, has a variety of biological activities and has shown significant inhibitory effects on a variety of tumours in vitro and in vivo. However, there are few studies on Shikonin in cervical cancer. In the present study, we found that Shikonin inhibited not only the proliferation but also the migration of cervical cancer cells. Our data showed that Shikonin inhibited the proliferation of HeLa and SiHa cells in a concentration- and time-dependent manner. In cervical cancer cells, Shikonin not only inhibited the phosphorylation of FAK, AKT and GSK3β but also inhibited the phosphorylation of FAK, AKT and GSK3β induced by EGF. Further exploring the mechanism, we found that Shikonin could inhibit the proliferation of cervical cancer cells by regulating the phosphorylation of the FAK/AKT/GSK3β pathway. In addition, Shikonin significantly inhibited cell migration and reduced the expression of proteins such as MTA1, TGFβ1 and VEGF. In conclusion, our study elucidated that Shikonin has an inhibitory effect on the proliferation and migration of cervical cancer cells, which may be mediated by the FAK/AKT/GSK3β signalling pathway. Our results suggest that Shikonin has the potential to become a clinical treatment for cervical cancer.

The Potential Oncogenic and MLN4924-Resistant Effects of CSN5 on Cervical Cancer Cells

2021 ◽  
Author(s):  
Huilin Zhang ◽  
Ping He ◽  
Qing Zhou ◽  
Yan Lu ◽  
Bingjian Lu
Keyword(s):  
Cell Cycle ◽  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cervical Cancer Cell ◽  
Cervical Cancers ◽  
Cervical Cancer Cells

Abstract BackgroundsCSN5, a member of Cop9 signalosome, is essential for protein neddylation. It has been supposed to serve as an oncogene in some cancers. However, the role of CSN5 has not been investigated in cervical cancer yet.MethodsData from TCGA cohorts and GEO dataset was analyzed to examine the expression profile of CSN5 in cervical cancers. The role of CSN5 on cervical cancer cell proliferation was investigated in cervical cancer cell lines, Siha and Hela, through CSN5 knockdown via CRISPR-CAS9. Western blot was used to detect the effect of CSN5 knockdown and overexpression. CCK8, clone formation assay and cell cycle assay were also employed. Besides, the role CSN5 knockdown in vivo was evaluated by xenograft tumor model. Moreover, MLN4924 was applied in Siha and Hela with CSN5 overexpression.ResultsWe found that downregulation of CSN5 in Siha and Hela cells inhibited cell proliferation in vitro and in vivo, and the inhibitory effects were largely rescued by CSN5 overexpression. Moreover, deletion of CSN5 caused cell cycle arrest rather than inducing apoptosis. Importantly, CSN5 overexpression confers resistance to the anti-cancer effects of MLN4924 (pevonedistat) in cervical cancer cells.ConclusionsOur findings demonstrated that CSN5 functions as an oncogene in cervical cancers and may serve as a potential indicator for predicting the effects of MLN4924 treatment in the future.

Quantification of DNA double-strand break induced by radiation in cervix cancer cells: in vitro study

2018 ◽  
Vol 18 (1) ◽  
pp. 52-54
Author(s):  
Sothing Vashum ◽  
Rabi Raja Singh I ◽  
Saikat Das ◽  
Mohammed Azharuddin KO ◽  
Prabhakaran Vasudevan
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Strand Break ◽  
Double Strand Break ◽  
Ionising Radiation ◽  
Dependent Manner ◽  
Survival Fraction ◽  
Dna Double Strand Break ◽  
Cervical Cancer Cells

AbstractAimDNA double-strand break (DSB) results in the phosphorylation of the protein, H.2AX histone. In this study, the effect of radiotherapy and chemotherapy on DNA DSB in cervical cancer cells is analysed by the phosphorylation of the protein.MethodsThe cervical cancer cells (HeLa cells) were cultured and exposed to ionising radiation. Radiation sensitivity was measured by clonogenic survival fraction after exposing to ionising radiation. Since the phosphorylation of H.2AX declines with time, the DNA damage was quantified at different time points: 1 hour, 3 hours and 1 week after exposed to the radiation. The analysis of γ-H.2AX was done by Western-blot technique. The protein expression was observed at different dose of radiation and combination of both radiation and paclitaxel.ResultsLow-dose hypersensitivity was observed. By 1 week after radiation at 0·5, 0·8 and 2 Gy, there was no expression of phosphorylated H.2AX. Previous experiments on the expression of phosphorylated H.2AX (γ-H.2AX) in terms of foci analysis was found to peak at 1 hour and subsequently decline with time. In cells treated with the DNA damaging agents, the expression of phosphorylated H.2AX decreases in a dose-dependent manner when treated with radiation alone. However, when combined with paclitaxel, at 0·5 Gy, the expression peaked and reduces at 0·8 Gy and slightly elevated at 2 Gy.FindingsIn this study, the peak phosphorylation was observed at 3 hour post irradiation indicating that DSBs are still left unrepaired.

scholarly journals Radiation enhancing effects of sanazole and gemcitabine in hypoxic breast and cervical cancer cells in vitro

2015 ◽  
Vol 3 ◽  
pp. 236-240
Author(s):  
Yue-Can Zeng ◽  
Rong Wu ◽  
Yu-Ping Xiao ◽  
Yan Xin ◽  
Feng Chi ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Breast And Cervical Cancer ◽  
Cervical Cancer Cells

Growth Inhibition of Human Cervical Cancer Cells with the Recombinant Adenovirusp53 in Vitro

1996 ◽  
Vol 60 (3) ◽  
pp. 373-379 ◽  
Author(s):  
Katsuyuki Hamada ◽  
Wei-Wei Zhang ◽  
Ramon Alemany ◽  
Judith Wolf ◽  
Jack A. Roth ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Growth Inhibition ◽  
Cancer Cells ◽  
Cervical Cancer Cells ◽  
Human Cervical Cancer Cells ◽  
Human Cervical Cancer

scholarly journals Upregulation of Long Non-Coding RNA Small Nucleolar RNA Host Gene 12 Contributes to Cell Growth and Invasion in Cervical Cancer by Acting as a Sponge for MiR-424-5p

2018 ◽  
Vol 45 (5) ◽  
pp. 2086-2094 ◽  
Author(s):  
Jing Dong ◽  
Qing Wang ◽  
Li Li ◽  
Zhang Xiao-jin
Keyword(s):  
Cervical Cancer ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Host Gene ◽  
Migration And Invasion ◽  
Small Nucleolar Rna ◽  
Cervical Cancer Cells ◽  
Cancer Tissues ◽  
Nucleolar Rna

Background/Aims: Cervical cancer, which is one of the most aggressive cancers affecting females, has high rates of recurrence and mortality. Small nucleolar RNA host gene 12 (SNHG12) is known to promote the progression of several cancers; however, its exact effects and molecular mechanisms in cervical cancer remain unknown. Methods: Real-time quantitative PCR was used to determine the expression level of SNHG12 in cervical cancer tissues and cell lines. Loss-of-function assays were performed to examine the effect of SNHG12 on the proliferation, apoptosis, migration and invasion of cervical cancer cells in vitro and tumor growth in vivo. Luciferase experiments were employed to explore the interactions between SNHG12 and miR-424-5p. Results: SNHG12 was found to be abnormally elevated in human cervical cancer tissues compared with paired adjacent normal tissues. Moreover, high SNHG12 expression in tumor tissues was significantly correlated with vascular involvement, lymph node metastasis, advanced FIGO stage and poor prognosis. Furthermore, the knockdown of SNHG12 was found to inhibit proliferation, migration and invasion of cervical cancer cells in vitro, and silencing SNHG12 was shown to suppress tumor growth in a nude mouse model. Mechanistic studies showed that SNHG12 functioned as an endogenous sponge for miR-424-5p, thereby downregulating the expression of miR-424-5p in cervical cancer. Furthermore, the inhibition of miR-424-5p in SNHG12-depleted cells partially reversed the effects on cervical cancer cell apoptosis, adhesion and invasion. Conclusion: In summary, our findings suggest that the tumor-promoting role of SNHG12 is to function as a molecular sponge, which negatively regulates miR-424-5p. These findings may provide a potent therapeutic target for cervical cancer.

Sign in / Sign up

Export Citation Format

Share Document