In Vitro Study of Carbamate-Linked Cationic Lipid for Gene Delivery Against 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.

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Targeted delivery of mesoporous silica nanoparticles loaded monastrol into cancer cells: an in vitro study

Applied Nanoscience ◽

10.1007/s13204-017-0593-8 ◽

2017 ◽

Vol 7 (8) ◽

pp. 549-555 ◽

Cited By ~ 5

Author(s):

Huzaifa Hanif ◽

Samina Nazir ◽

Kehkashan Mazhar ◽

Muhammad Waseem ◽

Shazia Bano ◽

...

Keyword(s):

Mesoporous Silica ◽

Silica Nanoparticles ◽

Cancer Cells ◽

Targeted Delivery ◽

Mesoporous Silica Nanoparticles ◽

In Vitro Study ◽

Vitro Study

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

Journal of Radiotherapy in Practice ◽

10.1017/s1460396918000456 ◽

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.

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