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Your search keyword '"Rong, Jiamin"' showing total 2 results
Start Over Author "Rong, Jiamin" Topic apoptosis
2 results on '"Rong, Jiamin"'

1. Histone H2A-peptide-hybrided upconversion mesoporous silica nanoparticles for bortezomib/p53 delivery and apoptosis induction.

Author

Rong J, Li P, Ge Y, Chen H, Wu J, Zhang R, Lao J, Lou D, and Zhang Y

Subjects
Antineoplastic Agents chemistry, Biocompatible Materials chemistry, Bortezomib chemistry, Drug Carriers chemistry, Drug Screening Assays, Antitumor, HeLa Cells, Humans, Nanoparticles chemistry, Particle Size, Porosity, Silicon Dioxide chemistry, Surface Properties, Tumor Cells, Cultured, Tumor Suppressor Protein p53 metabolism, Antineoplastic Agents pharmacology, Apoptosis drug effects, Biocompatible Materials pharmacology, Bortezomib pharmacology, Histones chemistry, Peptides chemistry, Tumor Suppressor Protein p53 genetics
Abstract

The design and development of advanced gene/drug codelivery nanocarrier with good biocompatibility for cancer gene therapy is desirable. Herein, we reported a gene delivery nanoplatform to synergized bortezomib (BTZ) for cancer treatment with histone H2A-hybrided, upconversion luminescence (UCL)-guided mesoporous silica nanoparticles [UCNPs(BTZ)@mSiO 2 -H2A]. The functionalization of H2A on the surface of UCNPs(BTZ)@mSiO 2 nanoparticles realized the improvement of biocompatibility and enhancement of gene encapsulation and transfection efficiency. More importantly, then UCNPs(BTZ)@mSiO 2 -H2A/p53 induced specific and efficient apoptotic cell death in p53-null cancer cells and restored the functional activity of tumor suppressor p53 by the success of co-delivery of BTZ/p53. Moreover, the transfection with UCNPs(BTZ)@mSiO 2 -H2A/p53 in p53-deficient non-small cell lung cancer cells changed the status of p53 and substantially enhanced the p53-mediated sensitivity of encapsulated BTZ inside the UCNPs(BTZ)@mSiO 2 /p53. Meanwhile, core-shell structured mesoporous silica nanoparticles UCNPs@mSiO 2 as an UCL agent can detect the real-time interaction of nanoparticles with cells and uptake/penetration processes. The results here suggested that the as-developed UCNPs(BTZ)@mSiO 2 -H2A/p53 nanoplatform with coordinating biocompatibility, UCL image, and sustained release manner might be desirable gene/drug codelivery nanocarrier for clinical cancer therapy., Competing Interests: Declaration of competing Interest The authors declare that there was no conflict of interest in the preparation of this manuscript., (Copyright © 2019 Elsevier B.V. All rights reserved.)

Published
2020
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2. Small molecule CDS-3078 induces G2/M phase arrest and mitochondria-mediated apoptosis in HeLa cells

Author

Zhang, Yuanxin, Li, Pengcheng, Rong, Jiamin, Ge, Yakun, Hu, Chenming, Bai, Xu, and Shi, Wei

Subjects
p53, G2/M arrest, apoptosis, Articles, HeLa cells, small-molecule
Abstract

The tumor suppressor p53 serves important roles in cell cycle arrest and apoptosis, and its activation increases the sensitivity of cancer cells to radiotherapy or chemotherapy. In the present study, the small molecule 2-[1-(4-(benzyloxy)phenyl)-3-oxoisoindolin-2-yl)-2-(4-methoxyphenyl)] acetic acid (CDS-3078) significantly increased p53 mRNA expression levels in a dose-dependent manner. Treatment with CDS-3078 increased p53 expression levels and p53-mediated activation of its downstream target genes in HeLa cells. Additionally, p53+/+ HeLa cells treated with CDS-3078 presented with dysfunctional mitochondria, as indicated by the decrease in Bcl-2 levels, the increase in Bcl-2 homologous antagonist killer and the increase in cytochrome c release from the mitochondria to the cytoplasm. The present results suggested that CDS-3078 treatment significantly induced G2/M phase cell cycle arrest. Therefore, CDS-3078 administration induced apoptosis via p53-mediated cell cycle arrest, causing mitochondrial dysfunction and resulting in apoptotic cell death in cervical cancer cells. Collectively, the present results suggested that CDS-3078 may be a potential anticancer agent.

Published
2020

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