Advances in nanomaterial based optical biosensing and bioimaging of apoptosis via caspase-3 activity: a review

Khalilzadeh, Balal; Shadjou, Nasrin; Kanberoğlu, Gülşah Saydan; Afsharan, Hadi; Guárdia, Miguel de la; Charoudeh, Hojjatollah Nozad; Ostadrahimi, Alireza; Rashidi, Mohammad‐Reza

doi:10.1007/s00604-018-2980-6

Cited by 67 publications

(36 citation statements)

References 71 publications

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“…Furthermore, Bax could also downregulate apoptosis and the mitochondrial membrane in mitochondria as a pro-apoptotic gene [33]. Caspases, such as cleaved caspase-3 and caspase-9, comprise a family of cysteine proteases that contribute to apoptosis and ultimately cell death [34,35], and Bax and Bcl2 are effective factors for the downstream activation of caspase protein [36]. In the present study, we found that Bax and active caspase-3/-9 were highly expressed, whereas Bcl-2 was decreased in AGS cells treated with vortioxetine.…”

Section: Discussionmentioning

confidence: 99%

Vortioxetine induces apoptosis and autophagy of gastric cancer AGS cells via the PI3K/AKT pathway

Wang

Zhu

et al. 2020

FEBS Open Bio

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Vortioxetine is a potent antagonist of the 5-hydroxytryptamine receptor and serotonin transporter and has been reported to function as an antidepressant in the treatment of major depressive disorder. However, its antitumor effects remain unclear. Here, we examined whether vortioxetine affects the characteristics of GC cells. Cell viability was measured by a colony formation assay and, in addition, cell invasion, migration and apoptosis assays were performed with a transwell assay and a flow cytometry assay. Protein levels were measured by western blotting. We found that vortioxetine inhibited the proliferation, invasion and migration abilities of AGS cells. Additionally, vortioxetine could induce apoptosis and autophagy by increasing the levels of Bax, active caspase-3/-9, Beclin-1 and light chain 3, as well as by downregulating Bcl-2 and P62. Further investigations indicated that vortioxetine regulated apoptosis and autophagy via activation of the phosphoinositide 3-kinase/AKT pathway. Taken together, our data suggest that vortioxetine has cytotoxic effects against GC AGS cells as a result of inhibiting proliferation, invasion and migration, as well as by inducing apoptosis and autophagy through the phosphoinositide 3-kinase/ AKT pathway.

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Section: Discussionmentioning

confidence: 99%

Vortioxetine induces apoptosis and autophagy of gastric cancer AGS cells via the PI3K/AKT pathway

Wang

Zhu

et al. 2020

FEBS Open Bio

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“…Once caspase‐3 is activated, apoptosis occurs. Importantly, as a proteolytic enzyme, caspase‐3 activity is mostly based on the presence of a specific cleavage fragment peptide (Khalilzadeh et al ; Lincoln et al ). Our Western blotting analysis results showed that cleaved caspase‐3 was significantly upregulated in the etoposide‐induced group compared to that in the untreated group.…”

Section: Discussionmentioning

confidence: 99%

Screening the expression of several miRNAs from TaqMan Low Density Array in traumatic brain injury: miR‐219a‐5p regulates neuronal apoptosis by modulating CCNA2 and CACUL1

Yan

et al. 2019

Journal of Neurochemistry

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Circulating microRNAs (miRNAs) have emerged as diagnostic and prognostic biomarkers for traumatic brain injury (TBI). However, a comprehensive characterization of the serum miRNA profile in patients with TBI and the roles of these potential markers in neuronal regulation have rarely been reported. In this study, the levels of 754 serum miRNAs were initially determined in two pooled samples of 15 severe traumatic brain injury (sTBI) patients and 15 healthy controls using a TaqMan Low Density Array. The markedly upregulated miRNAs in sTBI patients were subsequently validated individually by quantitative reverse-transcription PCR (RT-qPCR) in another larger cohort consisting of 81 sTBI patients, 81 mild traumatic brain injury (mTBI) patients and 82 age/sex-matched healthy controls. Seven miRNAs, including miR-103a-3p, miR-219a-5p, miR-302d-3p, miR-422a, miR-518f-3p, miR-520d-3p and miR-627, were significantly upregulated in both sTBI and mTBI patients compared with their expression in controls. Among these miRNAs, miR-219a-5p not only discriminated sTBI and mTBI patients from controls but also discriminated between sTBI and mTBI patients. We further show here that in the neuronal cell injury model, upregulated miR-219a-5p inhibits the expression of CCNA2 and CACUL1 and further regulates akt/Foxo3a and p53/Bcl-2 signaling pathways, causing a notable change in the expression of cleaved caspase-3, thereby inducing neuronal apoptosis. These results indicate that these seven selected miRNAs could serve as novel biomarkers for TBI. In particular, miR-219a-5p is a potentially valuable indicator of the diagnosis, prognosis of TBI and appears to regulate neuronal apoptosis and death. Keywords: biomarker, CACUL1, CCNA2, microRNA, miR-219a-5p, traumatic brain injury.

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“…MCF-7 and BT-20 cells were seeded in a 96-well plate at density15 × 10 3 for 24, and 48 h, treated with different concentrations of MT (i.e., 5, 10, 20, 30 and 40 µM) as five groups including (a), (b), (c), (d) and (d) described at section (2.9.1.) and then incubated for 24 and 48 h. Finally, cleavage of the caspase-3 substrate (N-acetyl-DEVD-p-nitroaniline) [42] was monitored by measuring the fluorescent density at emission and excitation wavelengths of 535 nm and 485 nm, respectively. Data were obtained from two independent experiments.…”

Section: Caspase-3 Activity Assaymentioning

confidence: 99%

Redox-Sensitive and Hyaluronic Acid-Functionalized Nanoparticles for Improving Breast Cancer Treatment by Cytoplasmic 17α-Methyltestosterone Delivery

et al. 2020

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Novel reduction-responsive hyaluronic acid–chitosan–lipoic acid nanoparticles (HACSLA-NPs) were designed and synthesized for effective treatment of breast cancer by targeting Cluster of Differentiation 44 (CD44)-overexpressing cells and reduction-triggered 17α-Methyltestosterone (MT) release for systemic delivery. The effectiveness of these nanoparticles was investigated by different assays, including release rate, 3-(4,5-Dimethylthiazol-2-Yl)-2,5-Diphenyltetrazolium Bromide (MTT), lactate dehydrogenase (LDH), caspase-3 activity, Rhodamine 123 (RH-123), and Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL). In vitro experiments revealed that Methyltestosterone/Hyaluronic acid–chitosan–lipoic acid nanoparticles (MT/HACSLA-NPs) illustrated a sustained drug release in the absence of glutathione (GSH), while the presence of GSH led to fast MT release. HACSLA-NPs also showed high cellular internalization via CD44 receptors, quick drug release inside the cells, and amended cytotoxicity against positive CD44 BT-20 breast cancer cell line as opposed to negative CD44, Michigan Cancer Foundation-7 (MCF-7) cell line. These findings supported that these novel reduction-responsive NPs can be promising candidates for efficient targeted delivery of therapeutics in cancer therapy.

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Advances in nanomaterial based optical biosensing and bioimaging of apoptosis via caspase-3 activity: a review

Cited by 67 publications

References 71 publications

Vortioxetine induces apoptosis and autophagy of gastric cancer AGS cells via the PI3K/AKT pathway

Vortioxetine induces apoptosis and autophagy of gastric cancer AGS cells via the PI3K/AKT pathway

Screening the expression of several miRNAs from TaqMan Low Density Array in traumatic brain injury: miR‐219a‐5p regulates neuronal apoptosis by modulating CCNA2 and CACUL1

Redox-Sensitive and Hyaluronic Acid-Functionalized Nanoparticles for Improving Breast Cancer Treatment by Cytoplasmic 17α-Methyltestosterone Delivery

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