scholarly journals Smart NIR-light and pH responsive doxorubicin-loaded GNRs@SBA-15-SH nanocomposite for chemo-photothermal therapy of cancer

Nanophotonics ◽  
2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Maryam Deinavizadeh ◽  
Alireza Kiasat ◽  
Nasrin Hooshmand ◽  
Mohammad Shafiei ◽  
Mohammad Sabaeian ◽  
...  

Abstract We designed novel biocompatible nanocomposite composed of gold nanorods coated with rod-like mesoporous silica SBA-15-SH particles, (GNRs@SBA-15-SH) as a new synergistic therapeutic device to deliver heat and drug to cancer cells for tumor eradication. For this purpose, doxorubicin (DOX) was loaded into GNRs@SBA-15-SH nanocomposites and studied their photothermal therapy, chemotherapy and the combined effect on the ablation of A549 cells in vitro using human lung cancer cells, A549. The results demonstrate the high photothermal efficacy of gold nanorods loaded into the nanocomposite, the thermo-responsive properties of GNRs@SBA-15-SH, the high loading capacity of DOX into the GNRs@SBA-15-SH and its biocompatibility. Synergistic chemo-photothermal of the GNRs@SBA-15-SH/DOX nanocomposite in the eradication of cancer cells under laser irradiation (808 nm), demonstrates the high potential of therapeutic efficacy of this combined therapy over monotherapies.

Author(s):  
Shihao Pei ◽  
Jia-Bei Li ◽  
Zhuo Wang ◽  
Yao Xie ◽  
Jiabo Chen ◽  
...  

Carbon monoxide (CO) can cause mitochondrial dysfunction, inducing apoptosis of cancer cells which sheds light on a potential alternative for cancer treatment. However, the existing CO-based compounds are inherently limited...


2016 ◽  
Vol 37 (7) ◽  
pp. 919-929 ◽  
Author(s):  
Guo-dong Yao ◽  
Jing Yang ◽  
Qiang Li ◽  
Ye Zhang ◽  
Min Qi ◽  
...  

Gene Therapy ◽  
2019 ◽  
Vol 27 (1-2) ◽  
pp. 51-61
Author(s):  
Juliana G. Xande ◽  
Ana P. Dias ◽  
Rodrigo E. Tamura ◽  
Mario C. Cruz ◽  
Bárbara Brito ◽  
...  

2009 ◽  
Vol 57 (13) ◽  
pp. 5777-5782 ◽  
Author(s):  
Sungwook Chae ◽  
Kyoung Ah Kang ◽  
Weon Young Chang ◽  
Min Jung Kim ◽  
Su Jae Lee ◽  
...  

2019 ◽  
Vol 51 (7) ◽  
Author(s):  
Jae-Rin Lee ◽  
Jong-Yoon Lee ◽  
Hyun-Ji Kim ◽  
Myong-Joon Hahn ◽  
Jong-Sun Kang ◽  
...  

AbstractChloride intracellular channel 1 (CLIC1) is a promising therapeutic target in cancer due to its intrinsic characteristics; it is overexpressed in specific tumor types and its localization changes from cytosolic to surface membrane depending on activities and cell cycle progression. Ca2+ and reactive oxygen species (ROS) are critical signaling molecules that modulate diverse cellular functions, including cell death. In this study, we investigated the function of CLIC1 in Ca2+ and ROS signaling in A549 human lung cancer cells. Depletion of CLIC1 via shRNAs in A549 cells increased DNA double-strand breaks both under control conditions and under treatment with the putative anticancer agent chelerythrine, accompanied by a concomitant increase in the p-JNK level. CLIC1 knockdown greatly increased basal ROS levels, an effect prevented by BAPTA-AM, an intracellular calcium chelator. Intracellular Ca2+ measurements clearly showed that CLIC1 knockdown significantly increased chelerythrine-induced Ca2+ signaling as well as the basal Ca2+ level in A549 cells compared to these levels in control cells. Suppression of extracellular Ca2+ restored the basal Ca2+ level in CLIC1-knockdown A549 cells relative to that in control cells, implying that CLIC1 regulates [Ca2+]i through Ca2+ entry across the plasma membrane. Consistent with this finding, the L-type Ca2+ channel (LTCC) blocker nifedipine reduced the basal Ca2+ level in CLIC1 knockdown cells to that in control cells. Taken together, our results demonstrate that CLIC1 knockdown induces an increase in the intracellular Ca2+ level via LTCC, which then triggers excessive ROS production and consequent JNK activation. Thus, CLIC1 is a key regulator of Ca2+ signaling in the control of cancer cell survival.


2002 ◽  
Vol 30 (02n03) ◽  
pp. 307-314 ◽  
Author(s):  
Hui-Chiu Chang ◽  
Wen-Chun Hung ◽  
Ming-Shyan Huang ◽  
Hseng-Kuang Hsu

Recent study indicated that the components of Toona sinensis Roemor have potent anti-inflammatory and analgesic effects. These components have also been reported to inhibit the growth of boils in vivo. In this study, we investigated the effect of crude extract from the leaves of Toona sinensis Roemor on the proliferation of A549 lung cancer cells. We found that the extract effectively blocked cell cycle progression by inhibiting the expression of cyclin D1 and E in A549 cells. Additionally, incubation of the extract led to activation of caspase-3-like proteases and apoptotic cell death. Conversely, the extract did not show any significant cytotoxic effect on primarily cultured human foreskin fibroblasts or MRC-5 human lung fibroblasts. Therefore, antiproliferative action of the extract is specific for tumor cells. Our results suggest that the components of Toona sinensis Roemor have potent anticancer effects in vitro and identification of the useful components in the extract may lead to the development of a novel class of anticancer drugs.


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