|
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
We also found that KZ induced NSCLC cell apoptosis by increasing the Bax/Bcl-2 ratio and by activating caspase-3 and caspase-9 leading to mitochondrial apoptosis, and upregulated CHOP and activatedcaspase-7 and caspase-12, which triggered the endoplasmic reticulum stress pathway.
|
31817093 |
2019 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Furthermore, western blot analysis revealed that in NSCLC cell lines, the combined treatment with gefitinib and ginsenoside Rg3 increased protein expression levels of pro-apoptotic proteins Bax and cleaved-caspase-3, whilst the expression level of anti-apoptotic protein Bcl-2 decreased.
|
30651886 |
2019 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The mitochondria-mediated apoptosis of NSCLC induced by L-Ru was also observed followed by the increase of apoptosis regulator B-cell lymphoma 2 associated X (BAX), and activation of caspase-3/-9.
|
30831390 |
2019 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Mechanistically, CDK 4/6 inhibition induces a proapoptotic transcriptional program through suppression of IAPs FOXM1 and Survivin, while simultaneously augmenting expression of SMAC and caspase-3 in an RB-dependent manner.<b>Conclusions:</b> This study uncovers a novel function of RB activation to induce cellular apoptosis through therapeutic administration of a palbociclib and provides a rationale for the clinical evaluation of CDK 4/6 inhibitors in the treatment of patients with NSCLC.<i></i>.
|
29311118 |
2018 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Here, we showed that Mcl-1, a pro-survival member of the Bcl-2 family, was cleaved by caspase-3 in non-small cell lung cancer (NSCLC) cells undergoing chemotherapeutic agent-triggered apoptosis.
|
29256070 |
2018 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
According to our experimental data, miR-24 inhibition could induce apoptosis by activating caspase 3 and suppress the viability and proliferation of NSCLC cells in vitro and in vivo.
|
30307120 |
2018 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In addition, simultaneously targeting both CD47 and autophagy in NSCLC xenograft models elicited enhanced antitumor effects, with recruitment of macrophages, activated caspase-3, and overproduction of ROS at the tumor site.
|
28351890 |
2017 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Triptolide reduced the viability of five non-small cell lung cancer (NSCLC) cells, the proliferation and self-renewal of pulmospheres, and levels of HA synthase 2 (HAS2), HAS3, HA, CD44, RHAMM, EGFR, Akt and ERK, but increased the cleavage of caspase 3 and PARP.
|
28460475 |
2017 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In conclusion, the reductive Apaf-1 regulated by miR-484 accelerated the NSCLC cell progression associated with the inhibition of apoptosis via down-regulating Caspase-3 and PARP cleavage.
|
28982084 |
2017 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In addition, increases in phosphatidylserine externalization and caspase-3 activity also confirmed the apoptotic effect of NCKU-21 in both NSCLC cell lines.
|
28945763 |
2017 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
<b>Methods</b>: In this study, we evaluated for the first time the prognostic value of Plk1 mRNA and protein expression in combination with the <i>TP53</i> mutation status (next generation sequencing), induction of apoptotic cell death (immunohistochemistry for cleaved caspase 3) and hypoxia (immunohistochemistry for carbonic anhydrase IX (CA IX)) in 98 NSCLC adenocarcinoma patients.
|
28638459 |
2017 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
This report proves that the fluorescent probe DEVD-TPE is highly sensitive to caspase-3 and has potential prospects in the rapid screening of NSCLC.
|
28265596 |
2017 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The present study aimed to analyze the possible impact of the CASP3 (-1337 C > G, rs1405937) polymorphism on the expression profile of CASP3 gene and ultimately its association in the development of non-small cell lung cancer.
|
26768747 |
2016 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Here we report that caspase3 (CASP3) and caspase7 (CASP7) are previously unidentified targets of miR-224 in NSCLC, and that miR-224 promotes lung cancer cells proliferation and migration in part by directly targeting CASP7 and down-regulating its expression.
|
26307684 |
2015 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Paris saponin I induces apoptosis via increasing the Bax/Bcl-2 ratio and caspase-3 expression in gefitinib-resistant non-small cell lung cancer in vitro and in vivo.
|
24718383 |
2014 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
This study reveals for the first time that the anticancer activity of DN was induced through regulation of the Bcl-2 family protein-mediated mitochondrial pathway and the subsequent caspase-3 activation in A549 cancer cells, thus supporting its potential role as a natural apoptosis-inducing agent for NSCLC.
|
25342427 |
2014 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Overall, although the effects of CHIR99021 and the combined application of CHIR99021 and Notch3-shRNA on the cell proliferation and apoptosis aren't completely similar in the three cell lines, our findings still indicate that Notch3 signaling can be activated by canonical Wnt signaling and a functional link between Wnt and Notch signaling pathways exists in NSCLC, at least, which partially is associated with their regulations on the expressions of cyclinA and caspase-3.
|
24367688 |
2013 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
MDM2 knockdown in p53 mutant NSCLC H2009 cells induced significant cell cycle arrest, apoptosis and growth inhibition through upregulation of p21 and activation of caspase-3.
|
23352573 |
2013 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Association of CASP3 polymorphism with hematologic toxicity in patients with advanced non-small-cell lung carcinoma treated with platinum-based chemotherapy.
|
22568453 |
2012 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
These results strongly suggest that CCL21/CCR7 prevents apoptosis by upregulating the expression of bcl-2 and by downregulating the expression of bax and caspase-3 potentially via the ERK pathway in A549 and H460 cells of NSCLC.
|
22438908 |
2012 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
In the present study, we found BITC (7·5 and 10 μm) and PEITC (12·5 and 20 μm) induced highly metastatic human non-small cell lung cancer L9981 cell apoptosis in a dose-dependent manner.Caspase-3 was activated.
|
21733335 |
2011 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Our results show that human Lon is upregulated in non-small-cell lung cancer (NSCLC) cell lines, and downregulation of Lon triggers caspase-3 mediated apoptosis.
|
21077998 |
2010 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Radiation-induced apoptosis and the activation of caspase-3 were more elevated by XIAP-siRNA in the H1299/mp53 cells than in H1299/ wtp53.
|
18575718 |
2008 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In addition, knock-down of Oct-4 expression in LC-CD133(+) can significantly inhibit the abilities of tumor invasion and colony formation, and increase apoptotic activities of caspase 3 and poly (ADP-ribose) polymerase (PARP).
|
18612434 |
2008 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In contrast to the cells transfected with wild-type survivin, or the control NSCLC-3/neo, those cells transfected with mutant survivin and treated with SN-38 --> PS-341 exhibited enhanced caspase 9 activity (> 2-fold), caspase 3 (> 2- to 3-fold) activity and cytotoxicity compared to the NSCLC-3/neo cells.
|
16827119 |
2006 |