scholarly journals Retraction: FOXC1 silencing promotes A549 cell apoptosis through inhibiting the PI3K/AKT/hedgehog/Gli2 signaling pathway

RSC Advances ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 4572-4572
Author(s):  
Laura Fisher
Keyword(s):  
Signaling Pathway ◽  
A549 Cell ◽  
Cell Apoptosis

Retraction of ‘FOXC1 silencing promotes A549 cell apoptosis through inhibiting the PI3K/AKT/hedgehog/Gli2 signaling pathway’ by Pei Wang et al., RSC Adv., 2018, 8, 33786–33793, DOI: 10.1039/C8RA06041J.

scholarly journals FOXC1 silencing promotes A549 cell apoptosis through inhibiting the PI3K/AKT/hedgehog/Gli2 signaling pathway

RSC Advances ◽  
2018 ◽  
Vol 8 (59) ◽  
pp. 33786-33793
Author(s):  
Pei Wang ◽  
Hongbing Ma ◽  
Yong Li ◽  
Dong Chen ◽  
Xiaohui Li ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Signaling Pathway ◽  
A549 Cell ◽  
Cell Apoptosis ◽  
Premature Death

Lung cancer begins in the lung and is a leading cause of premature death.

Role of Bm30kc6 gene in cell apoptosis and the silk gland degradation signaling pathway in Bombyx mori L.

2020 ◽  
Vol 105 (3) ◽  
Author(s):  
Ying Xiao ◽  
Lei‐lei Li ◽  
Asma Bibi ◽  
Ning Zhang ◽  
Ting Chen ◽  
...  
Keyword(s):  
Bombyx Mori ◽  
Signaling Pathway ◽  
Cell Apoptosis ◽  
Silk Gland ◽  
Bombyx Mori L

scholarly journals Retraction: Salvianolic acid B inhibits inflammatory response and cell apoptosis via the PI3K/Akt signaling pathway in IL-1β-induced osteoarthritis chondrocytes

RSC Advances ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 4441-4441
Author(s):  
Laura Fisher
Keyword(s):  
Inflammatory Response ◽  
Signaling Pathway ◽  
Cell Apoptosis ◽  
Akt Signaling ◽  
Salvianolic Acid B ◽  
Signalling Pathway ◽  
Akt Signaling Pathway ◽  
Salvianolic Acid ◽  
Osteoarthritis Chondrocytes

Retraction of ‘Salvianolic acid B inhibits inflammatory response and cell apoptosis via the PI3K/Akt signalling pathway in IL-1β-induced osteoarthritis chondrocytes’ by Bin Zhu et al., RSC Adv., 2018, 8, 36422–36429, DOI: 10.1039/C8RA02418A.

scholarly journals PLAUR Confers Resistance to Gefitinib Through EGFR/P-AKT/Survivin Signaling Pathway

2018 ◽  
Vol 47 (5) ◽  
pp. 1909-1924 ◽  
Author(s):  
Jian Zhou ◽  
Kwang Joo Kwak ◽  
Zuoren Wu ◽  
Dawei Yang ◽  
Jing Li ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Membrane Potential ◽  
Tyrosine Kinase ◽  
Lung Adenocarcinoma ◽  
Signaling Pathway ◽  
Cell Apoptosis ◽  
Mitochondrial Membrane ◽  
Human Lung ◽  
Nsclc Patients ◽  
Gefitinib Resistance

Background/Aims: Tyrosine kinase inhibitor gefitinib significantly improves the survival of patients with non-small-cell lung cancer (NSCLC) by inhibiting epidermal growth factor receptor (EGFR) tyrosine kinase. However, patients eventually develop resistance to gefitinib through uncharacterized mechanisms. It is known that plasminogen activator urokinase receptor (PLAUR) plays an important role in cell proliferation, migration and apoptosis. However, the role of PLAUR, particularly exosomal PLAUR in gefitinib resistance in NSCLC has not been reported. The aim of this study is to determine the relationship between PLAUR and gefitinib resistance. Methods: In this study, a tethered cationic lipoplex nanoparticle (TCLN) biochip containing molecular beacons was used as probes to detect PLAUR mRNA in plasma exosomes from patients with gefitinib-sensitive and -resistant NSCLC. In vitro, Real-time PCR was used to examine the expression of PLAUR mRNA and Western blot was applied to examine the expression of related proteins. The gene knockdown was achieved by Lentivirus based RNA silence technique. The cell counting kit-8 assay and EdU incorporation were used to examine cell proliferation. The flow cytometry was applied to determine cell apoptosis and cell cycle, while the mitochondrial membrane potential was measured by JC-1 dye assay. Signaling pathway affected by PLAUR knockdown was identified by cDNA Microarray. The effect of PLAUR knockdown on tumorigenesis was analyzed in vivo. Results: We found that the exosomal PLAUR mRNA in the plasma of gefitinib-resistant NSCLC patients was significantly increased compared to that of gefitinib-sensitive NSCLC patients. The PLAUR mRNA and soluble PLAUR protein were also significantly increased in gefitinib-resistant human lung adenocarcinoma PC9R cells compared to gefitinib-sensitive PC9 cells. Silencing PLAUR in PC9R cells impaired mitochondrial membrane potential and increased cell apoptosis via EGFR/p-AKT/survivin signaling pathway. Furthermore, EGFR was upregulated in the geftinib-resistant PC9R cells, and knockdown of EGFR significantly increased cell apoptosis. Conclusions: Taken together, our results demonstrated that PLAUR induces geftinib-resistance through EGFR/p-AKT/survivin signaling pathway in gefitinib-resistant human lung adenocarcinoma cells. PLAUR could be a novel therapeutic target for gefitinib-resistant NSCLC patients.

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