scholarly journals Lansoprazole Alone or in Combination With Gefitinib Shows Antitumor Activity Against Non-small Cell Lung Cancer A549 Cells in vitro and in vivo

2021 ◽  
Vol 9 ◽  
Author(s):  
Xiaoxia Zhao ◽  
Ning Zhang ◽  
Yingying Huang ◽  
Xiaojing Dou ◽  
Xiaolin Peng ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Small Cell Lung Cancer ◽  
Antitumor Effect ◽  
A549 Cells ◽  
Small Cell ◽  
Small Cell Lung ◽  
Cycle Arrest ◽  
G1 Cell Cycle Arrest

Lansoprazole (Lpz) is an FDA-approved proton pump inhibitor (PPI) drug for the therapy of acid-related diseases. Aiming to explore the new application of old drugs, we recently investigated the antitumor effect of Lpz. We demonstrated that the PPI Lpz played a tumor suppressive role in non-small cell lung cancer (NSCLC) A549 cells. Mechanistically, Lpz induced apoptosis and G0/G1 cell cycle arrest by inhibiting the activation of signal transducer and activator of transcription (Stat) 3 and the phosphoinositide 3-kinase (PI3K)/Akt and Raf/ERK pathways. In addition, Lpz inhibited autophagy by blocking the fusion of autophagosomes with lysosomes. Furthermore, Lpz in combination with gefitinib (Gef) showed a synergistic antitumor effect on A549 cells, with enhanced G0/G1 cell cycle arrest and apoptosis. The combination inhibited Stat3 phosphorylation, PI3K/Akt and Raf/ERK signaling, affecting cell cycle-related proteins such as p-Rb, cyclin D1 and p27, as well as apoptotic proteins such as Bax, Bcl-2, caspase-3, and poly (ADP-ribose) polymerase (PARP). In vivo, coadministration with Lpz and Gef significantly attenuated the growth of A549 nude mouse xenograft models. These findings suggest that Lpz might be applied in combination with Gef for NSCLC therapy, but further evidence is required.

3,3′,5,5′-tetramethoxybiphenyl-4,4′diol induces cell cycle arrest in G2/M phase and apoptosis in human non-small cell lung cancer A549 cells

2020 ◽  
Vol 326 ◽  
pp. 109133 ◽  
Author(s):  
Virginia Marcia Concato ◽  
Fernanda Tomiotto-Pellissier ◽  
Taylon Felipe Silva ◽  
Manoela Daiele Gonçalves ◽  
Bruna Taciane da Silva Bortoleti ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Small Cell Lung Cancer ◽  
Cell Cycle Arrest ◽  
Cell Lung Cancer ◽  
A549 Cells ◽  
Small Cell ◽  
Small Cell Lung ◽  
Cycle Arrest ◽  
M Phase

Acacetin-induced cell cycle arrest and apoptosis in human non-small cell lung cancer A549 cells

2004 ◽  
Vol 212 (1) ◽  
pp. 53-60 ◽  
Author(s):  
Ya-Ling Hsu ◽  
Po-Lin Kuo ◽  
Chi-Feng Liu ◽  
Chun-Ching Lin
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Small Cell Lung Cancer ◽  
Cell Cycle Arrest ◽  
Cell Lung Cancer ◽  
A549 Cells ◽  
Small Cell ◽  
Small Cell Lung ◽  
Cycle Arrest

scholarly journals ZNF674-AS1 suppresses non-small cell lung cancer growth through the miR-423-3p/p21 axis

2020 ◽  
Author(s):  
Yu Liu ◽  
Risheng Huang ◽  
Deyao Xie ◽  
Xiaoming Lin ◽  
Liangcheng Zheng
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Small Cell Lung Cancer ◽  
Cell Cycle Arrest ◽  
Cell Lung Cancer ◽  
Colony Formation ◽  
Small Cell ◽  
Small Cell Lung ◽  
Cycle Arrest ◽  
G1 Cell Cycle Arrest

Abstract Background: ZNF674-AS1, a recently characterized long noncoding RNA, shows prognostic significance in hepatocellualar carcinoma and glioma. However, the expression and function of ZNF674-AS1 in non-small cell lung cancer (NSCLC) is unclear. Methods: In this work, we investigated the expression of ZNF674-AS1 in 83 pairs of NSCLC specimens and adjacent noncancerous lung tissues. The clinical significance of ZNF674-AS1 in NSCLC was analyzed. The role of ZNF674-AS1 in NSCLC growth and cell cycle progression was explored. Results: Our data show that ZNF674-AS1 expression is decreased in NSCLC compared to normal tissues. ZNF674-AS1 downregulation is significantly correlated with advanced TNM stage and decreased overall survival of NSCLC patients. Overexpression of ZNF674-AS1 inhibits NSCLC cell proliferation, colony formation, and tumorigenesis, which is accompanied by a G0/G1 cell cycle arrest. Conversely, knockdown of ZNF674-AS1 enhances the proliferation and colony formation of NSCLC cells. Biochemically, ZNF674-AS1 overexpression increases the expression of p21 through downregulation of miR-423-3p. Knockdown of p21 or overexpression of miR-423-3p blocks ZNF674-AS1-mediated growth suppression and G0/G1 cell cycle arrest. In addition, ZNF674-AS1 expression is negatively correlated with miR-423-3p in NSCLC specimens. Conclusions: ZNF674-AS1 suppresses NSCLC growth by downregulating miR-423-3p and inducing p21. This work suggests the therapeutic potential of ZNF674-AS1 in the treatment of NSCLC.

Tannic Acid Inhibits Non-small Cell Lung Cancer (NSCLC) Stemness by Inducing G0/G1 Cell Cycle Arrest and Intrinsic Apoptosis

2020 ◽  
Vol 40 (6) ◽  
pp. 3209-3220 ◽  
Author(s):  
NIPIN SP ◽  
DONG YOUNG KANG ◽  
DOH HOON KIM ◽  
JI-SEUNG YOO ◽  
EUN SEONG JO ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Small Cell Lung Cancer ◽  
Cell Cycle Arrest ◽  
Tannic Acid ◽  
Small Cell ◽  
Intrinsic Apoptosis ◽  
Small Cell Lung ◽  
Cycle Arrest ◽  
G1 Cell Cycle Arrest

scholarly journals ZNF674-AS1 antagonizes miR-423-3p to induce G0/G1 cell cycle arrest in non-small cell lung cancer cells

2021 ◽  
Vol 26 (1) ◽  
Author(s):  
Yu Liu ◽  
Risheng Huang ◽  
Deyao Xie ◽  
Xiaoming Lin ◽  
Liangcheng Zheng
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Small Cell Lung Cancer ◽  
Cell Cycle Arrest ◽  
Cell Lung Cancer ◽  
Colony Formation ◽  
Small Cell ◽  
Small Cell Lung ◽  
Cycle Arrest ◽  
G1 Cell Cycle Arrest

Abstract Background ZNF674-AS1, a recently characterized long noncoding RNA, shows prognostic significance in hepatocellular carcinoma and glioma. However, the expression and function of ZNF674-AS1 in non-small cell lung cancer (NSCLC) are unclear. Methods In this work, we investigated the expression of ZNF674-AS1 in 83 pairs of NSCLC specimens and adjacent noncancerous lung tissues. The clinical significance of ZNF674-AS1 in NSCLC was analyzed. The role of ZNF674-AS1 in NSCLC growth and cell cycle progression was explored. Results Our data show that ZNF674-AS1 expression is decreased in NSCLC compared to normal tissues. ZNF674-AS1 downregulation is significantly correlated with advanced TNM stage and decreased overall survival of NSCLC patients. Overexpression of ZNF674-AS1 inhibits NSCLC cell proliferation, colony formation, and tumorigenesis, which is accompanied by a G0/G1 cell cycle arrest. Conversely, knockdown of ZNF674-AS1 enhances the proliferation and colony formation of NSCLC cells. Biochemically, ZNF674-AS1 overexpression increases the expression of p21 through downregulation of miR-423-3p. Knockdown of p21 or overexpression of miR-423-3p blocks ZNF674-AS1-mediated growth suppression and G0/G1 cell cycle arrest. In addition, ZNF674-AS1 expression is negatively correlated with miR-423-3p in NSCLC specimens. Conclusions ZNF674-AS1 suppresses NSCLC growth by downregulating miR-423-3p and inducing p21. This work suggests the therapeutic potential of ZNF674-AS1 in the treatment of NSCLC.

Cytotoxicity of withasteroids: withametelin induces cell cycle arrest at G2/M phase and mitochondria-mediated apoptosis in non-small cell lung cancer A549 cells

Tumor Biology ◽  
2016 ◽  
Vol 37 (9) ◽  
pp. 12579-12587 ◽  
Author(s):  
Poorna Chandra Rao ◽  
Sajeli Begum ◽  
Mohammad Ali Farboodniay Jahromi ◽  
Zahra Hosseini Jahromi ◽  
Saketh Sriram ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Small Cell Lung Cancer ◽  
Cell Cycle Arrest ◽  
Cell Lung Cancer ◽  
A549 Cells ◽  
Small Cell ◽  
Small Cell Lung ◽  
Cycle Arrest ◽  
M Phase
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