scholarly journals Parthenolide inhibits human lung cancer cell growth by modulating the IGF‑1R/PI3K/Akt signaling pathway

2020 ◽  
Vol 44 (3) ◽  
pp. 1184-1193
Author(s):  
Longhua Sun ◽  
Wenxin Yuan ◽  
Guilan Wen ◽  
Bentong Yu ◽  
Fei Xu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Signaling Pathway ◽  
Cancer Cell ◽  
Human Lung ◽  
Akt Signaling ◽  
Human Lung Cancer ◽  
Akt Signaling Pathway ◽  
Lung Cancer Cell ◽  
Cancer Cell Growth

scholarly journals Atypical Protein Kinase Cι Plays a Critical Role in Human Lung Cancer Cell Growth and Tumorigenicity

2005 ◽  
Vol 280 (35) ◽  
pp. 31109-31115 ◽  
Author(s):  
Roderick P. Regala ◽  
Capella Weems ◽  
Lee Jamieson ◽  
John A. Copland ◽  
E. Aubrey Thompson ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Protein Kinase ◽  
Cell Growth ◽  
Cancer Cell ◽  
Human Lung ◽  
Critical Role ◽  
Human Lung Cancer ◽  
Lung Cancer Cell ◽  
Cancer Cell Growth ◽  
Human Lung Cancer Cell

scholarly journals Inhibitory effects of norcantharidin against human lung cancer cell growth and migration

2010 ◽  
Vol 62 (4) ◽  
pp. 349-355 ◽  
Author(s):  
Jinling Luan ◽  
Huiying Duan ◽  
Qian Liu ◽  
Kazumi Yagasaki ◽  
Guoying Zhang
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Human Lung ◽  
Human Lung Cancer ◽  
Inhibitory Effects ◽  
Lung Cancer Cell ◽  
Cancer Cell Growth ◽  
Cell Growth And Migration ◽  
And Migration

scholarly journals Targeting PRMT5/Akt signalling axis prevents human lung cancer cell growth

2018 ◽  
Vol 23 (2) ◽  
pp. 1333-1342 ◽  
Author(s):  
Shikui Zhang ◽  
Yaqiong Ma ◽  
Xiaoyan Hu ◽  
Yonghua Zheng ◽  
Xiaoke Chen
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Human Lung ◽  
Human Lung Cancer ◽  
Lung Cancer Cell ◽  
Cancer Cell Growth ◽  
Human Lung Cancer Cell

Long non-coding RNA EPIC1 promotes human lung cancer cell growth

2018 ◽  
Vol 503 (3) ◽  
pp. 1342-1348 ◽  
Author(s):  
Bing Zhang ◽  
Hui-Yu Lu ◽  
Yun-Hong Xia ◽  
Ai-Gui Jiang ◽  
Yu-Xin Lv
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Human Lung ◽  
Human Lung Cancer ◽  
Lung Cancer Cell ◽  
Cancer Cell Growth ◽  
Human Lung Cancer Cell ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals Beclin1-induced Autophagy Abrogates Radioresistance of Lung Cancer Cells by Suppressing Osteopontin

2012 ◽  
Vol 53 (3) ◽  
pp. 422-432 ◽  
Author(s):  
Seung-Hee Chang ◽  
Arash Minai-Tehrani ◽  
Ji-Young Shin ◽  
Sungjin Park ◽  
Ji-Eun Kim ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Human Lung ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Lung Cancer Cell ◽  
Cancer Cell Growth ◽  
Human Lung Cancer Cells

Abstract Osteopontin (OPN) serves as an indicator of resistance to radiotherapy. However, the role of OPN in the development of acquired radioresistance in human lung cancer cells has not yet been fully elucidated. Therefore, the potential importance of OPN as a marker of lung cancer with a potential significant role in the development of radioresistance against repeated radiotherapy has prompted us to define the pathways by which OPN regulates lung cancer cell growth. In addition, autophagy has been reported to play a key role in the radiosensitization of cancer cells. Here, we report that increased OPN expression through induction of nuclear p53 following irradiation was inhibited by exogenous beclin-1 (BECN1). Our results clearly show that BECN1 gene expression led to induction of autophagy and inhibition of cancer cell growth and angiogenesis. Our results suggest that the induction of autophagy abrogated the radioresistance of the cancer cells. Interestingly, we showed that knockdown of OPN by lentivirus-mediated shRNA induced the autophagy of human lung cancer cell. Taken together, these results suggest that OPN and BECN1 can be molecular targets for overcoming radioresistance by controlling autophagy.

scholarly journals Suppression of human lung cancer cell growth and migration by berbamine

2009 ◽  
Vol 62 (4) ◽  
pp. 341-348 ◽  
Author(s):  
Huiying Duan ◽  
Jinling Luan ◽  
Qian Liu ◽  
Kazumi Yagasaki ◽  
Guoying Zhang
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Human Lung ◽  
Human Lung Cancer ◽  
Lung Cancer Cell ◽  
Cancer Cell Growth ◽  
Cell Growth And Migration ◽  
Human Lung Cancer Cell ◽  
And Migration

scholarly journals Activation of ERK and Mutual Regulation of Stat3 and SP1 Contribute to Inhibition of PDK1 Expression by Atractylenolide-1 in Human Lung Cancer Cells

2017 ◽  
Vol 43 (6) ◽  
pp. 2353-2366 ◽  
Author(s):  
Qian Xiao ◽  
Fang Zheng ◽  
JingJing Wu ◽  
Qing Tang ◽  
Wei Wang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Human Lung ◽  
Human Lung Cancer ◽  
Lung Cancer Cell ◽  
Cancer Cell Growth ◽  
Protein Expressions ◽  
Mutual Regulation

Background/Aims: Atractylodes macrocephula Koidz is an important ingredient in traditional Chinese herbs. One major bioactive compound, atractylenolide-1 (ATL-1), was reported to have anti-inflammatory and anti-tumor activities. However, the underlying molecular mechanism associated to this has not been well elucidated. Methods: Cell viability and cell cycle distribution were measured using 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) and flow cytometry assays, respectively. Western blot analysis was performed to examine the phosphorylation and protein expression of extracellular signaling-regulated kinase 1/2 (ERK1/2), signal transducer and activator of transcription 3 (Stat3), 3-phosphoinositide dependent protein kinase-1 (PDK1) and transcription factor SP1. QRT-PCR was used to examine the mRNA levels of PDK1 gene. Exogenously expressions of Stat3, PDK1 and SP1 were carried out by transient transfection assays. PDK1 promoter activity was measured by Secrete-Pair Dual Luminescence Assay Kit. A nude mice xenograft model was used to confirm the findings in vitro. Results: We showed that ATL-1 inhibited human lung cancer cell growth and induced cell cycle arrest. Furthermore, we found that ATL-1 stimulated phosphorylation of ERK1/2, inhibited phosphorylation and protein expressions of Stat3 and SP1; the latter were abrogated in the presence of MEK/ERK inhibitor PD98059. Moreover, ATL-1 reduced the protein, mRNA expression and promoter activity of PDK1. Intriguingly, exogenously expressed Stat3 and SP1 overcame ATL-1-inhibited SP1 and Stat3, and PDK1 protein expressions, respectively. Moreover, overexpression of PDK1 resisted the ATL-1-inhibited lung cancer cell growth. In consistent with the results in vitro, ATL-1 inhibited tumor growth, protein expressions of Stat3, SP1 and PDK1, and induced phosphorylation of ERK1/2 in vivo. Conclusion: In summary, our results show that ATL-1 inhibits lung cancer cell growth through activation of ERK1/2, followed by suppressing SP1 protein expression. ATL-1 also reduces phosphorylation and protein levels of Stat3. These are mutual regulation between Stat3 and SP1 proteins affected by ATL-1. This ultimately suppresses PDK1 gene expression. This study reveals a novel mechanism by which ATL-1 inhibits growth of lung cancer cells. Thus, targeting PDK1 pinpoints a potential in the lung cancer treatment.

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