Prevention and management of lung cancer in China

Hong, Qunying; Wu, Guohao; Qian, Guisheng; Hu, Chengping; Zhou, Jianying; Chen, Liangan; Liu, Weimin; Li, Shiyue; Wang, Kai; Wang, Qi; Zhang, Xiaoju; Li, Jing; Gong, Xin; Bai, Chunxue

doi:10.1002/cncr.29584

Cited by 221 publications

(187 citation statements)

References 18 publications

Supporting

Mentioning

186

Contrasting

Unclassified

Order By: Relevance

“…Lung cancer is the leading cause of cancer death worldwide, especially in China [1, 2]. Though multimodal therapies are often used in patients with non-small cell lung cancer (NSCLC), the overall prognosis of NSCLC remains poor [3].…”

Section: Introductionmentioning

confidence: 99%

MiR-140 Expression Regulates Cell Proliferation and Targets PD-L1 in NSCLC

Xie

Liang

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Programmed death ligand1(PD-L1) plays a role in the development and progression of non-small cell lung cancer (NSCLC). This study aimed to identify miRNA(s) that are responsible for regulation of expression of PD-L1 in NSCLC, and to investigate the role of PD-L1 in regulation of the cell cycle in NSCLC. Methods: We predicted the target miRNA of PD-L1, which was miR-140, using the online tools TargetScan and miBase. In NSCLC cells obtained from clinical specimens, in addition to A549 and NCI-H1650 cell cultures, western blots were used to detect the level of expression of proteins, while real-time PCR was used to determine the level of expression of PD-L1, miR-140, cyclin E, and β-actin. Transfection with miR-140 mimics, miR-140 inhibitors, and PD-L1 siRNA were conducted using commercial kits. To determine whether miR-140 directly binds PD-L1, a luciferase reporter gene with wild type or mutated PD-L1 was used. Cell viability was measured with the MTT assay, and PI staining was used for cell cycle analysis. Results: We found low expression of miR-140 and high expression of PD-L1 and cyclin E in NSCLC cells. Over-expression of miR-140 suppressed the expression of PD-L1 by directly binding its 3’ UTR, and was also associated with decreased expression of cyclin E and inhibition of cellular proliferation in A549 and NCI-H1650 cells. Inhibition of PD-L1, in the absence of manipulations to miR-140, also decreased the expression of cyclin E. Conclusion: We conclude that miR-140 directly suppresses PD-L1 and inhibits the miR-140/PD-L1/cyclin E pathway in NSCLC.

show abstract

Section: Introductionmentioning

confidence: 99%

MiR-140 Expression Regulates Cell Proliferation and Targets PD-L1 in NSCLC

Xie

Liang

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…According to the World Cancer Report 2014 issued by the World Health Organization (WHO), the incidence rate and mortality rate of lung cancer have boosted in the world, and rank first in all malignant tumors [1]. Among all types of lung cancers, Non-Small Cell Lung Cancer (NSCLC) occupies almost 80%, but the 5 y survival rate is only 13% [2,3].…”

Section: Introductionmentioning

confidence: 99%

Hypoxic microenvironment promotes proliferation and invasion of non-small cell lung cancer A549 Cells through Wnt/ÃÂ²-catenin signaling pathway

Ma¹,

He²,

Wang³

et al. 2018

biomedicalresearch

View full text Add to dashboard Cite

Objective: To study the effect of Wnt/β-catenin signaling pathway on hypoxia induced proliferation and invasion in lung cancer cell line A549. Methods: Cultured lung cancer A549 cells were treated with hypoxia for 24 h. The proliferation rates were detected by CCK8; the mRNA and protein expression levels of HIF-1α and β-catenin were detected by RT-PCR and Western blot; the effect of hypoxia on invasion ability of A549 cells were detected with Transwell method. Furthermore, β-catenin siRNA was used to investigate the role of β-catenin on hypoxia induced proliferation and invasion. Results: The results demonstrated that hypoxia could promote A549 cells proliferation and invasion. The mRNA and protein level of HIF-1α and β-catenin was upregulated by hypoxia treatment, whereas β-catenin siRNA could block these processes. Conclusion: Hypoxia promotes osteosarcoma cell line A549 proliferation and invasion by activating Wnt/β-catenin signaling pathway.

show abstract

“…Lung cancer, particularly non-small cell lung cancer (NSCLC), remains a challenging disease with high mortality worldwide [1-2]. Despite the tremendous mountainous progress in multidisciplinary therapy, the overall 5-year survival rate is still poor [3].…”

Section: Introductionmentioning

confidence: 99%

CNTN-1 Enhances Chemoresistance in Human Lung Adenocarcinoma Through Induction of Epithelial-Mesenchymal Transition by Targeting the PI3K/Akt Pathway

Zhang

Sun

et al. 2017

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Chemoresistance has been a major obstacle to the effective treatment of lung cancer. Previously, we found that contactin-1 (CNTN-1) is related to cisplatin resistance in lung adenocarcinoma. Here, we aimed to investigate the underlying mechanism behind the role of CNTN-1 in cisplatin resistance in lung adenocarcinoma. Methods: EMT-associated phenotypes, including alterations in cellular morphology and marker (E-cadherin, N-cadherin and Vimentin) expression, were compared between A549 cells and A549/DDP cells (a cisplatin-resistant cell line of lung adenocarcinoma with abnormal CNTN-1 expression) by using real-time time PCR and Western blotting. Other methods, including CNTN-1 overexpression in A549 cells and CNTN-1 knockdown in A549/DDP cells, were also used to investigate the role of CNTN-1 in mediating the EMT phenotype and thr resulting cisplatin resistance and malignant progression of cancer cells in vitro and in vivo. Results: A549/DDP cells exhibited an EMT phenotype and aggravated malignant behaviors. CNTN-1 knockdown in A549/DDP cells partly reversed the EMT phenotype, increased drug sensitivity, and attenuated the malignant progression whereas CNTN-1 overexpression in A549 cells resulted in the opposite trend. Furthermore, the PI3K/Akt pathway was involved in the effects of CNTN-1 on EMT progression in A549/DDP cells, verified by the xenograft mouse model. Conclusion: CNTN-1 promotes cisplatin resistance in human cisplatin-resistant lung adenocarcinoma through inducing the EMT process by activating the PI3K/Akt signaling pathway. CNTN-1 may be a potential therapeutic target to reverse chemoresistance in cisplatin-resistant lung adenocarcinoma.

show abstract

Prevention and management of lung cancer in China

Cited by 221 publications

References 18 publications

MiR-140 Expression Regulates Cell Proliferation and Targets PD-L1 in NSCLC

MiR-140 Expression Regulates Cell Proliferation and Targets PD-L1 in NSCLC

Hypoxic microenvironment promotes proliferation and invasion of non-small cell lung cancer A549 Cells through Wnt/ÃÂ²-catenin signaling pathway

CNTN-1 Enhances Chemoresistance in Human Lung Adenocarcinoma Through Induction of Epithelial-Mesenchymal Transition by Targeting the PI3K/Akt Pathway

Contact Info

Product

Resources

About

Prevention and management of lung cancer in China

Cited by 221 publications

References 18 publications

MiR-140 Expression Regulates Cell Proliferation and Targets PD-L1 in NSCLC

MiR-140 Expression Regulates Cell Proliferation and Targets PD-L1 in NSCLC

Hypoxic microenvironment promotes proliferation and invasion of non-small cell lung cancer A549 Cells through Wnt/ÃÂ²-catenin signaling pathway

CNTN-1 Enhances Chemoresistance in Human Lung Adenocarcinoma Through Induction of Epithelial-Mesenchymal Transition by Targeting the PI3K/Akt Pathway

Contact Info

Product

Resources

About

Hypoxic microenvironment promotes proliferation and invasion of non-small cell lung cancer A549 Cells through Wnt/ÃÂ²-catenin signaling pathway