Acid-sensing ion channels contribute to the effect of extracellular acidosis on proliferation and migration of A549 cells

Inflammatory reactions mediated by the NACHT, LRR, and PYD domain-containing protein 3 (NLRP3) inflammasome contributes to non-small-cell lung cancer (NSCLC) progression, particularly in patients with bacterial infections. Salidroside (SAL) has recently been shown to suppress lipopolysaccharide- (LPS-) induced NSCLC proliferation and migration, but its mechanism of action remains unclear. It has been shown that SAL improves metabolic inflammation in diabetic rodents through AMP-activated protein kinase- (AMPK-) dependent inhibition of the NLRP3 inflammasome. However, whether the NLRP3 inflammasome is regulated by SAL in NSCLC cells and how its underlying mechanism(s) can be determined require clarification. In this study, human lung alveolar basal carcinoma epithelial (A549) cells were treated with LPS, and the effects of SAL on cell proliferation, migration, AMPK activity, reactive oxygen species (ROS) production, and NLRP3 inflammasome activation were investigated. We found that LPS induction increases the proliferation and migration of A549 cells which was suppressed by SAL. Moreover, SAL protected A549 cells against LPS-induced AMPK inhibition, ROS production, and NLRP3 inflammasome activation. Blocking AMPK using Compound C almost completely suppressed the beneficial effects of SAL. In summary, these results indicate that SAL suppresses the proliferation and migration of human lung cancer cells through AMPK-dependent NLRP3 inflammasome regulation.

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Effect of Dai-Bai-Jie on the proliferation and migration of the A549 cells

Chinese Chemical Letters ◽

10.1016/j.cclet.2019.07.066 ◽

2020 ◽

Vol 31 (2) ◽

pp. 476-478

Author(s):

Binxin Lin ◽

Xinling Lu ◽

Nan Li ◽

Ning Xu ◽

Jin-Ming Lin

Keyword(s):

A549 Cells ◽

And Migration ◽

Proliferation And Migration

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Non-Small Cell Lung Cancer A549 cells induces HUVECs proliferation and migration through TRPV3 promoting the secretion of VEGF

10.21203/rs.2.10275/v2 ◽

2019 ◽

Keyword(s):

Lung Cancer ◽

Small Cell Lung Cancer ◽

Cell Lung Cancer ◽

A549 Cells ◽

Small Cell ◽

Small Cell Lung ◽

And Migration ◽

Proliferation And Migration

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Heat shock protein B8 promotes proliferation and migration in lung adenocarcinoma A549 cells by maintaining mitochondrial function

Molecular and Cellular Biochemistry ◽

10.1007/s11010-020-03896-3 ◽

2020 ◽

Author(s):

Ling-Ling Yu ◽

Yuan Wang ◽

Zu-Ke Xiao ◽

Sheng-Song Chen

Keyword(s):

Heat Shock ◽

Heat Shock Protein ◽

Lung Adenocarcinoma ◽

Mitochondrial Function ◽

A549 Cells ◽

Lung Adenocarcinoma A549 ◽

And Migration ◽

Proliferation And Migration

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Ion channels and transporters in the development of drug resistance in cancer cells

Philosophical Transactions of the Royal Society B Biological Sciences ◽

10.1098/rstb.2013.0109 ◽

2014 ◽

Vol 369 (1638) ◽

pp. 20130109 ◽

Cited By ~ 62

Author(s):

Else K. Hoffmann ◽

Ian H. Lambert

Keyword(s):

Drug Resistance ◽

Ion Channels ◽

Drug Uptake ◽

Multi Drug Resistance ◽

Drug Efflux ◽

Ion Transporters ◽

Drug Induced ◽

And Migration ◽

Induced Apoptosis ◽

Proliferation And Migration

Multi-drug resistance (MDR) to chemotherapy is the major challenge in the treatment of cancer. MDR can develop by numerous mechanisms including decreased drug uptake, increased drug efflux and the failure to undergo drug-induced apoptosis. Evasion of drug-induced apoptosis through modulation of ion transporters is the main focus of this paper and we demonstrate how pro-apoptotic ion channels are downregulated, while anti-apoptotic ion transporters are upregulated in MDR. We also discuss whether upregulation of ion transport proteins that are important for proliferation contribute to MDR. Finally, we discuss the possibility that the development of MDR involves sequential and localized upregulation of ion channels involved in proliferation and migration and a concomitant global and persistent downregulation of ion channels involved in apoptosis.

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Deficiency of Functional Iron-Sulfur Domains in ABCE1 Inhibits the Proliferation and Migration of Lung Adenocarcinomas By Regulating the Biogenesis of Beta-Actin In Vitro

Cellular Physiology and Biochemistry ◽

10.1159/000485090 ◽

2017 ◽

Vol 44 (2) ◽

pp. 554-566 ◽

Cited By ~ 5

Author(s):

Qian Yu ◽

Xu Han ◽

Da-Li Tian

Keyword(s):

Lung Cancer ◽

Cancer Metastasis ◽

A549 Cells ◽

Metastatic Progression ◽

Lung Cancer Metastasis ◽

And Migration ◽

Opposing Effects ◽

Proliferation And Migration

Background/Aims: ATP-binding cassette transporter E1 (ABCE1), a unique ABC superfamily member that bears two Fe-S clusters, is essential for metastatic progression in lung cancer. Fe-S clusters within ABCE1 are crucial for ribosome dissociation and translation reinitiation; however, whether these clusters promote tumor proliferation and migration is unclear. Methods: The interaction between ABCE1 and β-actin was confirmed using GST pull-down. The lung adenocarcinoma (LUAD) cell line A549 was transduced with lentiviral packaging vectors overexpressing either wild-type ABCE1 or ABCE1 with Fe-S cluster deletions (ΔABCE1). The role of Fe-S clusters in the viability and migration of cancer cells was evaluated using clonogenic, MTT, Transwell and wound healing assays. Cytoskeletal rearrangement was determined using immunofluorescent techniques. Results: Fe-S clusters were the key domains in ABCE1 involved in binding to β-actin. The proliferative and migratory capacity increased in cells overexpressing ABCE1. However, the absence of Fe-S clusters reversed these effects. A549 cells overexpressing ABCE1 exhibited irregular morphology and increased levels of cytoskeletal polymerization as indicated by the immunofluorescence images. In contrast, cells expressing the Fe-S cluster deletion mutant presented opposing effects. Conclusion: These results demonstrate the indispensable role of Fe-S clusters when ABCE1 participates in the proliferation and migration of LUADs by interacting with β-actin. The Fe-S clusters of ABCE1 may be potential targets for the prevention of lung cancer metastasis.

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Suppression of MiR130a-3p Using CRISPR/Cas9 Induces Proliferation and Migration of Non-Small Cell Lung Cancer Cell Line

The Indonesian Biomedical Journal ◽

10.18585/inabj.v13i4.1670 ◽

2021 ◽

Vol 13 (4) ◽

pp. 364-74

Author(s):

Nur Ainina Abdollah ◽

Nabil Izzatie Mohamad Safiai ◽

Muhammad Khairi Ahmad ◽

Kumitaa Theva Das ◽

Siti Razila Abdul Razak

Keyword(s):

Lung Cancer ◽

Small Cell Lung Cancer ◽

Cell Lung Cancer ◽

A549 Cells ◽

Lung Cancer Cell Line ◽

Small Cell ◽

Small Cell Lung ◽

Stem Loop ◽

And Migration ◽

Proliferation And Migration

BACKGROUND: Molecular alterations of microRNA130a (miR130a) are observed in many types of cancers, including non-small cell lung cancer (NSCLC). However, the role of miR130a in NSCLC has been poorly studied.METHODS: In this study, clustered regularly interspaced short palindromic repeat (CRISPR)-Cas9 was utilised to knockdown miR130a. The gRNA was designed to target the stem loop, 3’ and 5’ sites of miR130a and stably expressed in A549 cells. Post-treatment, mature levels of miR130a-3p and 5p were quantified, and proliferation and migration assays were conducted.RESULTS: Result showed significant suppression of miR130a-3p and -5p by two and three-fold respectively, when the CRISPR/Cas9 targeted at the 3’ site and stem loop of the miR130a gene. Suppression of miR130a-3p significantly increased the growth and migration of A549 cells, but no significant changes were observed in cells with suppressed expression of miR130a-5p.CONCLUSION: Our encouraging results highlight that the suppression of the miR130a is achievable using CRISPR/Cas9, and suppression of the miR-130a-3p could play an important role in the regulation of NSCLC.KEYWORDS: miR130a, CRISPR-Cas9, non-small cell lung cancer

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Mechanism of transmembrane and coiled‑coil domain 1 in the regulation of proliferation and migration of A549 cells

Oncology Letters ◽

10.3892/ol.2020.12020 ◽

2020 ◽

Vol 20 (5) ◽

pp. 1-1

Author(s):

Chen Yang ◽

Yuan Wang ◽

Jian-Qi Bai ◽

Jing-Ru Zhang ◽

Pei-Yan Hu ◽

...

Keyword(s):

Coiled Coil ◽

A549 Cells ◽

Coiled Coil Domain ◽

Regulation Of Proliferation ◽

And Migration ◽

Proliferation And Migration

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Inhibition of PAR-1 Receptor Signaling by Enoxaparin Reduces Cell Proliferation and Migration in A549 Cells

Anticancer Research ◽

10.21873/anticanres.13723 ◽

2019 ◽

Vol 39 (10) ◽

pp. 5297-5310 ◽

Cited By ~ 2

Author(s):

AZHAAR ALTURKISTANI ◽

NISANNE GHONEM ◽

VERNA-ANN POWER-CHARNITSKY ◽

ALEJANDRO PINO-FIGUEROA ◽

MATTIA M. MIGLIORE

Keyword(s):

Cell Proliferation ◽

A549 Cells ◽

Receptor Signaling ◽

Cell Proliferation And Migration ◽

And Migration ◽

Proliferation And Migration

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The Parotoid Gland Secretion from Peruvian Toad Rhinella horribilis (Wiegmann, 1833): Chemical Composition and Effect on the Proliferation and Migration of Lung Cancer Cells

Toxins ◽

10.3390/toxins12090608 ◽

2020 ◽

Vol 12 (9) ◽

pp. 608

Author(s):

Guillermo Schmeda-Hirschmann ◽

Jean Paulo de Andrade ◽

Marilú Roxana Soto-Vasquez ◽

Paul Alan Arkin Alvarado-García ◽

Charlotte Palominos ◽

...

Keyword(s):

Chemical Composition ◽

Cancer Cells ◽

Biological Effects ◽

A549 Cells ◽

Bioactive Substances ◽

M Phase ◽

Ic50 Values ◽

And Migration ◽

Induced Apoptosis ◽

Proliferation And Migration

Since Rhinella sp. toads produce bioactive substances, some species have been used in traditional medicine and magical practices by ancient cultures in Peru. During several decades, the Rhinella horribilis toad was confused with the invasive toad Rhinella marina, a species documented with extensive toxinological studies. In contrast, the chemical composition and biological effects of the parotoid gland secretions (PGS) remain still unknown for R. horribilis. In this work, we determine for the first time 55 compounds from the PGS of R. horribilis, which were identified using HPLC-MS/MS. The crude extract inhibited the proliferation of A549 cancer cells with IC50 values of 0.031 ± 0.007 and 0.015 ± 0.001 µg/mL at 24 and 48 h of exposure, respectively. Moreover, it inhibited the clonogenic capacity, increased ROS levels, and prevented the etoposide-induced apoptosis, suggesting that the effect of R. horribilis poison secretion was by cell cycle blocking before of G2/M-phase checkpoint. Fraction B was the most active and strongly inhibited cancer cell migration. Our results indicate that the PGS of R. horribilis are composed of alkaloids, bufadienolides, and argininyl diacids derivatives, inhibiting the proliferation and migration of A549 cells.

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