α7-Nicotinic acetylcholine receptor antagonist QND7 suppresses non-small cell lung cancer cell proliferation and migration via inhibition of Akt/mTOR signaling

Witayateeraporn, Wasita; Arunrungvichian, Kuntarat; Pothongsrisit, Sutthaorn; Doungchawee, Jeerapat; Vajragupta, Opa; Pongrakhananon, Varisa

doi:10.1016/j.bbrc.2019.11.018

Cited by 19 publications

(23 citation statements)

References 34 publications

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“…Lung cancer is one of the most commonly found carcinoma type and is an aggressive tumor with high incidence and mortality rate worldwide [1]. Non-small cell lung cancer (NSCLC) accounts for 80-85% of lung cancer diagnoses and is the major cause of lung cancer-associated mortality due to late-stage detection [2].…”

Section: Introductionmentioning

confidence: 99%

Circular RNA hsa_circ_0072309 inhibits non-small cell lung cancer progression by sponging miR-580-3p

et al. 2020

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Objective: Non-small cell lung cancer (NSCLC) continues to top the list of cancer mortalities worldwide. Early diagnosis and therapeutic interventions targeting NSCLC is becoming the world's significant challenge. Circular RNAs (circRNAs) are emerging as a group of potential cancer biomarkers. Materials and methods: Quantitative real-time PCR (qRT-PCR) was employed to examine the expression of circ 0072309 in NSCLC tissues and cell lines. Cell counting kit 8 (CCK-8), wound healing and Transwell assays were used to analyze cell proliferation, migration and invasion in A549 and H1299 cells. The relationship between circ 0072309 and miR-580-3 was analyzed by Luciferase reporter and RNA pull down assays. Results: We screened circ 0072309 from Gene Expression Omnibus and found that circ 0072309 was lowly expressed in NSCLC tissues and cell lines. The transfection of circ 0072309-overexpressing vector significantly suppressed the cell proliferation, migration and invasion in A549 and H1299 cells. We predicted that miR-580-3p is a target of circ 0072309 by using publicly available bioinformatic algorithms Circinteractome tool and confirmed that circ 0072309 directly bound to miR-580-3p. Furthermore, the addition of miR-580-3p mitigated the blockage of cell proliferation, migration and invasion induced by circ 0072309. Conclusions: These data showed that circ 0072309 inhibits the progression of NSCLC progression via blocking the expression of miR-580-3p. These findings revealed the anti-tumor role of circ 0072309 during the development of NSCLC and provided a novel diagnostic biomarker and potential therapy for NSCLC.

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Section: Introductionmentioning

confidence: 99%

Circular RNA hsa_circ_0072309 inhibits non-small cell lung cancer progression by sponging miR-580-3p

et al. 2020

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“…Apoptotic cell death was evaluated by apoptotic nuclei staining, as previously reported, [47] and annexin V/PI assays. For the annexin V/PI assay, after similar treatment for 48 h, the apoptotic cells were analyzed using a dead cell apoptosis kit according to the manufacturerʼs protocol (Invitrogen).…”

Section: Apoptosis Assaymentioning

confidence: 99%

Erianthridin Induces Non-small Cell Lung Cancer Cell Apoptosis through the Suppression of Extracellular Signal-regulated Kinase Activity

et al. 2020

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Due to the high mortality of lung cancer, natural derivative compounds have been promoted as versatile sources for anticancer drug discovery. Erianthridin, a phenanthrene compound isolated from Dendrobium formosum, exhibits intriguing apoptosis-inducing effects in non-small cell lung cancer cells. Apoptotic nuclei staining assays showed that apoptotic cells with DNA fragmentation and apoptotic bodies were apparent, and an increase in annexin V-FITC-positive cells were found in cells treated with erianthridin. The apoptosis protein markers for cleaved caspase-3 and cleaved poly-ADP-ribose polymerase were significantly upregulated in response to erianthridin. A mechanistic investigation revealed that erianthridin was able to attenuate extracellular signal-regulated kinase activity and thereby mediate apoptosis through the modulation of Bcl-2 family protein levels. U0126, an extracellular signal-regulated kinase inhibitor, augmented the apoptosis-inducing effect of erianthridin; in contrast, overexpression of exogenous extracellular signal-regulated kinase substantially abrogated erianthridin activity. Furthermore, an in vitro 3D tumorigenesis assay showed that erianthridin was able to potentially suppress lung cancer cell proliferation. This study is the first to report a promising cytotoxic effect of erianthridin, which provides preclinical evidence for further research and development of this compound.

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“…(i) nAChR single-nucleotide polymorphisms (SNPs) were associated with lung cancer cells [ 41 , 42 ], and nAChRs were shown to be involved in cancer cell proliferation and survival [ 43 , 44 , 45 , 46 ]. Interestingly, several subunits (including α5-7-10/β2-3) were identified in cancer cell lines, and selective nAChR inhibitors induced anti-tumour effects [ 47 , 48 ]. In addition, acetylcholine-signalling proteins were involved in the progression of lung cancer [ 49 ].…”

Section: Discussionmentioning

confidence: 99%

Nicotinic Receptor Subunits Atlas in the Adult Human Lung

Diabasana

Perotin

Belgacemi

et al. 2020

IJMS

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Nicotinic acetylcholine receptors (nAChRs) are pentameric ligand-gated ion channels responsible for rapid neural and neuromuscular signal transmission. Although it is well documented that 16 subunits are encoded by the human genome, their presence in airway epithelial cells (AECs) remains poorly understood, and contribution to pathology is mainly discussed in the context of cancer. We analysed nAChR subunit expression in the human lungs of smokers and non-smokers using transcriptomic data for whole-lung tissues, isolated large AECs, and isolated small AECs. We identified differential expressions of nAChRs in terms of detection and repartition in the three modalities. Smoking-associated alterations were also unveiled. Then, we identified an nAChR transcriptomic print at the single-cell level. Finally, we reported the localizations of detectable nAChRs in bronchi and large bronchioles. Thus, we compiled the first complete atlas of pulmonary nAChR subunits to open new avenues to further unravel the involvement of these receptors in lung homeostasis and respiratory diseases.

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α7-Nicotinic acetylcholine receptor antagonist QND7 suppresses non-small cell lung cancer cell proliferation and migration via inhibition of Akt/mTOR signaling

Cited by 19 publications

References 34 publications

Circular RNA hsa_circ_0072309 inhibits non-small cell lung cancer progression by sponging miR-580-3p

Circular RNA hsa_circ_0072309 inhibits non-small cell lung cancer progression by sponging miR-580-3p

Erianthridin Induces Non-small Cell Lung Cancer Cell Apoptosis through the Suppression of Extracellular Signal-regulated Kinase Activity

Nicotinic Receptor Subunits Atlas in the Adult Human Lung

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