Exosomes of A549 Cells Induced Migration, Invasion, and EMT of BEAS-2B Cells Related to let-7c-5p and miR-181b-5p

Abstract

As carriers containing abundant biological information, exosomes could deliver the property of donor cells to recipient cells. Emerging studies have shown that tumor cells could secrete a mass of exosomes into the microenvironment to regulate bystander cells. However, the underlying mechanisms of such a phenomenon remain largely unexplored. In this research, we purified and identified the exosomes of A549 cells and found that A549-cell-derived exosomes promoted BEAS-2B cells migration, invasion, and epithelial–mesenchymal transition (EMT). Importantly, we observed that let-7c-5p and miR-181b-5p were attenuated in A549-cell-derived exosomes compared to BEAS-2B-cell-derived exosomes. The analysis of miRNA expression level in BEAS-2B cells indicated that incubation with A549-cell-derived exosomes reduced the expression levels of let-7c-5p and miR-181b-5p. In transient transfections assay, we found that downregulation of let-7c-5p and miR-181b-5p simultaneously showed stronger promotion of BEAS-2B cells migration and invasion than individually. Moreover, exosomes secreted from A549 cells with upregulated expression of let-7c-5p and miR-181b-5p significantly reduce their regulatory effect on BEAS-2B cells. Bioinformatics analyses revealed that let-7c-5p and miR-181b-5p inhibit the EMT process mainly by regulating focal adhesion and mitogen-activated protein kinase (MAPK) signaling pathway. Thus, our data demonstrated that A549-cell-derived exosomal let-7c-5p and miR-181b-5p could induce migration, invasion, and EMT in BEAS-2B cells, which might be regulated through focal adhesion and MAPK signaling pathway. The expression level of let-7c-5p and miR-181b-5p may show great significance for the early diagnosis of lung cancer.

Audible Acoustic Wave Promotes EV Formation and Secretion from Adherent Cancer Cells via Mechanical Stimulation

“…It is now generally accepted that cancer cell-derived EVs have the ability to promote cancer metastasis. − Therefore, we evaluated the effect of EVs at 30 μg/mL on cancer cell migration and invasion and found no significant differences between AAW-promoted cancer cell-derived EVs and static cancer cell-derived EVs (Figure B,D,F,H,J). This result is consistent with previous studies in which EVs promote cancer cell migration and invasion . As a result, our findings indicate that the promotive function of EVs induced by the AAW method in facilitating cancer cell migration and invasion is maintained, which may help decipher the mechanism of EV-mediated cancer metastasis.…”

“…This result is consistent with previous studies in which EVs promote cancer cell migration and invasion. 51 As a result, our findings indicate that the promotive function of EVs induced by the AAW method in facilitating cancer cell migration and invasion is maintained, which may help decipher the mechanism of EV-mediated cancer metastasis. Thus, these results lay the foundation of enhancing EV production via AAW stimulation to boost cancer-EV-related basic research and translational investigation.…”

Serine/threonine kinase 36 induced epithelial-mesenchymal transition promotes docetaxel resistance in prostate cancer

“…In this study, reduced E-cadherin and increased N Cadherin and Vimentin levels were observed in cells overexpressing STK36, which suggested an interaction between STK36 and EMT. EMT can accelerate the motility and migration of cancer cells besides their morphological alteration 37 , 38 . The CCK8 and cell wound scratch assay confirmed the claim.…”

m6A modification of lncRNA PHKA1‐AS1 enhances Actinin Alpha 4 stability and promotes non‐small cell lung cancer metastasis

“…GAPDH served as endogenous reference of lncRNA and mRNA. ΔCt = Ct (target gene) ‒ Ct (GAPDH), ΔΔCt = ΔCt (treatment group) ‒ ΔCt (control group), and the relative expression of genes was calculated by formula 2 −ΔΔCt 44 . Table S1 displays the primers used in the study.…”