Manganese‐12 acetate suppresses the migration, invasion, and epithelial–mesenchymal transition by inhibiting Wnt/<b>β</b>‐catenin and PI3K/AKT signaling pathways in breast cancer cells

Ju, Hongping; Li, Yongxia; Xing, Xin; Miao, Xisong; Feng, Yun-Ping; Ren, Yunhui; Qin, Jing; Liu, Dian; Chen, Zihao; Yang, Zhaoyu

doi:10.1111/1759-7714.12584

Cited by 11 publications

(6 citation statements)

References 31 publications

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“…Numerous studies have reported that EMT is mediated by multiple pathways, including the Smad, MAP kinase (MAPK), and phosphatidylinositol 3-kinase (PI3K) pathways (13,22,41). Experimental Smad3-deficient mouse models of EMT and fibrosis demonstrated that Smad3 signaling is important in fibrosis (23).…”

Section: L1020mentioning

confidence: 99%

Resolvin D1 attenuates mechanical stretch-induced pulmonary fibrosis via epithelial-mesenchymal transition

Yang

Xia

et al. 2019

American Journal of Physiology-Lung Cellular and Molecular Phys

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Mechanical ventilation-induced pulmonary fibrosis plays an important role in the high mortality rate of acute respiratory distress syndrome (ARDS). Resolvin D1 (RvD1) displays potent proresolving activities. Epithelial-mesenchymal transition (EMT) has been proved to be an important pathological feature of lung fibrosis. This study aimed to investigate whether RvD1 can attenuate mechanical ventilation-induced lung fibrosis. Human lung epithelial (BEAS-2B) cells were pretreated with RvD1 for 30 min and exposed to acid for 10 min before being subjected to mechanical stretch for 48 h. C57BL/6 mice were subjected to intratracheal acid aspiration followed by mechanical ventilation 24 h later (peak inspiratory pressure 22 cmH2O, positive end-expiratory pressure 2 cmH2O, and respiratory rate 120 breaths/min for 2 h). RvD1 was injected into mice for 5 consecutive days after mechanical ventilation. Treatment with RvD1 significantly inhibited mechanical stretch-induced mesenchymal markers (vimentin and α-smooth muscle actin) and stimulated epithelial markers (E-cadherin). Tert-butyloxycarbonyl 2 (BOC-2), a lipoxin A4 receptor/formyl peptide receptor 2 (ALX/FPR2) antagonist, is known to inhibit ALX/FPR2 function. BOC-2 could reverse the beneficial effects of RvD1. The antifibrotic effect of RvD1 was associated with the suppression of Smad2/3 phosphorylation. This study demonstrated that mechanical stretch could induce EMT and pulmonary fibrosis and that treatment with RvD1 could attenuate mechanical ventilation-induced lung fibrosis, thus highlighting RvD1 as an effective therapeutic agent against pulmonary fibrosis associated with mechanical ventilation.

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Section: L1020mentioning

confidence: 99%

Resolvin D1 attenuates mechanical stretch-induced pulmonary fibrosis via epithelial-mesenchymal transition

Yang

Xia

et al. 2019

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…The migratory and invasive ability of prostate cancer cells was measured in a Transwell chamber [ 23 ]. Before the start of the invasion test, Matrigel should be applied to the membrane 6 hours in advance.…”

Section: Methodsmentioning

confidence: 99%

“…Transwell chamber [23]. Before the start of the invasion test, Matrigel should be applied to the membrane 6 hours in advance.…”

Section: Transwell Cell Migration and Invasion Assaymentioning

confidence: 99%

microRNA-877-5p exerts tumor-suppressive functions in prostate cancer through repressing transcription of forkhead box M1

et al. 2021

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The study aimed to investigate the significant potential role of miR-877-5p in Prostate cancer. The expression levels of miR-877-5p and forkhead box M1 (FOXM1) mRNA were detected by qRT-PCR. The prognostic significance of miR-877-5p in prostate cancer was investigated using Kaplan Meier analysis. Then, Cell Counting Kit-8 (CCK-8) and transwell assay were used to evaluate the effects of miR-877-5p on cell biological functions. The mechanism of miR-877-5p action on prostate cancer cells was investigated by luciferase activity assay with wide-type or mutation. miR-877-5p was lowly expressed both in prostate cancer tissues and cell lines compared with corresponding normal counterparts. Further, miR-877-5p was significantly correlated with Gleason score and TNM stage.Moreover, miR-877-5p may serve as an independent prognostic predictor. In addition, FOXM1 was checked as a direct target gene of miR-877-5p, and miR-877-5p can inhibit the expression of FOXM1 to restrain the growth, migration, and invasion abilities of prostate cancer cells. Taken together, miR-877-5p may act as a suppressor in prostate cancer and reduces cancer cell proliferation, migration and invasion by targeting FOXM1. miR-877-5p may serve as the effective biomarkers and therapeutic target for treating prostate cancer patients.

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“… 4 However, this approach can induce or aggravate lung damage, a condition referred to as mechanical ventilation-induced lung injury (VILI). 5 , 6 Adjuvant pharmacological approaches to reduce ARDS-associated pulmonary fibrosis have been highlighted as a potential means to improve morbidity and mortality rates. Over the past two decades, considerable research has focused on developing pharmacological therapies for ARDS, but results to date have been unsuccessful.…”

Section: Introductionmentioning

confidence: 99%

Wnt/β-Catenin Participates in the Repair of Acute Respiratory Distress Syndrome-Associated Early Pulmonary Fibrosis via Mesenchymal Stem Cell Microvesicles

Zhang

Tang

et al. 2022

DDDT

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Purpose The main aim of the present study was to establish whether mesenchymal stem cell microvesicles (MSC MVs) exert anti-fibrotic effects and investigate the mechanisms underlying these effects in a mouse model of acute respiratory distress syndrome (ARDS)-associated early pulmonary fibrosis. Methods An ARDS-associated pulmonary fibrosis model was established in mice by an intratracheal injection of lipopolysaccharide (LPS). At 1, 3, and 7 days after LPS-mediated injury, the lungs of mice treated with MSC MVs and untreated controls were carefully excised and fibrosis was assessed based on the extent of collagen deposition. In addition, the development of epithelial–mesenchymal transition (EMT) was evaluated based on loss of E-cadherin and zona occludens-1 (ZO-1) along with the acquisition of α-smooth muscle actin (α-SMA) and N-cadherin. Nuclear translocation and β-catenin expression analyses were also used to evaluate activation of the Wnt/β-catenin signaling pathway. Results Blue-stained collagen fibers were evident as early as 7 days after LPS injection. Treatment with MSC MVs suppressed pathological progression to a significant extent. MSC MVs markedly reversed the upregulation of N-cadherin and α-SMA and attenuated the downregulation of E-cadherin and ZO-1. The expression and nuclear translocation of β-catenin were clearly decreased on day 7 after MSC MV treatment. Conclusion Analyses indicated that MSC MVs could ameliorate ARDS-associated early pulmonary fibrosis via the suppression of EMT and might be related to Wnt/β-catenin transition signaling.

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Manganese‐12 acetate suppresses the migration, invasion, and epithelial–mesenchymal transition by inhibiting Wnt/β‐catenin and PI3K/AKT signaling pathways in breast cancer cells

Cited by 11 publications

References 31 publications

Resolvin D1 attenuates mechanical stretch-induced pulmonary fibrosis via epithelial-mesenchymal transition

Resolvin D1 attenuates mechanical stretch-induced pulmonary fibrosis via epithelial-mesenchymal transition

microRNA-877-5p exerts tumor-suppressive functions in prostate cancer through repressing transcription of forkhead box M1

Wnt/β-Catenin Participates in the Repair of Acute Respiratory Distress Syndrome-Associated Early Pulmonary Fibrosis via Mesenchymal Stem Cell Microvesicles

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