miRNA-128 modulates bone neoplasms cells proliferation and migration through the WNT/β-catenin and EMT signal pathways

Li, Yang; Long, Xiaotao; Wang, Ji; Peng, Jing; Shen, Kai

doi:10.1186/s13018-020-02164-w

Cited by 4 publications

(3 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The Wnt/β‐catenin is also found to be associated with tumour cell proliferation, apoptosis, cell cycle regulation, migration and metastasis 15 . As shown in Figure A, the expression of Wnt3a, Wnt5a and β‐catenin was significant down‐regulated in the cells treated with 20 mmol/L metformin.…”

Section: Resultsmentioning

confidence: 90%

lncRNA MALAT1 participates in metformin inhibiting the proliferation of breast cancer cell

Huang

Zhou

Zhang

et al. 2021

J Cellular Molecular Medi

View full text Add to dashboard Cite

In recent years, the repurposing of conventional and chemotherapeutic drugs is recognized as an alternative strategy for health care. The main purpose of this study is to strengthen the application of non‐oncological drug metformin on breast cancer treatment in the perspective of epigenetics. In the present study, metformin was found to inhibit cell proliferation, promote apoptosis and induce cell cycle arrest in breast cancer cells at a dose‐dependent manner. In addition, metformin treatment elevated acH3K9 abundance and decreased acH3K18 level. The expression of lncRNA MALAT1, HOTAIR, DICER1‐AS1, LINC01121 and TUG1 was up‐regulated by metformin treatment. In metformin‐treated cells, MALAT1 knock‐down increased the Bax/Bcl2 ratio and enhanced p21 but decreased cyclin B1 expression. The expression of Beclin1, VDAC1, LC3‐II, CHOP and Bip was promoted in the cells received combinatorial treatment of metformin and MALAT1 knock‐down. The reduced phosphorylation of c‐Myc was further decreased in the metformin‐treated cells in combination with MALAT1 knock‐down than metformin treatment alone. Taken together, these results provide a promising repurposed strategy for metformin on cancer treatment by modulating epigenetic modifiers.

show abstract

Section: Resultsmentioning

confidence: 90%

lncRNA MALAT1 participates in metformin inhibiting the proliferation of breast cancer cell

Huang

Zhou

Zhang

et al. 2021

J Cellular Molecular Medi

View full text Add to dashboard Cite

show abstract

“…Our study was similar to this previous research. β-catenin is known to be positively correlated with EMT process ( Li et al, 2021 ; Yiu et al, 2021 ). Therefore, the similar function between Wnt/β-catenin and tumor cell-derived exosomes might result in this similarity.…”

Section: Discussionmentioning

confidence: 99%

Tumor Cell-Derived Exosomal miR-770 Inhibits M2 Macrophage Polarization via Targeting MAP3K1 to Inhibit the Invasion of Non-small Cell Lung Cancer Cells

Liu

Luo

Wang

et al. 2021

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

BackgroundNon-small cell lung carcinoma (NSCLC) is a type lung cancer with high malignant behaviors. MicroRNAs (miRNAs) are known to be involved in progression of NSCLC. In order to explore potential targets for the treatment of NSCLC, bioinformatics tool was used to analyze differential expressed miRNAs between NSCLC and adjacent normal tissues.MethodsBioinformatics tool was used to find potential targets for NSCLC. Cell proliferation was investigated by Ki67 staining. Cell apoptosis was measured by flow cytometry. mRNA and protein expression in NSCLC cells were detected by RT-qPCR and Western-blot, respectively. Transwell assay was performed to test the cell migration and invasion. In order to investigate the function of exosomal miRNA in NSCLC, in vivo model of NSCLC was constructed.ResultsMiR-770 was identified to be downregulated in NSCLC, and miR-770 agomir could significantly inhibit NSCLC cell proliferation through inducing the apoptosis. Additionally, the metastasis of NSCLC cells was decreased by miR-770 agomir. MAP3K1 was identified to be the target mRNA of miR-770. Meanwhile, tumor cell-derived exosomal miR-770 inhibited M2 macrophage polarization via downregulation of MAP3K1, which in turn suppressed NSCLC cell invasion. Besides, tumor cell-derived exosomal miR-770 markedly decreased NSCLC tumor growth in vivo through suppressing M2 macrophage polarization.ConclusionTumor cell-derived exosomal miR-770 inhibits M2 macrophage polarization to inhibit the invasion of NSCLC cells via targeting MAP3K1. Thus, this study provided a new strategy for the treatment of NSCLC.

show abstract

“…205 Other newly identified EMT-related miRNAs include miR-27b-3p, 206 which promotes the generation of circulating tumor cells, and miRNA-490-3p, which promotes the metastasis of invasive ductal carcinoma. 207 Nonetheless, recent studies have reported that some miRNAs, such as miRNA-128 MiRNA-155-5p, 208,209 are able to hinder the EMT process through inhibition of diverse EMTrelated signaling pathways. With the increased understanding of miRNAs in EMT and TCP, different strategies focused on hindering miRNA function or miRNA delivery into tumor cells can be utilized to overcome cancer drug resistance.…”

Section: Epigenetic Mechanismsmentioning

confidence: 99%

Tumor cell plasticity in targeted therapy-induced resistance: mechanisms and new strategies

Pang

Yang

et al. 2023

Sig Transduct Target Ther

View full text Add to dashboard Cite

Despite the success of targeted therapies in cancer treatment, therapy-induced resistance remains a major obstacle to a complete cure. Tumor cells evade treatments and relapse via phenotypic switching driven by intrinsic or induced cell plasticity. Several reversible mechanisms have been proposed to circumvent tumor cell plasticity, including epigenetic modifications, regulation of transcription factors, activation or suppression of key signaling pathways, as well as modification of the tumor environment. Epithelial-to-mesenchymal transition, tumor cell and cancer stem cell formation also serve as roads towards tumor cell plasticity. Corresponding treatment strategies have recently been developed that either target plasticity-related mechanisms or employ combination treatments. In this review, we delineate the formation of tumor cell plasticity and its manipulation of tumor evasion from targeted therapy. We discuss the non-genetic mechanisms of targeted drug-induced tumor cell plasticity in various types of tumors and provide insights into the contribution of tumor cell plasticity to acquired drug resistance. New therapeutic strategies such as inhibition or reversal of tumor cell plasticity are also presented. We also discuss the multitude of clinical trials that are ongoing worldwide with the intention of improving clinical outcomes. These advances provide a direction for developing novel therapeutic strategies and combination therapy regimens that target tumor cell plasticity.

show abstract

miRNA-128 modulates bone neoplasms cells proliferation and migration through the WNT/β-catenin and EMT signal pathways

Cited by 4 publications

References 40 publications

lncRNA MALAT1 participates in metformin inhibiting the proliferation of breast cancer cell

lncRNA MALAT1 participates in metformin inhibiting the proliferation of breast cancer cell

Tumor Cell-Derived Exosomal miR-770 Inhibits M2 Macrophage Polarization via Targeting MAP3K1 to Inhibit the Invasion of Non-small Cell Lung Cancer Cells

Tumor cell plasticity in targeted therapy-induced resistance: mechanisms and new strategies

Contact Info

Product

Resources

About