MiRNA-based Therapeutic Strategy in Lung Cancer

Li, Guang; Fang, Jing; Wang, Ying; Wang, Hu; Sun, Chengcao

doi:10.2174/1381612823666170725141954

Cited by 28 publications

(16 citation statements)

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“…In addition, further experiments that shed light on XB130 protein expression in cancer and paracancerous tissues and perform correlations of the expression levels of the miR-30 family and XB130 in cancer tissues from patients with NSCLC are required to verify the findings of the present study. Combined with the low expression levels of miR-30 family members exhibited by patients with NSCLC (7,(11)(12)(13)(14), the present results supported the hypothesis that enhancing miR-30 family expression levels or silencing XB130 may provide improved survival benefit for patients with NSCLC (13,31,(36)(37)(38)(39). Figure 4.…”

Section: Discussionsupporting

confidence: 82%

Members of the miR‑30 family inhibit the epithelial‑to‑mesenchymal transition of non‑small‑cell lung cancer cells by suppressing XB130 expression levels

et al. 2020

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MicroRNAs (miRs) are associated with cancer metastasis. Aberrant expression levels of members of the miR-30 family have been observed in non-small-cell lung cancer (NSCLC). However, the effects of miR-30 family members on the epithelial-to-mesenchymal transition (EMT) of NSCLC cells and the underlying molecular mechanisms have not yet been fully elucidated. The present study investigated the effects of miR-30 family members on EMT, migration and invasion of NSCLC cells and found that overexpression of these miRs inhibited EMT via decreasing the expression levels of N-cadherin, β-catenin and SNAI1, along with weakened migration and invasion abilities. Then, XB130 was identified as a downstream target of the miR-30 family members. XB130-knockdown also inhibited EMT of NSCLC cells, whereas ectopic overexpression of XB130 partly rescued the suppressive effects of miR-30c and miR-30d on EMT. In conclusion, miR-30 family members inhibited EMT of NSCLC cells, partially via suppressing XB130 expression levels.

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Section: Discussionsupporting

confidence: 82%

Members of the miR‑30 family inhibit the epithelial‑to‑mesenchymal transition of non‑small‑cell lung cancer cells by suppressing XB130 expression levels

et al. 2020

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“…A single miRNA can influence the expression of several targets for degradation or translation repression, consequently their dysregulation can lead to human diseases, including cancer. Differentially expressed miRNAs were reported in diverse cancer types, such as breast [36], lung [37], prostate [38], and head and neck cancer [39]. The interest in the study of therapeutic strategies that act on miRNAs is linked to the fact that, by intervening therapeutically on a single molecule, it is possible to obtain multiple effects on the gene expression.…”

Section: Discussionmentioning

confidence: 99%

Mi-RNA-888-5p Is Involved in S-Adenosylmethionine Antitumor Effects in Laryngeal Squamous Cancer Cells

Pagano

Mosca

Vitiello

et al. 2020

Cancers

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(1) Purpose: The methyl donor S-Adenosylmethionine (AdoMet) has been widely explored as a therapeutic compound, and its application-alone or in combination with other molecules-is emerging as a potential effective strategy for the treatment and chemoprevention of tumours. In this study, we investigated the antitumor activity of AdoMet in Laryngeal Squamous Cell Carcinoma (LSCC), exploring the underlying mechanisms. (2) Results: We demonstrated that AdoMet induced ROS generation and triggered autophagy with a consistent increase in LC3B-II autophagy-marker in JHU-SCC-011 and HNO210 LSCC cells. AdoMet induced ER-stress and activated UPR signaling through the upregulation of the spliced form of XBP1 and CHOP. To gain new insights into the molecular mechanisms underlying the antitumor activity of AdoMet, we evaluated the regulation of miRNA expression profile and we found a downregulation of miR-888-5p. We transfected LSCC cells with miR-888-5p inhibitor and exposed the cells to AdoMet for 48 and 72 h. The combination of AdoMet with miR-888-5p inhibitor synergistically induced both apoptosis and inhibited cell migration paralleled by the up-regulation of MYCBP and CDH1 genes and of their targets. (3) Conclusion: Overall, these data highlighted that epigenetic reprogramming of miRNAs by AdoMet play an important role in inhibiting apoptosis and migration in LSCC cell lines.

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“…miRNAs are novel biomarkers for NSCLC (33). Recent studies described a novel therapeutic strategy based on miRNAs for patients with NSCLC (34). For example, miR-1298 suppresses tumor progression in NSCLC (35).…”

Section: Mapk10 Expression -----------------------------mentioning

confidence: 99%

Propofol suppresses the progression of non‑small cell lung cancer via downregulation of the miR‑21‑5p/MAPK10 axis

2020

Oncol Rep

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Non-small cell lung cancer (NSCLC) accounts for >80% of lung cancer cases and is the leading cause of cancer-associated mortality worldwide. Propofol is an anesthetic drug frequently used during tumor resection. It is also known to exert inhibitory effects on cancer. Although the role of propofol in NSCLC has been reported, its underlying mechanisms remain unknown. The present study aimed therefore to investigate the mechanisms of propofol action on NSCLC. Starbase V3.0 project was used to analyze the expression levels of microRNA-21-5p (miR-21-5p) and mitogen-activated protein kinase 10 (MAPK10) in NSCLC and adjacent normal tissues from patients with NSCLC and the association between miR-21-5p and MAPK10 expression level in NSCLC tissues. The correlation between MAPK10 expression and disease-free survival (DFS) in patients with NSCLC was analyzed using GEPIA software version 1.0. miR-21-5p and MAPK10 expression in tumor and adjacent normal tissues from patients with NSCLC was evaluated by reverse transcription-quantitative (RT-q) PCR and western blotting. Cell viability and apoptosis were assessed by using Cell Counting Kit-8 assay and flow cytometry, respectively. The interaction between miR-21-5p and MAPK10 was predicted by TargetScan/miRanda and verified by dual luciferase assay. The regulatory effect of propofol on miR-21-5p and MAPK10 expression in NSCLC cell lines was examined by RT-qPCR and western blotting. Starbase V3.0 project and the results of the present study indicated that tumor tissues presented a significantly lower MAPK10 level and a higher miR-21-5p level compared with the normal samples, and that miR-21-5p expression was negatively correlated with MAPK10 expression in the tumor tissues of patients with NSCLC. Furthermore, miR-21-5p targeted the 3'-untranslated region of MAPK10. In addition, compared with BEAS-2B cells, a higher miR-21-5p and a lower MAPK10 expression was observed in the NSCLC cell lines A549 and H1299, which was reversed by propofol. The overexpression of miR-21-5p abrogated the effects of propofol on A549 and H1299 cell viability and apoptosis by targeting MAPK10. Taken together, these findings demonstrated that propofol inhibited the viability and promoted the apoptosis of NSCLC cells by downregulating the miR-21-5p/MAPK10 axis.

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MiRNA-based Therapeutic Strategy in Lung Cancer

Cited by 28 publications

References 0 publications

Members of the miR‑30 family inhibit the epithelial‑to‑mesenchymal transition of non‑small‑cell lung cancer cells by suppressing XB130 expression levels

Members of the miR‑30 family inhibit the epithelial‑to‑mesenchymal transition of non‑small‑cell lung cancer cells by suppressing XB130 expression levels

Mi-RNA-888-5p Is Involved in S-Adenosylmethionine Antitumor Effects in Laryngeal Squamous Cancer Cells

Propofol suppresses the progression of non‑small cell lung cancer via downregulation of the miR‑21‑5p/MAPK10 axis

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