miR-550a-5p Functions as a Tumor Promoter by Targeting LIMD1 in Lung Adenocarcinoma

Guo, Zizhang; Ma, Zijuan; He, Yunjie; Jiang, Wei; Xia, Yang; Pan, Chunfeng; Wei, Ke; Shi, Yijun; Liang, Changhong; Chen, Yijiang

doi:10.3389/fonc.2020.570733

Cited by 9 publications

(5 citation statements)

References 30 publications

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“…Similar to our results, miR-550a-5p has been reported to function as a tumor promoter in colorectal cancer and lung adenocarcinoma [ 53 , 54 ]. However, currently no literature report elucidates the biological function of miR-550a-5p in breast cancer.…”

Section: Discussionsupporting

confidence: 92%

Circular RNA circCCDC85A inhibits breast cancer progression via acting as a miR-550a-5p sponge to enhance MOB1A expression

et al. 2022

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Background A growing body of evidence indicates that abnormal expression of circular RNAs (circRNAs) plays a crucial role by acting as molecular sponges of microRNAs (miRNAs) in various diseases, including cancer. In this study, we explored whether circCCDC85A could function as a miR-550a-5p sponge and influence breast cancer progression. Methods We detected the expression of circCCDC85A in breast cancer tissues and cells using fluorescence in situ hybridization (FISH) and quantitative reverse transcription polymerase chain reaction (qRT-PCR). CCK-8 and colony formation assay were used to detect the proliferative ability of breast cancer cells. Wound healing assay and transwell migration and invasion assays were used to detect the migrative and invasive abilities of breast cancer cells. We also examined the interactions between circCCDC85A and miR-550a-5p using FISH, RNA-binding protein immunoprecipitation (RIP), and luciferase reporter assay. Moreover, we performed luciferase reporter assay, qRT-PCR, and Western blot to confirm the direct targeting of miR-550a-5p to MOB1A. Results The expression of circCCDC85A in breast cancer tissues was obviously lower than that in normal breast tissues. Over-expression of circCCDC85A substantially inhibited the proliferative, migrative, and invasive ability of breast cancer cells, while knocking down of circCCDC85A enhanced the aforementioned properties of breast cancer cells. Moreover, enforced expression of circCCDC85A inhibits the oncogenic activity of miR-550a-5p and increases the expression of MOB1A targeted by miR-550a-5p. Further molecular mechanism research showed that circCCDC85A may act as a molecular sponge for miR-550a-5p, thus restoring miR-550a-5p-mediated targeting repression of tumor suppressor MOB1A in breast cancer cells. Conclusion Our findings provide novel evidence that circCCDC85A inhibits the progression of breast cancer by functioning as a molecular sponge of miR-550a-5p to enhance MOB1A expression.

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Section: Discussionsupporting

confidence: 92%

Circular RNA circCCDC85A inhibits breast cancer progression via acting as a miR-550a-5p sponge to enhance MOB1A expression

et al. 2022

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“…For example, interference of miR‐324‐3p impeded lung cancer progression via regulating ALX4 to inactivate the MAPK pathway 17 . Furthermore, upregulation of miR‐550a‐5p contributed to the growth of lung adenocarcinoma by suppressing LIMD1 18 . Additionally, Xiao et al suggested that miR‐7‐5p was conspicuously decreased in NSCLC, and its overexpression hindered NSCLC tumorigenesis through negatively regulating NOVA2 19 .…”

Section: Introductionmentioning

confidence: 99%

Propofol suppresses lung cancer tumorigenesis by modulating the circ‐ERBB2/miR‐7‐5p/FOXM1 axis

et al. 2021

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Background Propofol is a commonly used anesthetic for cancer surgery. Previous studies have shown that propofol has an anticancer role in various cancers, including lung cancer. This study aimed to investigate the role of propofol in lung cancer and its underlying mechanism. Methods Cell proliferation was determined by cell counting kit‐8 (CCK‐8) and colony formation assays. Flow cytometry and transwell assays were used to detect cell apoptosis and invasion, respectively. Glycolysis was evaluated by detecting glucose consumption, lactate production and ATP/ADP ratios. The levels of circular RNA erb‐b2 receptor tyrosine kinase 2 (circ‐ERBB2), microRNA‐7‐5p (miR‐7‐5p) and forkhead box M1 (FOXM1) were tested by quantitative real‐time PCR and Western blot. The binding relationship between miR‐7‐5p and circ‐ERBB2/FOXM1 was verified by dual‐luciferase reporter assay. Moreover, in vivo experiments were performed by establishing a mouse xenograft model. Results Propofol suppressed cell proliferation, invasion and glycolysis and expedited apoptosis in lung cancer cells. Circ‐ERBB2 and FOXM1 were upregulated, while miR‐7‐5p was decreased in lung cancer tissues and cells. Propofol suppressed lung cancer cell progression by regulating circ‐ERBB2. Additionally, miR‐7‐5p directly interacted with circ‐ERBB2 and FOXM1. Also, propofol played an antitumor role in lung cancer via modulating miR‐7‐5p or FOXM1. Moreover, circ‐ERBB2 knockdown enhanced the suppressive effect of propofol on tumor growth in vivo. Conclusions Propofol inhibited lung cancer progression via mediating circ‐ERBB2/miR‐7‐5p/FOXM1 axis, which might provide an effective therapeutic target for lung cancer therapy.

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“…As is well known, Limd1 (LIM domain-containing protein 1) is a member of the Zyxin proteins and is widely expressed in human tissues. Several previous studies have suggested the suppressor role of Limd1 in tumor diseases [ 39 ]. In cardiovascular disease, Limd1 has been reported to be functionally closely related to cardiac fibroblasts [ 40 ].…”

Section: Discussionmentioning

confidence: 99%

Upregulation of Biomarker Limd1 Was Correlated with Immune Infiltration in Doxorubicin-Related Cardiotoxicity

Zhang

Hao

et al. 2023

Mediators of Inflammation

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Doxorubicin is one of the most common antitumor drugs. However, cardiotoxicity’s side effect limits its clinical applicability. In the present study, Gene Expression Omnibus (GEO) datasets were applied to reanalyze differentially expressed genes (DEGs) and construct weighted correlation network analysis (WGCNA) modules of doxorubicin-induced cardiotoxicity in wild-type mice. Several other bioinformatics analyses were performed to pick out the hub gene, and then the correlation between the hub gene and immune infiltration was evaluated. In total, 120 DEGs were discovered in a mouse model of doxorubicin-induced cardiotoxicity, and PF-04217903, propranolol, azithromycin, etc. were found to be potential drugs against this pathological condition. Among all the DEGs, 14 were further screened out by WGCNA modules, of which Limd1 was upregulated and finally regarded as the hub gene after being validated in other GEO datasets. Limd1 was upregulated in the peripheral blood mononuclear cell (PBMC) of the rat model, and the area under curve (AUC) of the receiver operating characteristic curve (ROC) in diagnosing cardiotoxicity was 0.847. The GSEA and PPI networks revealed a potential immunocyte regulatory role of Limd1 in cardiotoxicity. The proportion of “dendritic cells activated” in the heart was significantly elevated, while “macrophage M1” and “monocytes” declined after in vivo doxorubicin application. Finally, Limd1 expression was significantly positively correlated with “dendritic cells activation’ and negatively correlated with “monocytes” and “macrophages M1’. In summary, our results suggested that limd1 is a valuable biomarker and a potential inflammation regulator in doxorubicin-induced cardiotoxicity.

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miR-550a-5p Functions as a Tumor Promoter by Targeting LIMD1 in Lung Adenocarcinoma

Cited by 9 publications

References 30 publications

Circular RNA circCCDC85A inhibits breast cancer progression via acting as a miR-550a-5p sponge to enhance MOB1A expression

Circular RNA circCCDC85A inhibits breast cancer progression via acting as a miR-550a-5p sponge to enhance MOB1A expression

Propofol suppresses lung cancer tumorigenesis by modulating the circ‐ERBB2/miR‐7‐5p/FOXM1 axis

Upregulation of Biomarker Limd1 Was Correlated with Immune Infiltration in Doxorubicin-Related Cardiotoxicity

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