MiR‐195 and miR‐497 suppress tumorigenesis in lung cancer by inhibiting SMURF2‐induced TGF‐β receptor I ubiquitination

Chae, Dong Kyu; Park, Jin‐Young; Cho, Moonsoo; Ban, Eunmi; Jang, Mihue; Yoo, Young Sook; Kim, Eunice Eun Kyeong; Baik, Ja Hyun; Song, Eun Joo

doi:10.1002/1878-0261.12581

Cited by 58 publications

(42 citation statements)

References 50 publications

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“…In prostate cancer, miR-195 inhibits tumor progression [79,80]. Other solid tumors in which this microRNA have been investigated in include CRC [81,82], lung cancer [76,[83][84][85], gastric cancer [86], cervical cancer [87], breast cancer [88], etc. The common bonds found between proteins and their corresponding molecules include hydrophobic amino acids and H-bonds.…”

Section: Discussionmentioning

confidence: 99%

Gene Expression Alterations and Molecular Analysis of CHEK1 in Solid Tumors

Fadaka

Bakare

Sibuyi

et al. 2020

Cancers

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Alterations in the Checkpoint kinase (CHEK1) gene, its regulation, and the possible clinical outcomes in human solid tumors have not been previously examined. Therefore, the present study was carried out to evaluate the expression of CHEK1 in solid tumors as well as the mechanism by which it can be regulated through non-coding RNAs. The expression of CHEK1 was investigated using Oncomine analysis. cBioPortal, Kaplan–Meier Plotter, and PrognoScan were performed to identify the prognostic roles of this gene in solid tumors. The copy number alteration, mutation, interactive analysis, and visualization of the altered networks were performed by cBioPortal. The molecular binding analysis was carried out by Schrodinger suite, PATCHDOCK, and discovery studio visualizer. The study demonstrated that the CHEK1 gene was differentially expressed in four different cancers, and that reduced CHEK1 mRNA expression is an unfavorable prognostic factor for patients with gastric and colorectal cancer. The molecular docking results showed that the CHEK1 gene can be regulated by microRNAs (miR-195-5p) due to the number of stable hydrogen atoms observed within the distance of 2.0 Å and the favorable amino acids (Ala221, Ile353, Ile365, Ile756, Val797, Val70, Val154, Ile159, Val347, Tyr804, Phe811, Tyr815, and Phe156) identified in the binding pocket of the argonaute protein. Due to the possibility of CHEK1’s involvement in solid tumors, it may potentially be a target for therapeutic intervention in cancer. Further studies into the interaction between CHEK1 and other co-expressed genes may give further insight into other modes of regulation of this gene in cancer patients.

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Section: Discussionmentioning

confidence: 99%

Gene Expression Alterations and Molecular Analysis of CHEK1 in Solid Tumors

Fadaka

Bakare

Sibuyi

et al. 2020

Cancers

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“…The peripheral T-cell subsets, on the other hand, in particular central and effector memory T cells, were not affected under steady-state conditions (Fig. 4C,D nonhematopoietic cancer settings [22][23][24][25][26][27][28]. To investigate this in more detail, we crossed miR-497/195 fl/fl mice with a ubiquitous Cre deleter strain to generate miR-497/195 À/À mice lacking the cluster in all tissues.…”

Section: Immune Cell Homeostasis and Function Are Not Affected Upon Lmentioning

confidence: 99%

Differential roles of miR‐15a/16‐1 and miR‐497/195 clusters in immune cell development and homeostasis

et al. 2020

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MicroRNAs (miRNAs) post-transcriptionally repress almost all genes in mammals and thereby form an additional layer of gene regulation. As such, miRNAs impact on nearly every physiological process and have also been associated with cancer. Prominent examples of such miRNAs can be found in the miR-15 family, composed of the bicistronic clusters miR-15a/ 16-1, miR-15b/16-2, and miR-497/195. In particular, the miR-15a/16-1 cluster is deleted in almost two thirds of all chronic B lymphocytic leukemia (CLL) cases, a phenotype that is also recapitulated by miR-15a/16-1deficient as well as miR-15b/16-2-deficient mice. Under physiological conditions, those two clusters have been implicated in T-cell function, and B-cell and natural killer (NK) cell development; however, it is unclear whether miR-497 and miR-195 confer similar roles in health and disease. Here, we have generated a conditional mouse model for tissue-specific deletion of miR-497 and miR-195. While mice lacking miR-15a/16-1 in the hematopoietic compartment developed clear signs of CLL over time, aging mice deficient for miR-497/195 did not show such a phenotype. Likewise, loss of miR-15a/16-1 impaired NK and early B-cell development, whereas miR-497/195 was dispensable for these processes. In fact, a detailed analysis of miR-497/195-deficient mice did not reveal any effect on steady-state hematopoiesis or immune cell function. Unexpectedly, even whole-body deletion of the cluster was well-tolerated and had no obvious impact on embryonic development or healthy life span. Therefore, we postulate that the miR-497/195 cluster is redundant to its paralog clusters or that its functional relevance is restricted to certain physiological and pathological conditions.

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“…In vivo studies of xenograft model revealed the repressed-effect of miR-195 on tumor growth. 18 More importantly, a previous study identified that miR-195 was downregulated in liposarcoma tissues. 19 Thus, it was needed to explore the character and potential mechanism of miR-195 in liposarcoma.…”

Section: Introductionmentioning

confidence: 97%

<p>miR-195 Serves as a Tumor Suppressor in the Progression of Liposarcoma by Targeting OSBP</p>

Cao¹,

Li²,

Han³

et al. 2020

OTT

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Background: Liposarcoma was considered as a soft tissue kind of sarcoma with one-fifth in the sarcoma cases of adults. The aim of this study was to explore the role and the potential mechanisms of miR-195 in liposarcoma. Methods: Quantitative real-time PCR (qRT-PCR) was conducted to measure the expression of microRNA-195 (miR-195) and oxysterol-binding protein (OSBP) in liposarcoma. Cell proliferation was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT). Cell migration was measured by wound healing and transwell assays. Cell cycle phases and apoptosis were examined using flow cytometry analysis. Caspase-3 activity was detected by commercial kit. Binding sites between miR-195 and OSBP were predicted through bioinformatics analysis and confirmed by dual-luciferase reporter assay and RNA immunoprecipitation (RIP). Western blot was used to analyze OSBP level. Xenograft tumor assays were performed to observe the effect of miR-195 overexpression on tumor growth in vivo. Results: miR-195 expression was decreased, whereas OSBP was increased in liposarcoma tissues and cells. Besides, miR-195 upregulation suppressed the proliferative and migrative abilities and induced inhibition on cell growth and promotion on apoptosis in SW872 and 93T449 cells. Mechanically, miR-195 functioned as a suppressor by regulating OSBP expression. Furthermore, OSBP overexpression inverted the effects of miR-195 on cell growth, migration and apoptosis in SW872 and 93T449 cells. miR-195 overexpression also suppressed tumor growth in vivo. Conclusion: miR-195 suppressed cell growth, migration and elevated cell apoptosis via OSBP in liposarcoma.

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MiR‐195 and miR‐497 suppress tumorigenesis in lung cancer by inhibiting SMURF2‐induced TGF‐β receptor I ubiquitination

Cited by 58 publications

References 50 publications

Gene Expression Alterations and Molecular Analysis of CHEK1 in Solid Tumors

Gene Expression Alterations and Molecular Analysis of CHEK1 in Solid Tumors

Differential roles of miR‐15a/16‐1 and miR‐497/195 clusters in immune cell development and homeostasis

<p>miR-195 Serves as a Tumor Suppressor in the Progression of Liposarcoma by Targeting OSBP</p>

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