miR‐335 inhibited cell proliferation of lung cancer cells by target Tra2β

Liu, Jian; Bian, Tingting; Feng, Jia; Li, Qian; Zhang, Jianguo; Jiang, Daishan; Zhang, Qing; Li, Xiaoli; Liu, Yifei; Shi, Jiahai

doi:10.1111/cas.13452

Cited by 46 publications

(38 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Li et al found that miR-93-5p played an inhibitory role in the proliferation and metastasis of CC cells, and it could suppress the development of HPV-positive CC by targeting BTG3. 12 These studies suggest that the abnormal expression of miRNAs may affect the malignant progression of CC. It has been reported that miR-145-5p is down-regulated in a variety of human cancers, such as breast cancer 13 and bladder cancer 14 , and plays an inhibitory role in tumor growth.…”

Section: Introductionmentioning

confidence: 97%

<p>miR-145-5p Regulates the Proliferation, Migration and Invasion in Cervical Carcinoma by Targeting KLF5</p>

Cao¹,

Pan²,

Tang³

et al. 2020

OTT

View full text Add to dashboard Cite

Objective: Cervical carcinoma (CC) is a serious threat to women's health and few effective therapeutic methods have been discovered. The purpose of this study is to explore the underlying mechanism of miR-145-5p in CC. Methods: Bioinformatics methods were employed to analyze the gene expression data of CC from TCGA database. qRT-PCR was used to detect the expression of miR-145-5p and KLF5 in CC cells, and Western blot was employed for the examination of KLF5 protein level. The targeted relationship between miR-145-5p and KLF5 was verified by a dualluciferase reporter assay. Moreover, CCK-8, wound healing assay and transwell invasion assay were used to analyze the effects of miR-145-5p overexpression or KLF5 silencing on the proliferation, migration and invasion of CC cells. Results: miR-145-5p was shown to be down-regulated in CC tissues and cells, while KLF5 was up-regulated. miR-145-5p could bind to the complementary sequence within the wild type KLF5 3ʹUTR rather than the mutant one. In addition, miR-145-5p could effectively down-regulate KLF5, in turn inhibiting the proliferation, migration and invasion of CC cells. Conclusion: miR-145-5p regulates the proliferation, migration and invasion of CC cells by targeting KLF5.

show abstract

Section: Introductionmentioning

confidence: 97%

<p>miR-145-5p Regulates the Proliferation, Migration and Invasion in Cervical Carcinoma by Targeting KLF5</p>

Cao¹,

Pan²,

Tang³

et al. 2020

OTT

View full text Add to dashboard Cite

show abstract

“…In NSCLC, miRNAs may have potential roles in modulating metastases, either by inhibition or reconstitution of their functions [20]. In several human cancers, hsa-miR-335 has multiple roles in carcinogenesis [21][22][23][24]. Although little is known of the role of miR-335-3p in lung cancer, in several other cancers, miR-335-3p is down-regulated [25][26][27][28].…”

Section: Introductionmentioning

confidence: 99%

Upregulation of the Coatomer Protein Complex Subunit beta 2 (COPB2) Gene Targets microRNA-335-3p in NCI-H1975 Lung Adenocarcinoma Cells to Promote Cell Proliferation and Migration

Jiang

et al. 2020

Med Sci Monit

View full text Add to dashboard Cite

Departmental sources Background: The coatomer protein complex subunit beta 2 (COPB2) gene is upregulated and promotes cell proliferation in some cancer cells. This study aimed to investigate the role of microRNA (miRNA) targeting by COPB2 gene expression in human lung adenocarcinoma cell lines, including NCI-H1975 cells. Material/Methods: COPB2 expression in normal human bronchial epithelial cells and lung adenocarcinoma cells was measured by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blot. NCI-H1975 human lung adenocarcinoma cells were transfected with short-interfering COPB2 (siCOPB2). Cell apoptosis and cell proliferation were evaluated by flow cytometry and Cell Counting Kit-8 (CCK-8) assays, respectively. The transwell assay evaluated cell migration. Targeting of miR-335-3p by COPB2 was predicted using TargetScan 7.2 and verified using a dual-luciferase reporter assay in NCI-H1975 cells. MiR-335-3p mimics were transfected into NCI-H1975 cells. The further functional analysis included detection of protein expression for cyclin D1, tissue inhibitor matrix metalloproteinase-1 (TIMP-1), matrix metallopeptidase 9 (MMP9), Bcl-2, and Bax, to verify the role of miR-335-3p targeting by COPB2 in lung adenocarcinoma cells. Results: COPB2 was upregulated in lung adenocarcinoma cells and was a direct target of miR-335-3p mimics. COPB2 knockdown promoted cell apoptosis, inhibited cell migration and proliferation in NCI-H1975 cells. The effects of COPB2 knockdown on NCI-H1975 cells were increased by miR-335-3p mimics, which also further reduced the expression levels of cyclin D1, MMP9, and Bcl-2 and further increased TIMP-1 and Bax by siCOPB2. Conclusions: This study showed that COPB2 was the functional target of miR-335-3p in NCI-H1975 human adenocarcinoma cells.

show abstract

“…In this context, the Tra2b protein (the transformer 2 beta homolog) is particularly interesting as it is considered one of the most important splicing factors involved in RNA processing needed for both normal (e.g., brain development) and pathological (e.g., cancer) cell proliferation [75,76]. The RNA binding protein Rbmx, also known as heterogenous nuclear ribonucleoprotein G (hnRNPG), also functions as an important protein, being involved in the regulation of gene expression and alternative splicing.…”

Section: Discussionmentioning

confidence: 99%

A Neuroprotective Dose of Isatin Causes Multilevel Changes Involving the Brain Proteome: Prospects for Further Research

Медведев

Kopylov

Buneeva

et al. 2020

IJMS

View full text Add to dashboard Cite

Isatin (indole-2,3-dione) is an endogenous regulator, exhibiting a wide range of biological and pharmacological activities. At doses of 100 mg/kg and above, isatin is neuroprotective in different experimental models of neurodegeneration. Good evidence exists that its effects are realized via interaction with numerous isatin-binding proteins identified in the brain and peripheral tissues studied. In this study, we investigated the effect of a single dose administration of isatin to mice (100 mg/kg, 24 h) on differentially expressed proteins and a profile of the isatin-binding proteins in brain hemispheres. Isatin administration to mice caused downregulation of 31 proteins. However, these changes cannot be attributed to altered expression of corresponding genes. Although at this time point isatin influenced the expression of more than 850 genes in brain hemispheres (including 433 upregulated and 418 downregulated genes), none of them could account for the changes in the differentially expressed proteins. Comparative proteomic analysis of brain isatin-binding proteins of control and isatin-treated mice revealed representative groups of proteins sensitive to isatin administration. Control-specific proteins (n = 55) represent specific targets that interact directly with isatin. Appearance of brain isatin-binding proteins specific to isatin-treated mice (n = 94) may be attributed to the formation of new clusters of protein–protein interactions and/or novel binding sites induced by a high concentration of this regulator (ligand-induced binding sites). Thus, isatin administration produces multiple effects in the brain, which include changes in gene expression and also profiles of isatin-binding proteins and their interactomes. Further studies are needed for deeper insight into the mechanisms of the multilevel changes in the brain proteome induced by isatin. In the context of the neuroprotective action, these changes may be aimed at interruption of pathological links that begin to form after initiation of pathological processes.

show abstract

miR‐335 inhibited cell proliferation of lung cancer cells by target Tra2β

Cited by 46 publications

References 26 publications

<p>miR-145-5p Regulates the Proliferation, Migration and Invasion in Cervical Carcinoma by Targeting KLF5</p>

<p>miR-145-5p Regulates the Proliferation, Migration and Invasion in Cervical Carcinoma by Targeting KLF5</p>

Upregulation of the Coatomer Protein Complex Subunit beta 2 (COPB2) Gene Targets microRNA-335-3p in NCI-H1975 Lung Adenocarcinoma Cells to Promote Cell Proliferation and Migration

A Neuroprotective Dose of Isatin Causes Multilevel Changes Involving the Brain Proteome: Prospects for Further Research

Contact Info

Product

Resources

About