miR‐212‐5p exerts tumor promoter function by regulating the Id3/PI3K/Akt axis in lung adenocarcinoma cells
| Autor: | Yang Yang, Fang-Fang Chen, Hai‐yan Xi, Yin Wang, Ning Sun, Bai‐zeng Yu, Xiao-Jun Li |
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| Rok vydání: | 2020 |
| Předmět: |
Male
0301 basic medicine Lung Neoplasms Carcinogenesis Physiology Clinical Biochemistry Adenocarcinoma of Lung Apoptosis Biology medicine.disease_cause Mice Phosphatidylinositol 3-Kinases 03 medical and health sciences 0302 clinical medicine Cell Movement Carcinoma Non-Small-Cell Lung microRNA medicine Animals Humans Gene silencing Neoplasm Invasiveness Protein kinase B PI3K/AKT/mTOR pathway Cell Proliferation Mice Inbred BALB C Tumor microenvironment Akt/PKB signaling pathway Cell Biology Prognosis Neoplasm Proteins Gene Expression Regulation Neoplastic MicroRNAs 030104 developmental biology Tumor progression 030220 oncology & carcinogenesis Carcinogens Cancer research Heterografts Inhibitor of Differentiation Proteins Proto-Oncogene Proteins c-akt Signal Transduction |
| Zdroj: | Journal of Cellular Physiology. 235:7273-7282 |
| ISSN: | 1097-4652 0021-9541 |
| Popis: | microRNAs may function as oncogenes or tumor suppressor genes that play crucial roles in human carcinogenesis and cancer development. Growing evidence revealed that the tumor suppressor Id3 is involved in tumor progression, carcinogenesis, and the tumor microenvironment. We identified miR-212-5p as a negative posttranscriptional modulator of Id3. Dual luciferase reporter assay was used to verify that Id3 is a direct target gene of miR-212-5p. Id3 was lowly expressed and miR-212-5p was highly expressed in non-small-cell lung cancer (NSCLC) tissues and cells. In addition, we found that NSCLC patients having a higher level of miR-212-5p expression had a shorter survival time. Besides this, miR-212-5p could directly target Id3 and reduce its expression. miR-212-5p overexpression significantly accelerated cell proliferation, migration, and invasion by reversing the effects of Id3. Id3 overexpression by silencing miR-212-5p expression suppressed phosphatidylinositol 3 kinase (PI3K)/Akt activity and consequently promoted apoptosis and inhibited cell proliferation in lung cancer cells. Consistent with the in vitro results, a xenograft mouse model was used to validate the fact that miR-212-5p could promote tumorigenesis by targeting Id3 and activate the PI3K/Akt pathway in vivo as well. Taken together, the present results indicated that miR-212-5p may be involved in progression of NSCLC through the PI3K/Akt signaling pathway by targeting Id3. |
| Databáze: | OpenAIRE |
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