Retracted: Micro RNA‐21 promotes glioma cell proliferation and inhibits senescence and apoptosis by targeting SPRY 1 via the PTEN/PI 3K/AKT signaling pathway
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Summary: Aims: Our study aims to investigate the effect of micro RNA‐21 (miR‐21) on the proliferation, senescence, and apoptosis of glioma cells by targeting SPRY 1 via the PTEN/PI 3K/AKT signaling pathway. Methods: Glioma tissues and brain tissues were collected for this study after surgical decompression for traumatic brain injury. RT‐qPCR was employed to measure mRNA levels of miR‐21, SPRY 1, PTEN,PI 3K, and AKT, and Western blotting was conducted to determine protein levels of SPRY 1, PTEN,PI 3K, AKT, p‐AKT, Caspase‐3, Caspase‐9, P53, GSK 3, and p‐GSK 3. Human glioma U87 cells were assigned into the blank, negative control (NC), miR‐21 mimics, miR‐21 inhibitors, si RNA‐SPRY 1, and miR‐21 inhibitors + si RNA‐SPRY 1 groups, with human HEB cells serving as the normal group. Cell proliferation, cell cycle, and apoptosis were determined by MTT and flow cytometry, respectively. Results: Compared with control group, an increased expression of miR‐21, PI 3K, AKT, p‐AKT, P53, and p‐GSK 3, and a decreased expression of SPRY 1, PTEN, Caspase‐3, and Caspase‐9 were observed in the glioma group, and no significant differences were found in the expression of GSK 3. SPRY 1 was verified to be the target gene of miR‐21. Compared with the blank and NC groups, levels of PI 3K, AKT, p‐AKT, P53, and p‐GSK 3 increased while levels of SPRY 1, PTEN, Caspase‐3, and Caspase‐9 decreased in the miR‐21 mimics and si RNA‐SPRY 1 groups; the miR‐21 inhibitors group reversed the tendency; furthermore, the miR‐21 inhibitors group showed decreased cell proliferation but promoted apoptosis, which were opposite to the results of the miR‐21 mimics and si RNA‐SPRY 1 groups. Conclusion: Micro RNA‐21 might promote cell proliferation and inhibit cell senescence and apoptosis of human glioma cells by targeting SPRY 1 via the PTEN/PI 3K/AKT signaling pathway.
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miR-21 is overexpressed in almost all cancer types, and its upregulation promotes cell proliferation, invasion, and metastatic behavior.
“miR-21 is a well-known miRNA, found to be overexpressed in almost all cancer types, where its upregulation promotes cell proliferation, invasion, and metastatic behavior.”
From Potential Therapeutic Effects of Exosomes Packed With a miR-21-Sponge Construct in a Rat Model of Glioblastoma (2019) · cites this paper as [22]
miR-21 targets several genes such as PDCD4, TIMP3, and RECK, which are key regulators of apoptotic and metastatic pathways.
“miR-21 targets several genes such as PDCD4, TIMP3, and RECK, which are key regulators of apoptotic and metastatic pathways (17–23).”
From Potential Therapeutic Effects of Exosomes Packed With a miR-21-Sponge Construct in a Rat Model of Glioblastoma (2019) · cites this paper as [22]
Overexpressed miR-21 in cell lines can increase the proliferation rate and malignant behavior of the cells.
“Our data on the effects of miR-21 enriched exosomes is in agreement with the previous reports demonstrating that overexpressed miR-21 in cell lines can increase the proliferation rate and malignant behavior of the cells (17–23).”
From Potential Therapeutic Effects of Exosomes Packed With a miR-21-Sponge Construct in a Rat Model of Glioblastoma (2019) · cites this paper as [22]
Cites
MicroRNA-21 Targets a Network of Key Tumor-Suppressive Pathways in Glioblastoma Cells
Papagiannakopoulos, T., Shapiro, A., & Kosik, K. S. (2008) · Cancer Research · doi:10.1158/0008-5472.can-08-1305 · Cited by 705 · see citing works
MicroRNA-21 down-regulates the expression of tumor suppressor PDCD4 in human glioblastoma cell T98G
Chen, Y., Liu, W., Chao, T., Zhang, Y., Yan, X., Gong, Y., Qiang, B., Yuan, J., Sun, M., & Peng, X. (2008) · Cancer Letters · doi:10.1016/j.canlet.2008.06.034 · Cited by 217 · see citing works
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Monfared, H., Jahangard, Y., Nikkhah, M., Mirnajafi-Zadeh, J., & Mowla, S. J. (2019) · Frontiers in Oncology · doi:10.3389/fonc.2019.00782 · Cited by 123 · see citing works
- Authors
- Chai, C., Song, L., Han, S., Li, X., & Li, M.
- Affiliations
- Henan Provincial People's Hospital (CN)
- Department of Neurosurgery the First Affiliated Hospital of Zhengzhou University Zhengzhou China
- Department of Gastroenterology Henan Provincial People's Hospital Zhengzhou China
- Department of Oncology Henan Provincial People's Hospital Zhengzhou China
- Corresponding author
- Li, Ming
- ORCID
- Li, Ming
- Venue
- CNS Neuroscience & Therapeutics
- Publisher
- Wiley
- Published
- 2018-01-05
- Volume
- 24
- Issue
- 5
- Pages
- 369-380
- ISSN
- 1755-5930 (ISSN-L)
- 1755-5949
- PMC
- PMC6489721
- OpenAlex
- W2782704938
- Cited by
- 89
- References
- 2
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 5 · 2023: 15 · 2022: 12 · 2021: 18 · 2020: 22 · 2019: 10 · 2018: 4
- FWCI
- 4.07
- Type
- journal article
- Language
- en
- Status
- Retracted
- Update notices
- retraction (2021-01-25)
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- CNS Neuroscience & Therapeutics (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- International Business Machines Corporation
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer-related molecular mechanisms research
- Health Sciences › Medicine › Genetics › Glioma Diagnosis and Treatment
- Keywords
- miR-21, SPRY1, glioma, PTEN/PI3K/AKT signaling pathway, cell proliferation, cellular senescence, apoptosis, caspase-3, caspase-9, p53, glycogen synthase kinase-3, traumatic brain injury, U87 cells, cell cycle, cell migration and invasion
- MeSH terms
- Adolescent, Adult, Aged, Brain, Brain Neoplasms, Cell Cycle, Female, Glioma, Humans, Male, Membrane Proteins, Middle Aged, Phosphoproteins, Signal Transduction, Cellular Senescence, Apoptosis, Phosphatidylinositol 3-Kinases, MicroRNAs, Cell Line, Tumor, Cell Proliferation, Proto-Oncogene Proteins c-akt, PTEN Phosphohydrolase, Young Adult
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