Anti-miRNA-221 sensitizes human colorectal carcinoma cells to radiation by upregulating PTEN

Xue, Qi; Sun, Kai; Deng, Haijun; Lei, Shangtong; Dong, Jinqiao; Li, Guoxin

doi:10.3748/wjg.v19.i48.9307

Cited by 41 publications

(37 citation statements)

References 36 publications

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“…Knockout of these miRNAs results in increased PTEN levels, which in turn lead to suppressed Akt activity and increased apoptosis, and most importantly, to enhanced radiosensitivity in various cancer cell lines (57). These results are in agreement with observations by other authors reporting studies using gastric (58) and colorectal cancer cell lines (54). Furthermore, PTEN is a known target of miR-21.…”

Section: Mirnas Regulating Relevant Cellular Signaling Pathwayssupporting

confidence: 91%

“…One wellknown tumor suppressor gene is PTEN (phosphatase and tensin homolog), which acts by negatively regulating the PKB (protein kinase B, Akt) signaling pathway. This mechanism is critical for the regulation of the cell cycle, cell growth and apoptosis (54,56). In recent years, several authors have identified numerous miRNAs that can interfere with the PTEN pathway.…”

Section: Mirnas Regulating Relevant Cellular Signaling Pathwaysmentioning

confidence: 99%

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MicroRNAs and Their Impact on Radiotherapy for Cancer

et al. 2016

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Section: Mirnas Regulating Relevant Cellular Signaling Pathwayssupporting

confidence: 91%

Section: Mirnas Regulating Relevant Cellular Signaling Pathwaysmentioning

confidence: 99%

MicroRNAs and Their Impact on Radiotherapy for Cancer

et al. 2016

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“…Previous studies have demonstrated that aberrant activation of the PI3K/Akt signaling pathway has a significant role in tumorigenesis and tumor metastasis (14). PTEN functions as a tumor suppressor by negatively regulating the PI3K/Akt signaling pathway (22). miRNAs, including miR-17-5p and miR29b, have been reported to regulate the expression of PTEN (19,23).…”

Section: Introductionmentioning

confidence: 99%

Downregulation of miR-221/222 by a microRNA sponge promotes apoptosis in oral squamous cell carcinoma cells through upregulation of PTEN

et al. 2016

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MicroRNA-221 and microRNA-222 (miR-221/222) have been identified as oncogenes and confirmed to be overexpressed in various types of cancer. However, the regulation mechanism of miR-221/222 in oral squamous cell carcinoma (OSCC) remains to be fully elucidated. Previously, an miR-221/222 sponge was successfully constructed and its effect on the downregulation of miR-221/222 expression was investigated. In the present study, the dual luciferase reporter assay revealed a phosphatase and tensin homolog (PTEN) deletion on chromosome 10 to be a target gene of miR-221/222. It was also demonstrated that miR-221/222 suppression by transfection with an miR-221/222 sponge in vitro resulted in upregulation of PTEN. Notably, the proliferation and invasiveness of the miR-221/222 sponge-transfected cells was significantly inhibited, while apoptosis was promoted, when determined by Cell Counting Kit-8, Transwell assays and flow cytometry. The results of the present study prove that miR-221/222 may downregulate the expression of PTEN in OSCC cells and function as oncogenes, providing a novel insight into the underlying mechanism of OSCC tumorigenesis. The present study suggests that upregulating the expression of PTEN by downregulation of miR-221/222 may be a potential treatment for OSCC.

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“…Recently, several studies discovered that miRNA interference is the main method by which PTEN inactivation occurs after gene transcription. Among the 940 miRNAs previously discovered, miR‐21a, miR‐17‐92, miR‐425, miR‐181a, miR‐26a, miR‐221, and miR‐222 have been shown to degrade or to inhibit mRNA translation by complementary binding to the 3′UTR of PTEN mRNA, consequently inducing tumorigenesis . miR‐21a is located on fragile sites of chromosome 17q23.2, which is detected much earlier and which has attracted public concern .…”

Section: Introductionmentioning

confidence: 99%

“…Among the 940 miRNAs previously discovered, miR-21a, miR-17-92, miR-425, miR-181a, miR-26a, miR-221, and miR-222 have been shown to degrade or to inhibit mRNA translation by complementary binding to the 3 0 UTR of PTEN mRNA, consequently inducing tumorigenesis. [5][6][7][8][9][10] miR-21a is located on fragile sites of chromosome 17q23.2, which is detected much earlier and which has attracted public concern. 11 Accumulating evidence suggests that it is aberrantly expressed in many tissues, which may result in hepatocellular carcinoma (HCC), 12 non-small cell lung cancer, 13 leukemia 14 or Cowden syndrome.…”

Section: Introductionmentioning

confidence: 99%

miR‐21a negatively modulates tumor suppressor genes PTEN and miR‐200c and further promotes the transformation of M2 macrophages

Qin

Han

et al. 2017

Immunol Cell Biol

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miR-21a is well-known to inhibit PTEN expression. We have previously shown that PTEN suppressed the transformation of M2 macrophages in the tumor microenvironment. Therefore, we hypothesized that miR-21a could influence M2 macrophage transformation by regulating PTEN expression. In this study, we identified how miR-21a reduced the expression of both PTEN mRNA and protein in murine macrophage cell lines and primary macrophages. Moreover, opposite effects were identified upon the use of a miR-21a inhibitor. Using a cytokine array, we identified the cytokines closely associated with miR-21a-mediated macrophage transformation to the M2 phenotype. miR-21a mimics could also enhance the migratory ability of murine breast cancer 4T1 cells, the growth of breast cancer in vivo and CD206 intratumor expression. In addition, quantitative PCR (qPCR) and methylation-specific PCR analysis showed that miR-21a enhanced miR-200c methylation and then decreased miR-200c and PTEN expression. These effects could be reversed by treatment with 5'-Aza, a DNA-demethylating agent. MiR-200c was predicted to target the PTEN 3'UTR, but qPCR illustrated the miR-200c mimic that increased PTEN expression, and 5'-Aza could enhance its effect. The above results indicate that miR-21a negatively modulates two tumor suppressor genes, miR-200c and PTEN, thereby promoting M2 macrophage transformation. This demonstrates that miR-21a represents a novel target for improving the overall tumor microenvironment.

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Anti-miRNA-221 sensitizes human colorectal carcinoma cells to radiation by upregulating PTEN

Abstract: Anti-miR-221 can enhance the radiosensitivity of CRC cells by upregulating PTEN.

Cited by 41 publications

References 36 publications

MicroRNAs and Their Impact on Radiotherapy for Cancer

MicroRNAs and Their Impact on Radiotherapy for Cancer

Downregulation of miR-221/222 by a microRNA sponge promotes apoptosis in oral squamous cell carcinoma cells through upregulation of PTEN

miR‐21a negatively modulates tumor suppressor genes PTEN and miR‐200c and further promotes the transformation of M2 macrophages

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