Long non-coding RNA XIST regulates miR-106b-5p/P21 axis to suppress tumor progression in renal cell carcinoma

Sun, Kai; Jia, Zhiyuan; Duan, Ranran; Yan, Zechen; Jin, Zhibo; Liang, Yan; Li, Qi; Yang, Jinjian

doi:10.1016/j.bbrc.2019.01.116

Cited by 46 publications

(23 citation statements)

References 25 publications

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“…In our study, targeting XIST significantly reduced cell viability and increased cell apoptosis in vitro in U2OS cells, and targeting XIST suppressed tumorigenesis in vivo. Our findings are similar to those of the recent reports [31,32] and contrary to the results of recent reports [33,34]. However, the underlying mechanism by which XIST mediates gene expression and participates in tumorigenesis remains to be clarified.…”

Section: Discussionsupporting

confidence: 86%

Targeting XIST induced apoptosis of human osteosarcoma cells by activation of NF-kB/PUMA signal

Gao

Chen

et al. 2019

Bioengineered

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The long noncoding RNA X-inactive specific transcript (XIST) plays vital roles in tumor progression. However, the underlying mechanisms remain unclear. This study investigated the effects and mechanisms of targeting XIST on osteosarcoma (OS) cells in vitro and in vivo. We used shRNA to knockdown XIST to evaluate cell growth and apoptosis in U2OS cells in vitro and xenograft formation in vivo. An observed relationship between XIST and the p53 upregulated modulator of apoptosis (PUMA) and nuclear factor-kappa B (NF-kB) pathway was further explored by using small interfering RNA (siRNA). Our results showed that suppression of XIST by short hairpin RNA (shRNA) impeded U2OS cell growth, induced apoptosis and lessened OS xenograft tumor growth. Targeting XIST increased NF-kB-dependent PUMA upregulation in U2OS cells. Upregulation of PUMA is correlated with suppression of XIST-induced apoptosis in U2OS cells. Therefore, inhibition of XIST could promote U2OS cell death via activation of NF-kB/PUMA pathways.

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Section: Discussionsupporting

confidence: 86%

Targeting XIST induced apoptosis of human osteosarcoma cells by activation of NF-kB/PUMA signal

Gao

Chen

et al. 2019

Bioengineered

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“…Upregulation of CDKN1A expression mimicked, while CDKN1A knockdown reversed the suppressive effects of miR-106b-5p inhibitor transfection on OS cell proliferation and cell cycle progression. Similarly, miR-106-5p targeting CDKN1A has been reported in gastric cancer (33) and renal cell carcinoma (34). The present study hypothesized that knockdown of miR-106b-3p inhibited proliferation via G0/G1 cell cycle arrest by negatively regulating CDKN1A.…”

Section: Discussionsupporting

confidence: 52%

miR‑106b‑5p promotes cell proliferation and cell cycle progression by directly targeting CDKN1A in osteosarcoma

He¹,

Chen²,

Liu³

et al. 2020

Exp Ther Med

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MicroRNA (miR)-106b-5p has been reported to act as both an oncogene and tumor suppressor in several tumors. The aim of the present study was to investigate the biological function of miR-106b-5p in osteosarcoma (OS). miR-106b-5p expression was observed to be significantly increased in OS tissues and cell lines. MTT assay and flow cytometry analysis determined that miR-106b-5p inhibitor transfection suppressed OS cell proliferation and induced cell cycle G0/G1 phase arrest. Furthermore, bioinformatics analysis and a luciferase reporter assay demonstrated that cyclin-dependent kinase inhibitor 1A (CDKN1A) was a potential target of miR-106b-5p. p21 protein expression was found to be significantly increased by miR-106b-5p downregulation in OS cells. Further analysis demonstrated that CDKN1A was downregulated in OS tissues and was negatively correlated with miR-106b-5p expression. Furthermore, upregulation of CDKN1A expression mimicked, whilst CDKN1A knockdown reversed the suppressive effects of miR-106b-5p inhibitor on OS cell proliferation and cell cycle progression. In summary, the present data suggested that miR-106b-5p promotes cell proliferation and cell cycle progression by directly targeting CDKN1A in OS.

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“…In our study, we found that CTC‐specific miR106b was positively related to the expression level of vimentin in CTCs. It has been reported that overexpression of miR‐106b was observed in a variety of human tumors, which plays an oncogenic role in tumor progression and prognosis, including colorectal cancer , gastric cancer , hepatocellular carcinoma , glioma tumors , renal cell carcinoma , and head and neck squamous cell carcinomas . MiR‐106b plays a functional role in promoting proliferation, migration, and invasion of cancer cells both in vitro and in vivo .…”

Section: Discussionmentioning

confidence: 99%

Incorporating MicroRNA into Molecular Phenotypes of Circulating Tumor Cells Enhances the Prognostic Accuracy for Patients with Metastatic Breast Cancer

et al. 2019

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Background The molecular phenotype of circulating tumor cells (CTCs) was associated with clinical outcome of patients with breast cancer. CTCs isolated from patients with metastatic breast cancer (MBC) display a unique microRNA (miRNA) expression profile. The aim of this study was to enhance the prognostic accuracy of the CTC phenotype in patients with MBC, by incorporating miRNA into a combined prediction model. Subjects, Materials, and Methods CTCs were detected by CellSearch and enriched by magnetic cell sorting. miRNA deep sequencing and quantitative polymerase chain reaction were used to screen and verify potentially CTC‐specific miRNA candidates. Patients with MBC were enrolled from two independent cohorts, and overall survival (OS) and chemotherapy response were analyzed. Results We screened and identified that miR‐106b was an upregulated molecule in patients with MBC with CTC ≥5/7.5 mL (n = 16) compared with patients with CTC = 0/7.5 mL (n = 16) and healthy donors (n = 8). The expression of CTC‐specific miR‐106b correlated with vimentin and E‐cadherin in CTC and acted as an independent factor for predicting OS (hazard ratio 2.157, 95% confidence interval [CI] 1.098–4.239, p = .026). Although CTC‐specific miR‐106b, E‐cadherin, and vimentin showed a prognostic potential independently, the prognostic performance for OS based on the combination of three markers was significantly enhanced in Cohort 1 (area under the curve [AUC] 0.752, 95% CI 0.658–0.847, n = 128) and further validated in Cohort 2 (AUC 0.726, 95% CI 0.595–0.856, n = 91). Besides, a combined model incorporating miR‐106b was associated with therapy response. Conclusion The phenotypic assemblies of CTC incorporating miR‐106b show enhanced prognostic accuracy of overall survival in patients with MBC. Implications for Practice In order to enhance the prognostic accuracy of the circulating tumor cell (CTC) phenotype in patients with metastatic breast cancer (MBC), this study screened and identified a CTC‐specific microRNA (miRNA), miR‐106b, as an upregulated molecule based on the comparison of miRNA profile between CTCs, primary tumors, and healthy blood donors. By incorporating miR‐106b into a combined prediction model, the prognostic accuracy of the CTC phenotype for patients with MBC was greatly improved in both the training and validation cohorts. This work provides clinical evidence supporting the prognostic potential of CTC‐specific miRNA for patients with MBC. These results indicate that developing CTC‐specific miRNAs as new biomarkers will help to further optimize personalized therapy.

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Long non-coding RNA XIST regulates miR-106b-5p/P21 axis to suppress tumor progression in renal cell carcinoma

Cited by 46 publications

References 25 publications

Targeting XIST induced apoptosis of human osteosarcoma cells by activation of NF-kB/PUMA signal

Targeting XIST induced apoptosis of human osteosarcoma cells by activation of NF-kB/PUMA signal

miR‑106b‑5p promotes cell proliferation and cell cycle progression by directly targeting CDKN1A in osteosarcoma

Incorporating MicroRNA into Molecular Phenotypes of Circulating Tumor Cells Enhances the Prognostic Accuracy for Patients with Metastatic Breast Cancer

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