Identification of microR-106b as a prognostic biomarker of p53-like bladder cancers by ActMiR

Lee, Eunjee; Collazo-Lorduy, Ana; Castillo-Martín, Mireia; Gong, Yixuan; Wang, Li; Oh, William K.; Galsky, Matthew D.; Cordon‐Cardo, Carlos; Zhu, Jun

doi:10.1038/s41388-018-0367-0

Cited by 22 publications

(20 citation statements)

References 41 publications

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“…With context to malignancies, miR-532 has been reported as a prognostic biomarker for bladder cancer. Moreover, it has been shown to be associated with the Warburg effect in ovarian cancer 10,11 . Although miR-532 has been reported to be dysregulated in adenoma, its expression pattern and molecular function in CRC remain undefined.…”

Section: Introductionmentioning

confidence: 99%

MiR-532-3p suppresses colorectal cancer progression by disrupting the ETS1/TGM2 axis-mediated Wnt/β-catenin signaling

Cai

et al. 2019

Cell Death Dis

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The expression panel of plasma microRNA defined miR-532-3p as a valuable biomarker for colorectal adenoma (CRA). However, its expression pattern and function in colorectal cancer (CRC) have remained unclear. The present study investigated the expression levels of miR-532-3p and found that it was in situ downregulated both in CRA and CRC. Moreover, it functioned as a sensitizer for chemotherapy in CRC by inducing cell cycle arrest and early apoptosis via its activating effects on p53 and apoptotic signaling pathways. In addition, miR-532-3p was found to restrain cell growth, metastasis, and epithelial–mesenchymal transition (EMT) phenotype of CRC. A study on the mechanism behind these effects revealed that miR-532-3p directly binds to 3′UTR regions of ETS1 and TGM2, ultimately repressing the canonical Wnt/β-catenin signaling. Further investigation showed that TGM2 was transcriptionally regulated by ETS1 and ETS1/TGM2 axis served as a vital functional target of miR-532-3p in suppressing CRC progression. To conclude, miR-532-3p mimics could act as potential candidate for molecular therapy in CRC through inactivation of the canonical Wnt/β-catenin signaling and enhancement of chemosensitivity.

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Section: Introductionmentioning

confidence: 99%

MiR-532-3p suppresses colorectal cancer progression by disrupting the ETS1/TGM2 axis-mediated Wnt/β-catenin signaling

Cai

et al. 2019

Cell Death Dis

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“…Some examples include the amplification of miR-106b-5p triggering stem cell-like properties of hepatocellular carcinoma cells (12), miR-106b-5p conferring proliferative advantage and inhibiting apoptosis in non-small cell lung cancer and overexpression of miR-106b-5p attenuating invasion and metastasis in colorectal cancer (27). By contrast, miR-106b-5p is reported to inhibit metastasis in colorectal cancer (27) and is associated with better survival in bladder cancer (28). However, whether miR-106-5p functions as an oncogene or tumor suppressor in OS still remains unclear.…”

Section: Discussionmentioning

confidence: 99%

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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“…Multiple microRNAs have been reported to play a regulatory role in cell senescence. For example, miR-30 inhibits both p16 INK4A and p53, two key senescence effectors, leading to efficient senescence disruption (32). miR-137 targets KDM4A mRNA during RAS-induced senescence and activates both the p53 and Rb pathways (33).…”

Section: Discussionmentioning

confidence: 99%

Epstein–Barr virus miR-BART3-3p promotes tumorigenesis by regulating the senescence pathway in gastric cancer

Wang

Zheng

Qin

et al. 2019

Journal of Biological Chemistry

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Edited by Qi-Qun TangEpstein-Barr virus-associated gastric cancer (EBVaGC) accounts for about 10% of all gastric cancer cases and has unique pathological and molecular characteristics. EBV encodes a large number of microRNAs, which actively participate in the development of EBV-related tumors. Here, we report that EBV-miR-BART3-3p (BART3-3p) promotes gastric cancer cell growth in vitro and in vivo. Moreover, BART3-3p inhibits the senescence of gastric cancer cells induced by an oncogene (RAS G12V ) or chemotherapy (irinotecan). LMP1 and EBNA3C encoded by EBV have also been reported to have antisenescence effects; however, in EBVaGC specimens, LMP1 expression is very low, and EBNA3C is not expressed. BART3-3p inhibits senescence of gastric cancer cells in a nude mouse model and inhibits the infiltration of natural killer cells and macrophages in tumor by altering the senescence-associated secretory phenotype (SASP). Mechanistically, BART3-3p directly targeted the tumor suppressor gene TP53 and caused down-regulation of p53's downstream target, p21. Analysis from clinical EBVaGC samples also showed a negative correlation between BART3-3p and TP53 expression. It is well known that mutant oncogene RAS G12V or chemotherapeutic drugs can induce senescence, and here we show that both RAS G12V and a chemotherapy drug also can induce BART3-3p expression in EBV-positive gastric cancer cells, forming a feedback loop that keeps the EBVaGC senescence at a low level. Our results suggest that, although TP53 is seldom mutated in EBVaGC, its expression is finely regulated such that EBV-encoded BART3-3p may play an important role by inhibiting the senescence of gastric cancer cells.

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Identification of microR-106b as a prognostic biomarker of p53-like bladder cancers by ActMiR

Cited by 22 publications

References 41 publications

MiR-532-3p suppresses colorectal cancer progression by disrupting the ETS1/TGM2 axis-mediated Wnt/β-catenin signaling

MiR-532-3p suppresses colorectal cancer progression by disrupting the ETS1/TGM2 axis-mediated Wnt/β-catenin signaling

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

Epstein–Barr virus miR-BART3-3p promotes tumorigenesis by regulating the senescence pathway in gastric cancer

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