miR-22 in tumorigenesis

Song, Su Jung; Pandolfi, Pier Paolo

doi:10.4161/cc.27027

Cited by 26 publications

(25 citation statements)

References 8 publications

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“…Previous studies have suggested that miR-22 functions in multiple cellular processes, including proliferation, differentiation, senescence and apoptosis and that their dysregulation is a hallmark of human cancer [43]. MiR-22 has been determined to be a regulator or an inhibitor in diverse cancers, including osteosarcoma, prostate cancer, cervical cancer, lung cancer, [44]breast cancer[45], colorectal cancer[46], gastric cancer [47, 48], ovarian cancer[49], acute myeloid leukemia[50], medulloblastomas[51], endometrial endometrioid carcinomas[52], esophageal squamous cell carcinoma[53] and hepatocellular carcinoma[54].…”

Section: Discussionmentioning

confidence: 99%

Response of MiRNA-22-3p and MiRNA-149-5p to Folate Deficiency and the Differential Regulation of MTHFR Expression in Normal and Cancerous Human Hepatocytes

Liu

et al. 2017

PLoS ONE

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Background/AimsFolic acid (FA) is a core micronutrient involved in DNA synthesis/methylation, and the metabolism of FA is responsible for genomic stability. MicroRNAs may affect gene expression during folate metabolism when cellular homeostasis is changed. This study aimed to reveal the relationship between FA deficiency and the expression of miR-22-p/miR-149-5p and the targeted regulation of miR-22-3p/miR-149-5p on the key folate metabolic gene Methylenetetrahydrofolate reductase (MTHFR).MethodsNormal (HL-7702 cells) and cancerous (QGY-7703 cells) human hepatocytes were intervened in modified RPMI 1640 with FA deficiency for 21 days. The interaction between MTHFR and the tested miRNAs was verified by Dual-Luciferase Reporter Assays. The changes in the expression of miR-22-3p/miR-149-5p in response to FA deficiency were detected by Poly (A) Tailing RT-qPCR, and the expression of MTHFR at both the transcriptional and translational levels was determined by RT-qPCR and Western blotting, respectively.ResultMiR-22-3p/miR-149-5p directly targeted the 3’UTR sequence of the MTHFR gene. FA deficiency led to an upregulation of miR-22-3p/miR-149-5p expression in QGY-7703/HL-7702 cells, while the transcription of MTHFR was decreased in QGY-7703 cells but elevated in HL-7702 cells. Western blotting showed that FA deficiency resulted in a decline of the MTHFR protein in QGY-7703 cells, whereas in HL-7702 cells, the MTHFR protein level remained constant.ConclusionThe results suggested that miR-22-3p/miR-149-5p exert different post-transcriptional effects on MTHFR under conditions of FA deficiency in normal and cancerous human hepatocytes. The results also implied that miR-22-3p/miR-149-5p might exert anticancer effects in cases of long-term FA deficiency.

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Section: Discussionmentioning

confidence: 99%

Response of MiRNA-22-3p and MiRNA-149-5p to Folate Deficiency and the Differential Regulation of MTHFR Expression in Normal and Cancerous Human Hepatocytes

Liu

et al. 2017

PLoS ONE

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“…All animal experiments were approved by the Medical Ethics Committee of The Second Hospital Affiliated to Tianjin Medical University (Tianjin, China). An RCC xenograft mouse model was created by subcutaneous injection of 1x10 7 Caki-1 cells transfected with LV-MALAT1 shRNA or LV-MALAT1 scramble to SPF nude mice. When sacrificed, the weight of mice was ~25 g. The tumor volume was evaluated every 5 days until 30 days after the development of a palpable tumor according to the formula (a x b 2 )/2, where a and b are the largest diameter and the perpendicular diameter, respectively.…”

Section: Rcc Xenograftsmentioning

confidence: 99%

“…Previous research has revealed that miRNA-22 (miR-22) is lowly expressed in breast cancer, esophageal squamous cell carcinoma, gastric and colorectal cancer. miR-22 inhibited cell growth, migration and epithelial-mesenchymal transition in the above-mentioned cancers (7)(8)(9)(10)(11). It was reported that miR-22 inhibited the invasion and migration of gastric cancer cells by downregulating the expression of MMP-14 and Snail (12).…”

Section: Introductionmentioning

confidence: 97%

Long non‑coding RNA MALAT1 correlates with cell viability and mobility by targeting miR‑22‑3p in renal cell carcinoma via the PI3K/Akt pathway

Zhong

Ma²,

2018

Oncol Rep

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Renal cell carcinoma (RCC) is one of the most common types of cancer of the urinary tract in the world. Long non-coding RNA MALAT1 (lncR-MALAT1) is upregulated in RCC and is associated with the proliferation and migration of RCC. The present study aimed to investigate the regulating role of lncR-MALAT1 in RCC as well as the possible underlying mechanisms. The relative expression of MALAT1 and miR-22-3p in RCC tumor tissues and cell lines was detected by qRT-PCR. CCK-8 and wound healing assay were used to evaluate cell proliferation and migration ability. Western blot analysis was used to detect the expression of Ki-67, proliferating cell nuclear antigen (PCNA), matrix metalloproteinase-3 (MMP-3), migration and invasion inhibitory protein (MIIP), p-PI3K and p-Akt. The relationship between MALAT1 and miR-22-3p was examined by bioinformatic prediction analysis and luciferase reporter assay. Immunofluorescence was used to detect the activation of Akt. MALAT1 was highly expressed and the expression of miR-22-3p was suppressed in RCC tissues and cell lines. ShRNA-mediated knockdown of MALAT1 significantly inhibited the viability and mobility of RCC cells in vitro and in vivo. Further experiments revealed that miR-22-3p was a target of MALAT1 and that miR-22-3p inhibitor abolished the effect of MALAT1 shRNA on cell proliferation, migration and inactivation of PI3K/AKT pathway. In conclusion, lncR-MALAT1 affected the proliferation and migration of RCC cells by targeting miR-22-3p through the inactivation of the PI3K/Akt signaling pathway.Abbreviations: MALAT1, metastasis-associated lung adenocarcinoma transcript 1; lncRNA, long non-coding RNA; RCC, renal cell carcinoma; miRNA, microRNA; MMP-3, matrix metaloproteinase-3; PCNA, proliferating cell nuclear antigen; MIIP, migration and invasion inhibitory protein; FBS, fetal bovine serum

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“…More recent evidence has identified miR-22 as a potent proto-oncogenic miRNA that deranges the epigenetic landscape of the cell (144). miR-22 has been shown to enhance the repopulating capacity and stem cell function of hematopoietic stem/progenitor cells (145).…”

Section: Cancer Cell ‘Stemness’ and The Epigenomementioning

confidence: 99%