MicroRNA485-3p negatively regulates the transcriptional co-repressor <i>CtBP1</i> to control the oncogenic process in osteosarcoma cells

Du, Kaili; Zhang, Chi; Lou, Zhenkai; Guo, Peiyu; Zhang, Fan; Wang, Bing; Chen, Lingqiang; Zhang, Chunqiang

doi:10.7150/ijbs.26335

Cited by 29 publications

(24 citation statements)

References 36 publications

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“…miR-485-3p functions as a tumor-suppressor in different types of cancers and signaling pathways. For example, low expression of miR-485-3p was observed in osteosarcoma that negatively regulate CtBP1, a transcription co-repressor, which can associate with epigenetic enzymes for regulating downstream genes like Bax, Bim, E-cadherin, PUMA, p16, p21, and PTEN (22). Decreased expression of miR-485-3p was clarifi ed to be age-dependent in lung adenocarcinoma (24).…”

Section: Discussionmentioning

confidence: 99%

“…Emerging evidences demonstrate that miR-485-3p can act as an oncogene in gastric cancer (16), hepatocellular carcinoma (17,18), prostate cancer (19,20), and lymphoma (21). In contrast, studies showed that miR-485-3p can act as a tumor-suppressor in osteosarcoma (22), NSCLC lung cancer (23,24), glioblastoma (25) and breast cancer (26). However, its role in initiation and progression of colorectal cancer has remained disputed.…”

Section: Introductionmentioning

confidence: 99%

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miR-485-3p suppresses colorectal cancer via targeting TPX2

Taherdangkoo¹,

Nezhad²,

Hajjari³

et al. 2020

BLL

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BACKGROUND: Colorectal cancer (CRC), is the third most common cancer type. MicroRNAs and their roles in cancer progression have gained considerable attention in the scientifi c community. miR-485-3p has been identifi ed to be abnormally expressed in different types of cancer, but its expression level, biological function, and underlying pathways are still unclear in CRC. Targeting Protein for Xenopus kinesin-like protein 2 (TPX2) is a nuclear protein which plays vital roles in cancer progression and mitotic spindle assembly. TPX2 is overexpressed in various malignancies and has been predicted as an indirect target of miR-485-3p. This study aims to investigate the miR-485-3p and TPX2 expression level, their potential correlation, and underlying molecules like P53 and P21 in forty-one pairs of colorectal cancer tissues compared to matched non-cancerous ones. MATERIALS AND METHODS: We used forty-one pairs of CRC fresh tissue samples and their adjacent normal ones for RNA extraction. After cDNA synthesis, the expression level of miR-485-3p, TPX2, P53 and P21 were determined by Real-time PCR. RESULTS AND CONCLUSIONS: The results revealed that miR-485-3p was signifi cantly downregulated and TPX2 was highly upregulated in CRC tissues. Moreover, miR-485-3p was negatively correlated with TPX2 expression and positively correlated with P21 expression. We present miR-485-3p as a suppressor for colorectal cancer (Tab. 2, Fig. 8, Ref.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

miR-485-3p suppresses colorectal cancer via targeting TPX2

Taherdangkoo¹,

Nezhad²,

Hajjari³

et al. 2020

BLL

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“…Some studies have revealed that miRNAs may be involved in the regulation of CtBPs. For example, Du and colleagues found that miR-485-3p negatively regulates the expression of CtBP1 by directly binding to its 3'-untranslated region (3'-UTR) [46]. Deng and colleagues identified that miR-137 can repress the expression of CtBP1 by binding to its 3'-UTR [39].…”

Section: Discussionmentioning

confidence: 99%

DNA methylation is involved in the pathogenesis of osteoarthritis by regulating CtBP expression and CtBP-mediated signaling

et al. 2020

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Osteoarthritis (OA) is a common type of arthritis. Chronic inflammation is an important contributor to the pathogenesis of OA. The maturation and secretion of proinflammatory cytokines are controlled by inflammasomes, especially NLRP1 (NLR Family Pyrin Domain Containing 1) and NLRP3. In this study, we identified a transactivation mechanism of NLRP3 mediated by CtBPs (C-terminal-binding proteins). We found that both the mRNA and protein levels of CtBPs were significantly increased in OA biopsies. Analyzing the profiles of differentially expressed genes in CtBP-knockdown and overexpression cells, we found that the expression of NLRP3 was dependent on CtBP levels. By the knockdown or overexpression of transcription factors that potentially bind to the promoter of NLRP3, we found that only AP1 could specifically regulate the expression of NLRP3. Using immunoprecipitation (IP) and Co-IP assays, we found that AP1 formed a transcriptional complex with a histone acetyltransferase p300 and CtBPs. The knockdown of any member of this transcriptional complex resulted in a decrease in the expression of NLRP3. To explore the underlying mechanism of CtBP overexpression, we analyzed their promoters and found that they were abundant in CpG islands. Treatment with the DNA methylation inhibitor 5-aza-2′deoxycytidine (AZA) or knockdown of DNMTs (DNA methyltransferases) resulted in the overexpression of CtBPs, while overexpression of DNMTs caused the reverse effects on CtBP expression. Collectively, our results suggest that the decreased DNA methylation levels in the promoters of CtBPs upregulate their expression. Increased CtBPs associated with p300 and AP1 to form a transcriptional complex and activate the expression of NLRP3 and its downstream signaling, eventually aggravating the inflammatory response and leading to the pathogenesis of OA.

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“…For example, miR-485-3p was demonstrated to directly interact with the 3′-UTR of CtBP1, while the expression of miR-485-3p was associated with the DNA methylation of CpG islands in its promoter. When treating with 5′-AZA, miR-485-3p was upregulated to inhibit OS cell development by reducing CtBP1 expression [69]. High methylation levels in the CpG sites of miR-7 promoter were decreased by treating 5′-AZA, thus promoting miR-7 expression in OS cells.…”

Section: Osteosarcomamentioning

confidence: 99%

DNA methylation of noncoding RNAs: new insights into osteogenesis and common bone diseases

Xia

Cen

et al. 2020

Stem Cell Res Ther

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Bone diseases such as osteoarthritis, osteoporosis, and bone tumor present a severe public health problem. Osteogenic differentiation is a complex process associated with the differentiation of different cells, which could regulate transcription factors, cytokines, many signaling pathways, noncoding RNAs (ncRNAs), and epigenetic modulation. DNA methylation is a kind of stable epigenetic alterations in CpG islands without DNA sequence changes and is involved in cancer and other diseases, including bone development and homeostasis. ncRNAs can perform their crucial biological functions at the RNA level, and many findings have demonstrated essential functions of ncRNAs in osteogenic differentiation. In this review, we highlight current researches in DNA methylation of two relevant ncRNAs, including microRNAs and long noncoding RNAs, in the initiation and progression of osteogenesis and bone diseases.

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MicroRNA485-3p negatively regulates the transcriptional co-repressor CtBP1 to control the oncogenic process in osteosarcoma cells

Cited by 29 publications

References 36 publications

miR-485-3p suppresses colorectal cancer via targeting TPX2

miR-485-3p suppresses colorectal cancer via targeting TPX2

DNA methylation is involved in the pathogenesis of osteoarthritis by regulating CtBP expression and CtBP-mediated signaling

DNA methylation of noncoding RNAs: new insights into osteogenesis and common bone diseases

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