MYC upregulated LINC00319 promotes human acute myeloid leukemia (AML) cells growth through stabilizing SIRT6

Zhang, Yanni; Huang, Zhenguang; Sheng, Fen; Yin, Zhaoyang

doi:10.1016/j.bbrc.2018.12.133

Cited by 29 publications

(21 citation statements)

References 30 publications

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“…Here, we have identified a novel lncRNA LINC00319 as a key regulator of miR-3127, and showed that LINC00319 can downregulate the expression of miR-3127 in BCA cells by functioning as a miRNA sponge. LINC00319 was highly expressed in many human tumors and associated with poorer survival of patients (Zhou et al, 2017;Li et al, 2018;Zhang et al, 2018Zhang et al, , 2019Song and Yin, 2019). LINC00319 was shown to promote the proliferative, migratory and invasive capabilities of tumor cells by stabilizing SIRT6 (Zhang et al, 2019) or by interacting with miR-1207 (Song and Yin, 2019), miR-450 (Zhang et al, 2018) and miR-32 (Zhou et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

“…LINC00319 was highly expressed in many human tumors and associated with poorer survival of patients (Zhou et al, 2017;Li et al, 2018;Zhang et al, 2018Zhang et al, , 2019Song and Yin, 2019). LINC00319 was shown to promote the proliferative, migratory and invasive capabilities of tumor cells by stabilizing SIRT6 (Zhang et al, 2019) or by interacting with miR-1207 (Song and Yin, 2019), miR-450 (Zhang et al, 2018) and miR-32 (Zhou et al, 2017). Interestingly, a recent study revealed a direct interaction between lncRNA LINC00319 and miR-3127 in cervical cancer cells, and demonstrated that LINC00319 promotes migration, invasion and epithelial-mesenchymal transition process via regulating miR-3127 (Yang et al, 2020).…”

Section: Discussionmentioning

confidence: 99%

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LINC00319-Mediated miR-3127 Repression Enhances Bladder Cancer Progression Through Upregulation of RAP2A

Wang

Meng

2020

Front. Genet.

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Recent studies suggested that microRNA-3127 (miR-3127) was dysregulated in multiple tumor types and has important roles in tumorigenesis and cancer progression. However, its biological roles and the mechanisms that regulate its expression in bladder cancer (BCA) remain to be determined. The expression level of miR-3127 was measured in BCA tissues and its cellular functions were examined using both in vitro and in vivo experiments. The interaction between miR-3127 and long non-coding RNA (lncRNA) LINC00319 was explored using RNA immunoprecipitation assay and luciferase reporter assays. We showed that miR-3127 expression was significantly downregulated in human BCA tissues and BCA cell lines. Lower miR-3127 levels were associated with worse survival in BCA patients. The overexpression of miR-3127 impaired BCA cell proliferation and invasion, and the knockdown of miR-3127 enhanced BCA cell proliferation and invasion in vitro. Importantly, miR-3127 was able to suppress cell growth in vivo. We demonstrated that miR-3127 repressed the proliferation and invasion of BCA cells though directly targeted the 3-UTR of RAP2A, which served as a novel oncogene in BCA cells. The suppression of cell proliferation and invasion caused by miR-3127 overexpression could be partially abrogated by ectopic expression of RAP2A. Furthermore, high expression of LINC00319 was correlated with adverse survival in BCA patients. LINC00319 could bind directly with miR-3127 and inhibited its expression, and the tumor-promoting effects of LINC00319 could be reversed by re-expression of miR-3127 in BCA cells. Our findings indicated that lncRNA LINC00319-mediated miR-3127 repression promotes BCA progression through the upregulation of RAP2A. The re-introduction of miR-3127 or inhibition of LINC00319 might represent a promising therapeutic strategy for BCA treatment.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

LINC00319-Mediated miR-3127 Repression Enhances Bladder Cancer Progression Through Upregulation of RAP2A

Wang

Meng

2020

Front. Genet.

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“…Low SIRT6 expression has been reported in pancreatic cancer, colorectal cancer, and HCC [77,79]. However, several recent studies have reported that SIRT6 functions as a tumor promoter in other human cancers, such as skin squamous cell carcinoma, papillary thyroid cancer and acute myeloid leukemia (AML) [72,98,99]. SIRT6 promotes COX-2 expression by inhibiting AMPK signaling, thereby increasing cell proliferation and survival in the skin epidermis.…”

Section: Tumorigenesismentioning

confidence: 99%

“…In papillary thyroid cancer, SIRT6 promotes tumorigenesis by enhancing HIF-1α stability and prolonging its protein half-life [98]. Moreover, SIRT6 upregulation rescues the suppressive effect of LINC00319 (a long noncoding RNA, lncRNA) on AML cell growth [99].…”

Section: Tumorigenesismentioning

confidence: 99%

The Roles of Sirtuin Family Proteins in Cancer Progression

Zhao

Hou

et al. 2019

Cancers

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Sirtuin family members are characterized by either mono-ADP-ribosyltransferase or deacylase activity and are linked to various cancer-related biological pathways as regulators of transcriptional progression. Sirtuins play fundamental roles in carcinogenesis and maintenance of the malignant phenotype, mainly participating in cancer cell viability, apoptosis, metastasis, and tumorigenesis. Although sirtuin family members have a high degree of homology, they may play different roles in various kinds of cancer. This review highlights their fundamental roles in tumorigenesis and cancer development and provides a critical discussion of their dual roles in cancer, namely, as tumor promoters or tumor suppressors.

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“…More important, the mRNA expression level of FOXP4 was decreased by the knockdown of IGF2BP2 (Figure 2E). Mechanistically, lncRNAs can upregulate mRNAs by binding to RBPs to stabilize mRNAs (Lan et al, 2018; Zhang et al, 2018). In this regard, we conducted RIP assay to validate the binding of IGF2BP2 to FOXP4 (Figure 2F).…”

Section: Resultsmentioning

confidence: 99%

YY1‐induced upregulation of FOXP4‐AS1 and FOXP4 promote the proliferation of esophageal squamous cell carcinoma cells

Yang

et al. 2020

Cell Biology International

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Esophageal squamous cell carcinoma (ESCC) belongs to one of the most common malignant tumors worldwide and possesses high mortality. Long non‐coding RNAs (lncRNAs) have been demonstrated to be essential biological participants in the progression of ESCC. On the basis of bio‐informatics prediction, forkhead box P4 antisense RNA 1 (FOXP4‐AS1) and forkhead box P4 (FOXP4) were upregulated in esophageal carcinoma samples and were positively correlated with each other. The present study aimed to explore the function of FOXP4‐AS1 and FOXP4 in ESCC cells. Function assays disclosed that knockdown of FOXP4‐AS1 or FOXP4 efficiently suppressed cell proliferation and induced cell apoptosis. Moreover, FOXP4‐AS1 positively regulated FOXP4 by interacting with insulin‐like growth factor 2 mRNA‐binding protein 2 (IGF2BP2) to stabilize FOXP4 messenger RNA. In addition, FOXP4‐AS1 could upregulate the expression of FOXP4 by sponging miR‐3184‐5p. Finally, we found that Yin Yang 1 (YY1) is a transcription factor that can transcriptionally activate both FOXP4‐AS1 and FOXP4 in ESCC cells. In a word, YY1‐induced upregulation of FOXP4‐AS1 and FOXP4 promote the proliferation of ESCC cells

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MYC upregulated LINC00319 promotes human acute myeloid leukemia (AML) cells growth through stabilizing SIRT6

Cited by 29 publications

References 30 publications

LINC00319-Mediated miR-3127 Repression Enhances Bladder Cancer Progression Through Upregulation of RAP2A

LINC00319-Mediated miR-3127 Repression Enhances Bladder Cancer Progression Through Upregulation of RAP2A

The Roles of Sirtuin Family Proteins in Cancer Progression

YY1‐induced upregulation of FOXP4‐AS1 and FOXP4 promote the proliferation of esophageal squamous cell carcinoma cells

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