Long noncoding RNA TUG1 promotes proliferation and inhibits apoptosis in multiple myeloma by inhibiting miR-29b-3p

Liu, Dahai; Wang, Jianfeng; Liu, Meihan

doi:10.1042/bsr20182489

Cited by 21 publications

(27 citation statements)

References 36 publications

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“…Recently, increasing studies suggested that lncRNAs could function as sponges to bind to specific miRNAs to modulate downstream target gene, which were involved in many biological process [27, 28]. TUG1 was also reported to be involved in diverse human diseases by functioning as a ceRNA to sponge a variety of miRNAs such as miR-26a [13], miR-212-3p [29], and miR-29b [30]. Consistent with those reports, in this study, we found that TUG1 was associated with cell proliferation, apoptosis, invasion, and angiogenesis of trophoblast cells through sponging miR-29b, which decipher the essential role of TUG1 in the pathogenesis of PE, and as far as we know, this was the first study that reported the TUG1-regulated pathogenesis of PE by directly targeting miR-29b as a ceRNA.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: lncRNA TUG1 modulates proliferation, apoptosis, invasion, and angiogenesis via targeting miR-29b in trophoblast cells

Li¹,

Zhang

Su³

et al. 2019

Hum Genomics

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Background Pre-eclampsia (PE) is regarded as the leading cause of maternal and neonatal morbidity and mortality. Nevertheless, the potential mechanism for the regulation of trophoblast behaviors and the pathogenesis of PE remain largely elusive. Recently, accumulating evidence emphasized that aberrant expression of long non-coding RNAs (lncRNAs) functions as imperative regulators in human diseases, including PE. Thus, identifying PE-related specific lncRNAs to uncover the underlying molecular mechanism is of much significance. However, the functional roles and underlying mechanisms of lncRNAs in PE progression remain unclear. Method Placenta tissues obtained from patients with PE and healthy pregnant women were performed to measure TUG1 expression by qRT-PCR analysis. Transient transfections were conducted to alter TUG1 expression. Cell Counting Kit-8 (CCK-8) and flow cytometry assays were carried out to assess cell proliferation and apoptosis, respectively. Transwell and tube formation assays were performed to measure the capacity of cell invasion and angiogenesis. Moreover, the luciferase reporter assay was subjected to verify the binding relationship between TUG1 and miR-29b. Western blot analysis was performed to detect the expression of key proteins in the PI3K/AKT and ERK pathway. Results Here, we identified a lncRNA, TUG1, which was notably decreased in placental samples of PE patients. Functional experiments of loss- or gain-of-function assays also verified that ectopic expression of TUG1 promoted cell proliferation, invasion, and angiogenesis, but negatively regulated cell apoptosis, whereas TUG1 inhibition presented the opposite effects. Furthermore, mechanistic researches revealed that TUG1 could act as a molecular sponge for miR-29b, thus regulating MCL1, VEGFA, and MMP2 to modulate PE development. Conclusions Taken together, our findings demonstrated that TUG1 exerts as a critical role in PE progression, which might furnish a novel therapeutic marker for PE treatment.

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Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: lncRNA TUG1 modulates proliferation, apoptosis, invasion, and angiogenesis via targeting miR-29b in trophoblast cells

Li¹,

Zhang

Su³

et al. 2019

Hum Genomics

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“…Additionally, TUG1 promotes cancer progression through accelerating cell proliferation and inhibiting cell apoptosis (Kuang, Zhang, Hua, Dong, & Li, 2016; Li, Chen, Zhang, & Liu, 2018; Li, Zhang, Liu, & Chen, 2018). It has also been reported that TUG1 promotes multiple myeloma cell proliferation and inhibits apoptosis by suppressing miR‐29b‐3p (Liu, Wang, & Liu, 2019), and TUG1 induces cardiac hypertrophy through sponging miR‐29b‐3p (Zou, Wang, Tang, & Wen, 2019). Moreover, TUG1 promotes OC cell proliferation and invasion by regulating WNT/β‐catenin pathway (Liu, Liu et al, 2018), or regulates angiogenesis by regulating expression of LRG1 (Fan, Li, et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

“…lncRNA turine up‐regulated gene 1 (TUG1) contributes to the photoreceptor formation and retina development and locates at chromosome band 22q12 (Young, Matsuda, & Cepko, 2005). A variety of studies demonstrated that TUG1 is highly expressed in multiple cancers, and it has been found to contribute to carcinogenesis in laryngocarcinoma (Zhuang, Liu, & Wu, 2019), osteosarcoma (Yu, Hu, et al, 2019), multiple myeloma (Liu, Wang, & Liu, 2019), pancreatic cancer (Hui et al, 2019), melanoma (Wang, Liu, Ren, Wang, & Liu, 2019), and OC (Fan, Li, et al, 2019). Previous studies have illustrated that TUG1 promotes cancer progression by regulating LRG1 secretion through modulating tumor growth factor‐β pathway (Fan, Li, et al, 2019), and by promoting cell proliferation and invasion through regulating WNT/β‐catenin pathway (Liu et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

RETRACTED: Long noncoding RNA TUG1 facilitates cell ovarian cancer progression through targeting MiR‐29b‐3p/MDM2 axis

Yang

Xin

et al. 2020

The Anatomical Record

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Ovarian cancer (OC) is one of the most aggressive female cancers in the world. OC trends to be diagnosed at an advanced stage with abdominal metastasis. Our study explored the biological function and underlying mechanism of lncRNA on OC cell proliferation and migration. The expression of turine upregulated gene 1 (TUG1) in human OC tissues and cell lines was measured by qRT-PCR. OC cell proliferation, viability, migration, and invasion were measured by MTT assays, colony formation assays, and transwell assays in vitro. Furthermore, the nude mice xenograft model was established to determine the effects of TUG1 in vivo. The relationship between TUG1 and miR-29b-3p, as well as miR-29b-3p and MDM2 were identified using the luciferase reporter assays. We showed that the expression of TUG1 and MDM2 were significantly increased, but the expression of miR-29b-3p was remarkably decreased in OC tissues and cell lines. Knockdown of TUG1 strongly inhibited the ability of cell proliferation, colony formation, migration, and invasion in vitro. The relationship between TUG1 and miR-29b-3p, or miR-29b-3p and MDM2 were predicted by StarBase and miRanda online software. Besides, miR-29b-3p reversed the positive effect of TUG1 on the OC cell proliferation, migration, and invasion through inhibiting MDM2 expression and increasing p53 phosphorylation level. Moreover, knockdown of TUG1 suppressed tumor growth in vivo. Taken all together, this study shows that TUG1 plays a crucial oncogenic role and facilitates cell proliferation, migration, and invasion in OC through regulating miR-29b-3p/MDM2 axis.

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“…Increasing evidence indicates that the aberrant expression of long non-coding RNAs (lncRNAs) are closely associated with the development and prognosis of various types of cancer, including MM [5]. Liu et al [6] reported that lncRNA TUG1 were significantly up-regulated in MM samples and cell lines, and that down-regulation of TUG1 markedly inhibited MM cell proliferation and promoted apoptosis. LncRNA Small Nucleolar RNA Host Gene 16 (SNHG16), an SNHG member, is up-regulated and functions as an oncogene in pancreatic cancer [7] and gastric cancer [8].…”

Section: Introductionmentioning

confidence: 99%

Knockdown of lncRNA SNHG16 suppresses multiple myeloma cell proliferation by sponging miR-342-3p

et al. 2020

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Background: Aberrant expression of long non-coding RNAs (lncRNAs) is closely associated with development and prognosis of human cancers. LncRNA SNHG16 is reportedly involved in human cancer; however, its roles in multiple myeloma (MM) remain unclear. Methods: In this study, we investigated the function and molecular mechanisms of SNHG16 in MM. MM cells were transfected with si-SNHG16 or si-NC. SNHG16 expression levels was measured by qRT-PCR. Cell proliferation was monitored using the MTS. Flow cytometry assay was performed to measure the cell cycle and apoptosis. Luciferase reporter assay were performed to confirm the sponged miRNAs of SNHG16. Results: SNHG16 expression was up-regulated in MM tissues. SNHG16 knockdown suppressed cell proliferation, arrested cell cycle transition from G1 to S phase, and promoted the apoptosis of MM cells. Moreover, SNHG16 knockdown promoted cleaved-Caspase-3, cleaved-Caspase-9, Foxa3a, and Bax expression, while markedly inhibiting CCND1, Bcl-2, Cyclin D1, PI3K, and p-AKT expression in MM cells. miR-342-3p was a direct target of SNHG16. SNHG16 knockdown significantly increased miR-342-3p expression in MM cells. Overexpression miR-342-3p markedly suppressed cell proliferation, arrested cell cycle transition from G1 to S phase, and promoted apoptosis of MM cells. Overexpression of miR-342-3p markedly promoted cleaved-Caspase-3/-9, Foxa3a, and Bax expression, and inhibited CCND1, Bcl-2, Cyclin D1, PI3K, and p-AKT expression in MM cells. Additionally, repression of miR-342-3p could rescue the effect of SNHG16 knockdown on MM cell proliferation, cycle arrest, apoptosis, and related protein expression. Conclusion: Knockdown of lncRNA SNHG16 suppresses MM cell proliferation by sponging miR-342-3p, implicating SNHG16 as a novel therapeutic target for MM.

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Long noncoding RNA TUG1 promotes proliferation and inhibits apoptosis in multiple myeloma by inhibiting miR-29b-3p

Cited by 21 publications

References 36 publications

RETRACTED ARTICLE: lncRNA TUG1 modulates proliferation, apoptosis, invasion, and angiogenesis via targeting miR-29b in trophoblast cells

RETRACTED ARTICLE: lncRNA TUG1 modulates proliferation, apoptosis, invasion, and angiogenesis via targeting miR-29b in trophoblast cells

RETRACTED: Long noncoding RNA TUG1 facilitates cell ovarian cancer progression through targeting MiR‐29b‐3p/MDM2 axis

Knockdown of lncRNA SNHG16 suppresses multiple myeloma cell proliferation by sponging miR-342-3p

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