Long non-coding RNA TUG1 enhances chemosensitivity in non-small cell lung cancer by impairing microRNA-221-dependent PTEN inhibition

Guo, Shouwu; Zhang, Lei; Zhang, Yuehua; Wu, Zheng; He, Dongwei; Li, Xing; Wang, Zhiyu

doi:10.18632/aging.102271

Cited by 40 publications

(46 citation statements)

References 34 publications

(39 reference statements)

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“…10 Studies based on transcriptomics and genomics show that approximately 75% of human DNA transcribed to RNA is not translated into protein. 11,12 Many such RNA sequences exceed a length of 200 nucleotides and are termed long non-coding RNAs (lncRNAs). Several investigative reports applying various experimental techniques have demonstrated that these lncRNAs influence many essential physiological functions, including the differentiation of cell lineages 13,14 and immunological reactions.…”

Section: Introductionmentioning

confidence: 99%

TUG1 long non‐coding RNA enlists the USF1 transcription factor to overexpress ROMO1 leading to hepatocellular carcinoma growth and metastasis

Liu

Qiu

et al. 2020

MedComm

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Hepatocellular carcinoma (HCC) is a prevalent and highly aggressive cancer. Long non-coding RNAs (lncRNAs) are recognized as potential molecular targets for HCC and are currently under increased research focus. Here, we investigate the regulatory processes underlying the axis of the lncRNA taurine upregulated gene 1 (TUG1), Upstream Transcription Factor 1 (USF1), and reactive oxygen species modulator 1 (ROMO1) in the propagation and metastasis of HCC cells. Distribution of lncRNA TUG1 was found to be prominent in HCC cell cytoplasm and nuclei. LncRNA TUG1 conscripted the USF1 transcription factor to enhance the promoter function of ROMO1. Enlisting the USF1 transcription factor to increase ROMO1 expression following upregulation of TUG1 lncRNA enhanced HCC Huh7 cell proliferation, motility, and metastasis. Rapid tumor proliferation in nude mice provided in vivo verification. The importance of the lncRNA TUG1/USF1/ROMO1 complex as a target for HCC therapy is a key result of this investigation which is exemplified by its role in regulating the proliferation, motility, and metastasis of HCC cells.

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Section: Introductionmentioning

confidence: 99%

TUG1 long non‐coding RNA enlists the USF1 transcription factor to overexpress ROMO1 leading to hepatocellular carcinoma growth and metastasis

Liu

Qiu

et al. 2020

MedComm

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“…Recently, TUG1 was characterized as a new oncogene and found to be upregulated in multiple human cancers (50)(51)(52)(53)(54)(55)(56). TUG1 was upregulated in OC tissues and cells and was positively correlated with advanced disease and poor prognosis.…”

Section: Discussionmentioning

confidence: 99%

miR‑1299/NOTCH3/TUG1 feedback loop contributes to the malignant proliferation of ovarian cancer

Pei

Lou

et al. 2020

Oncol Rep

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Recent studies have revealed the oncogenic role of notch reporter 3 (NOTCH3) in ovarian cancer (OC). However, the possible regulators and mechanisms underlying notch receptor 3 (NOTCH3)-mediated behaviors in OC remain to be completely investigated. In the present study, we aimed to identify regulators of NOTCH3 and their interactions underlying the pathogenesis of OC. Bioinformatics analysis and luciferase reporter assay were used to identify potential regulatory miRNAs and lncRNAs of NOTCH3 in OC. Several in vivo and in vitro assays were performed to evaluate their effects on the proliferative ability mediated by NOTCH3. We identified microRNA-1299 (miR-1299) as a novel negative regulator of NOTCH3. miR-1299 was downregulated in OC and was found to be considerably correlated with tumor differentiation. Upregulation of miR-1299 inhibited cell proliferation, colony formation, and 5-ethynyl-2'-deoxyuridine (EdU) incorporation, as well as induced cell cycle arrest in the G0G1 phase in OC cells. Overexpression of miR-1299 in xenograft mouse models suppressed tumor growth in vivo. The lncRNA taurine upregulated gene 1 (TUG1), acting as a sponge of miR-1299, was found to upregulate NOTCH3 expression and promote cell proliferation in OC through the competing endogenous RNA mechanism. In addition, TUG1 was found to be a potential downstream target of NOTCH3, forming a miR-1299/NOTCH3/TUG1 feedback loop in the development of OC. Collectively, our findings improve the understanding of NOTCH3-mediated regulation in OC pathogenesis and facilitate the development of miRNA-and lncRNA-directed diagnostics and therapeutics against this disease.

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“…In recent years, lncRNA TUG1 emerges as a new player in gene regulation in lung-related diseases (29)(30)(31). Many studies have indicated that TUG1 is downregulated in lung-related diseases, including acute lung injury (ALI) (29) and non-small cell lung cancer (NSCLC) (32).…”

Section: Discussionmentioning

confidence: 99%

Long Non-coding RNA TUG1 Modulates Expression of Elastin to Relieve Bronchopulmonary Dysplasia via Sponging miR-29a-3p

Zhong

Wang

et al. 2020

Front. Pediatr.

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Objective: Multiple studies have highlighted that long non-coding RNAs (lncRNAs) may exert paramount roles in relieving bronchopulmonary dysplasia (BPD). The aim of our investigation is to probe the role and mechanism of lncRNA taurine upregulated gene 1 (TUG1) in BPD. Methods:The current mouse model of BPD was simulated by induction of hyperoxia, and hyperoxia-induced mouse type II alveolar epithelial (MLE-12) (MLE-12) cells were established as a cellular model. Quantitative real-time polymerase chain reaction (qRT-PCR) was applied to determine relative expressions of TUG1, miR-29a-3p, and elastin (ELN). We assessed cell apoptosis by TdT-mediated dUTP-biotin nick-end labeling (TUNEL) staining. Western blot was used for detection of apoptosis-related proteins. Moreover, cell viability was tested by cell counting kit-8 (CCK-8) assay. Inflammatory factors were measured by enzyme-linked immunosorbent assay (ELISA). Dual-luciferase reporter (DLR) assay was employed to confirm relationship between genes.Results: Upregulation of miR-29a-3p was found in lung tissues of BPD mice compared with lung tissues without BPD, while downregulations of TUG1 and ELN were discovered in BPD tissues in comparison with tissues without BPD. Increasing TUG1 was shown to alleviate lung injury of BPD mice and promote proliferation of hyperoxia-induced MLE-12 cells. Meanwhile, TUG1 inhibited inflammatory response and cell apoptosis in lung tissues of BPD mice and hyperoxia-induced MLE-12 cells. miR-29a-3p was targeted by TUG1 and negatively modulated by TUG1. ELN was inversely regulated by miR-29a-3p. Meantime, suppressive effects of TUG1 on apoptosis and inflammation were reversed by decreasing ELN or increasing miR-29a-3p in hyperoxia-induced MLE-12 cells.Conclusion: lncRNA TUG1 relieved BPD through regulating the miR-29a-3p/ELN axis, which provided a therapeutic option to prevent or ameliorate BPD.

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Long non-coding RNA TUG1 enhances chemosensitivity in non-small cell lung cancer by impairing microRNA-221-dependent PTEN inhibition

Cited by 40 publications

References 34 publications

TUG1 long non‐coding RNA enlists the USF1 transcription factor to overexpress ROMO1 leading to hepatocellular carcinoma growth and metastasis

TUG1 long non‐coding RNA enlists the USF1 transcription factor to overexpress ROMO1 leading to hepatocellular carcinoma growth and metastasis

miR‑1299/NOTCH3/TUG1 feedback loop contributes to the malignant proliferation of ovarian cancer

Long Non-coding RNA TUG1 Modulates Expression of Elastin to Relieve Bronchopulmonary Dysplasia via Sponging miR-29a-3p

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