Overexpression of the long noncoding RNA TRHDE‐AS1 inhibits the progression of lung cancer via the miRNA‐103/KLF4 axis

Zhuan, Bing; Lu, Yuting; Chen, Qian; Zhao, Xiaona; Li, Ping; Yan, Qun; Zhao, Yang

doi:10.1002/jcb.29029

Cited by 34 publications

(21 citation statements)

References 28 publications

(43 reference statements)

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“…Although the roles of numerous miRNAs in malignant tumors have been reported, little research has revealed the function of miR-103 on tumor progression (41). miR-103 has been reported to have a tumor suppressor effect on NSCLC (42), however, to the best of our knowledge, a comprehensive assessment of the effects of miR-103 on all processes in NSCLC cells has not been performed.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑103 modulates tumor progression by targeting KLF7 in non‑small cell lung cancer

Yuan

2020

Int J Mol Med

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Numerous studies have identified that microRNAs (miRs) play a crucial role in the tumorigenesis of non-small cell lung cancer (NSCLC). However, to the best of our knowledge, the physiological function of miR-103 in NSCLC is not fully understood. Experiments in the present study revealed that miR-103 expression was increased in NSCLC cell lines. In addition, a series of methods, including MTT, colony formation, 5-ethynyl-2'-deoxyuridine, Transwell, wound healing, flow cytometric, reverse transcription-quantitative PCR and western blot assays, were performed, which revealed that overexpression of miR-103 enhanced cell growth, migration, invasion and epithelial-mesenchymal transition (EMT), and suppressed apoptosis of A549 and H1299 cells. Additionally, a dual-luciferase reporter assay indicated that miR-103 directly targets the 3'-untranslated region of Kruppel-like factor 7 (KLF7), and KLF7 expression was negatively regulated by miR-103 expression. Furthermore, the present findings demonstrated that miR-103 promoted EMT via regulating the Wnt/β-catenin signaling pathway in NSCLC. Collectively, the current results demonstrated that miR-103 serves a tumorigenesis role in NSCLC development by targeting KLF7, at least partly via the Wnt/β-catenin signaling pathway. Consequently, these findings indicated that miR-103/KLF7/Wnt/β-catenin may provide a novel insight into underlying biomarkers for improving the diagnosis and treatment of NSCLC.

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Section: Discussionmentioning

confidence: 99%

MicroRNA‑103 modulates tumor progression by targeting KLF7 in non‑small cell lung cancer

Yuan

2020

Int J Mol Med

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“…In NSCLC the expression of KLF4 is negatively regulated by various microRNAs: miR-25, miR-103, miR-145 and miR-3120-5p [ 69 , 73 , 74 , 75 ]. KLF4 expression is positively regulated by metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), a long non-coding RNA (lncRNA) that has been demonstrated to function as an oncogene [ 74 ].…”

Section: Lung Cancermentioning

confidence: 99%

“…This regulation is indirect as MALAT1 directly targets miR-145 and in this way it reduces the inhibitory effects of miR-145 on KLF4 activity [ 74 ]. Thyrotropin Releasing Hormone Degrading Enzyme (TRHDE)-Antisense RNA 1 (TRHDE-AS1) is another lncRNA positively regulating the expression of KLF4, and this regulation is most likely mediated by miR-103 [ 75 ]. These findings emphasize the importance of non-coding RNAs in the regulation of KLF4 activity.…”

Section: Lung Cancermentioning

confidence: 99%

Recent Discoveries on the Involvement of Krüppel-Like Factor 4 in the Most Common Cancer Types

Taracha-Wisniewska

Kotarba

Dworkin

et al. 2020

IJMS

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Krüppel-like factor 4 (KLF4) is a transcription factor highly conserved in evolution. It is particularly well known for its role in inducing pluripotent stem cells. In addition, KLF4 plays many roles in cancer. The results of most studies suggest that KLF4 is a tumor suppressor. However, the functioning of KLF4 is regulated at many levels. These include regulation of transcription, alternative splicing, miRNA, post-translational modifications, subcellular localization, protein stability and interactions with other molecules. Simple experiments aimed at assaying transcript levels or protein levels fail to address this complexity and thus may deliver misleading results. Tumor subtypes are also important; for example, in prostate cancer KLF4 is highly expressed in indolent tumors where it impedes tumor progression, while it is absent from aggressive prostate tumors. KLF4 is important in regulating response to many known drugs, and it also plays a role in tumor microenvironment. More and more information is available about upstream regulators, downstream targets and signaling pathways associated with the involvement of KLF4 in cancer. Furthermore, KLF4 performs critical function in the overall regulation of tissue homeostasis, cellular integrity, and progression towards malignancy. Here we summarize and analyze the latest findings concerning this fascinating transcription factor.

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“…gov/nuccore/NR_026837). This long non-coding RNA is found in the cytoplasm and binds directly to miR-103 in samples of human lung, inhibiting parameters of human lung cancer progression (Zhuan et al, 2019). Individuals challenged with FIGURE 1 | A map of candidates for transcriptional regulation of Trhde expression predicted by bioinformatic analysis.…”

Section: Trhde Gene Transcripts Protein Structure Isoforms and Spementioning

confidence: 99%

The Thyrotropin-Releasing Hormone-Degrading Ectoenzyme, a Therapeutic Target?

et al. 2020

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Thyrotropin releasing hormone (TRH: Glp-His-Pro-NH 2) is a peptide mainly produced by brain neurons. In mammals, hypophysiotropic TRH neurons of the paraventricular nucleus of the hypothalamus integrate metabolic information and drive the secretion of thyrotropin from the anterior pituitary, and thus the activity of the thyroid axis. Other hypothalamic or extrahypothalamic TRH neurons have less understood functions although pharmacological studies have shown that TRH has multiple central effects, such as promoting arousal, anorexia and anxiolysis, as well as controlling gastric, cardiac and respiratory autonomic functions. Two G-protein-coupled TRH receptors (TRH-R1 and TRH-R2) transduce TRH effects in some mammals although humans lack TRH-R2. TRH effects are of short duration, in part because the peptide is hydrolyzed in blood and extracellular space by a M1 family metallopeptidase, the TRH-degrading ectoenzyme (TRH-DE), also called pyroglutamyl peptidase II. TRH-DE is enriched in various brain regions but is also expressed in peripheral tissues including the anterior pituitary and the liver, which secretes a soluble form into blood. Among the M1 metallopeptidases, TRH-DE is the only member with a very narrow specificity; its best characterized biological substrate is TRH, making it a target for the specific manipulation of TRH activity. Two other substrates of TRH-DE, Glp-Phe-Pro-NH 2 and Glp-Tyr-Pro-NH 2, are also present in many tissues. Analogs of TRH resistant to hydrolysis by TRH-DE have prolonged central efficiency. Structure-activity studies allowed the identification of residues critical for activity and specificity. Research with specific inhibitors has confirmed that TRH-DE controls TRH actions. TRH-DE expression by b2-tanycytes of the median eminence of the hypothalamus allows the control of TRH flux into the hypothalamus-pituitary portal vessels and may regulate serum thyrotropin secretion. In this review we describe the critical evidences that suggest that modification of TRH-DE activity in tanycytes, and/or in other brain regions, may generate beneficial consequences in some central and metabolic disorders and identify potential drawbacks and missing information needed to test these hypotheses.

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Overexpression of the long noncoding RNA TRHDE‐AS1 inhibits the progression of lung cancer via the miRNA‐103/KLF4 axis

Cited by 34 publications

References 28 publications

MicroRNA‑103 modulates tumor progression by targeting KLF7 in non‑small cell lung cancer

MicroRNA‑103 modulates tumor progression by targeting KLF7 in non‑small cell lung cancer

Recent Discoveries on the Involvement of Krüppel-Like Factor 4 in the Most Common Cancer Types

The Thyrotropin-Releasing Hormone-Degrading Ectoenzyme, a Therapeutic Target?

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