MiR-365 regulates lung cancer and developmental gene thyroid transcription factor 1

Qi, Ji; Rice, Stephen L.; Salzberg, Anna C.; Runkle, E. Aaron; Liao, Jason; Zander, Dani S.; Mu, David

doi:10.4161/cc.11.1.18576

Cited by 75 publications

(71 citation statements)

References 46 publications

(52 reference statements)

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“…S1). This was somewhat unexpected in view of our reported finding that in NCI-H441 cells, TGF-␤ represses TTF-1 expression by up-regulating miR-365, which targets TTF-1 (36). There are several putative explanations to reconcile the opposite observations of TGF-␤ effects on TJ gene transcription between the two cell systems (e.g.…”

Section: Discussioncontrasting

confidence: 43%

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Occludin Is a Direct Target of Thyroid Transcription Factor-1 (TTF-1/NKX2–1)

Runkle

Rice

et al. 2012

Journal of Biological Chemistry

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Background: TTF-1, an amplified lung oncogene, also suppresses lung cancer metastasis, whereas the occludin phenotype in lung carcinomas is poorly understood. Results: TTF-1 transactivates occludin and occludin expression, reversing metastatic characteristics of lung cancer cells. Conclusion: Transcriptional regulation of occludin by TTF-1 negates metastatic properties of lung carcinoma cells. Significance: This study describes a novel extension of the multipronged anti-metastatic activity of TTF-1.

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Section: Discussioncontrasting

confidence: 43%

“…Approximately 300 ng of total RNA was reverse transcribed as described previously (36). Reactions were performed using TaqMan reagents and normalized to ␤-actin.…”

Section: Methodsmentioning

confidence: 99%

Occludin Is a Direct Target of Thyroid Transcription Factor-1 (TTF-1/NKX2–1)

Runkle

Rice

et al. 2012

Journal of Biological Chemistry

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“…The abnormal expression of microRNAs (miRNAs/miRs) has been implicated in the pathogenesis of numerous tumor types, including PTC (10)(11)(12). miRNAs are a group of short, endogenous, non-protein-coding and single-stranded RNA molecules 18-25 nucleotides in length (13).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑335 is downregulated in papillary thyroid cancer and suppresses cancer cell growth, migration and invasion by directly targeting ZEB2

Kan

Yang

2017

Oncol Lett

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Abstract. MicroRNAs (miRs) are a group of short, endogenous, non-protein-coding and single-stranded RNAs that regulate gene expression by binding to the 3'-untranslated region (3'UTR) of mRNAs, which results in their degradation or translational repression. The aim of the present study was to investigate the expression and function of miR-335 in human papillary thyroid cancer (PTC). Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was performed to quantify the relative miR-335 expression levels in PTC tissues and cell lines. The effect of miR-335 on the proliferation, migration and invasion of PTC cells was assessed by an MTT assay, and transwell migration and invasion assays, respectively. Dual-luciferase reporter assays were employed to explore whether miR-335 directly targeted the 3'UTR of the potential target gene zinc finger E-box binding homeobox 2 (ZEB2). RT-qPCR and western blotting were adopted to assess the effect of miR-335 on the mRNA and protein expression of ZEB2. RT-qPCR revealed that miR-335 was downregulated in PTC tissues and cell lines. The MTT assay and transwell migration and invasion assays demonstrated that the overexpression of miR-335 significantly inhibited the proliferation, migration and invasion of PTC cells. ZEB2 was identified as a direct target of miR-335 with computational analysis, which was confirmed with a dual-luciferase reporter assay, RT-qPCR and western blotting. The knockdown of ZEB2 significantly inhibited the proliferation, migration and invasion of PTC cells, indicating that ZEB2 may be a functional target of miR-335. Taken together, these findings suggested that miR-335 functioned as a tumor suppressor and suppressed the growth and metastatic behavior of PTC cells by targeting ZEB2. IntroductionThyroid cancer is the most common subtype of endocrine malignancy, with 300,000 new cases per year, and ~40,000 mortalities per year, worldwide (1). The incidence of thyroid cancer has increased in recent decades (2). It can be categorized into four major histologic groups, including papillary thyroid cancer (PTC), follicular thyroid cancer, poorly differentiated carcinoma and anaplastic thyroid cancer (3). PTC accounts for 80-90% of all thyroid cancer cases (4).A number of factors have been demonstrated to be associated with PTC progression, including genetic factors, environmental exposure, epigenetic alteration, nodular disease of the thyroid and radiation exposure (5,6). The prognosis of PTC patients is associated with their age, tumor size, lymph node invasion and distant metastasis (7). Currently, the standard therapeutic treatment for PTC is complete thyroidectomy followed by radioiodine and levothyroxine therapy (8). However, ~10% of patients with PTC develop recurrence and metastasis, which are associated with poor prognosis (9). Thus, it is necessary to characterize the molecular mechanisms of PTC initiation and development, and to develop novel, targeted therapies for PTC.The abnormal expression of microRNAs (miRNAs/miRs) has been implicated in ...

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“…Moreover, miR-365 feeds back to the TGF signaling pathway by specifically up-regulating TGF␤2 (Fig. 2B) (82). The observation of miR-365 repressing NKX2-1 was later reproduced in a separate study (83).…”

Section: Data Placing Nkx2-1 Firmly In a Microrna-based Signaling Netmentioning

confidence: 71%

“…This implies the putative existence of genetic selection pressure to lose the repressive miR-365 that would otherwise suppress amplified NKX2-1. Intriguingly, a signaling loop exists among TGF␤, miR-365, and NKX2-1, with TGF␤ up-regulating miR-365 via the mir-365-1 precursor gene, which in turn represses NKX2-1 (82). Moreover, miR-365 feeds back to the TGF signaling pathway by specifically up-regulating TGF␤2 (Fig.…”

Section: Data Placing Nkx2-1 Firmly In a Microrna-based Signaling Netmentioning

confidence: 99%

The Complexity of Thyroid Transcription Factor 1 with Both Pro- and Anti-oncogenic Activities

2013

Journal of Biological Chemistry

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After the original identification of thyroid transcription factor 1 (TTF-1 or NKX2-1) biochemical activity as a transcriptional regulator of thyroglobulin in 1989, the bulk of the ensuing research has concentrated on elucidating the roles of NKX2-1 in the development of lung and thyroid tissues. Motivated by its specific expression pattern, pathologists adopted the NKX2-1 immunoreactivity to distinguish pulmonary from nonpulmonary nonthyroid adenocarcinomas. Interestingly, the concept of NKX2-1 as an active participant in lung tumorigenesis did not take hold until 2007. This minireview contrasts the recent advancements of NKX2-1-related observations primarily in the realm of pulmonary malignancies.

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MiR-365 regulates lung cancer and developmental gene thyroid transcription factor 1

Cited by 75 publications

References 46 publications

Occludin Is a Direct Target of Thyroid Transcription Factor-1 (TTF-1/NKX2–1)

Occludin Is a Direct Target of Thyroid Transcription Factor-1 (TTF-1/NKX2–1)

MicroRNA‑335 is downregulated in papillary thyroid cancer and suppresses cancer cell growth, migration and invasion by directly targeting ZEB2

The Complexity of Thyroid Transcription Factor 1 with Both Pro- and Anti-oncogenic Activities

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