Upregulation of mi<scp>R</scp>‐372 and ‐373 associates with lymph node metastasis and poor prognosis of oral carcinomas

Tu, Hsi Feng; Chang, Kuo Wei; Cheng, Hui; Liu, Chung Ji

doi:10.1002/lary.25464

Cited by 42 publications

(33 citation statements)

References 39 publications

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“…Our data show that miR-372 is aberrantly expressed in a half of PAds and in the majority of both atypical PAds and PCas, where it is also present at significantly higher levels than in PAds. Therefore, aggressive behavior in parathyroid tumors appears to be associated with enriched expression of the embryonic miR-372, similar to what was reported for glioma, colorectal and oral cancers (Yamashita et al 2012, Chen et al 2015, Tu et al 2015. In this context, it is noteworthy that PAts showed a miR-372 expression pattern close to that detected in PCas.…”

Section: Discussionsupporting

confidence: 81%

“…In parathyroid tumor cells, miR-372 represses the cell cycle genes CDKN1A/p21, LATS2 and cyclin D1 thereby explaining the slow proliferating nature of this neoplasm, and potentially protects parathyroid cells from apoptotic stimuli, such as exposure to chemotherapeutics. miR-372 has been shown to play a substantial role in several human cancers, where it is either upregulated (Voorhoeve et al 2006, Cho et al 2009, Yamashita et al 2012, Li et al 2013, Chen et al 2015, Tu et al 2015, Liu et al 2016 or downregulated (Tian et al 2011, Huang et al 2015, Liu et al 2016. Our data show that miR-372 is aberrantly expressed in a half of PAds and in the majority of both atypical PAds and PCas, where it is also present at significantly higher levels than in PAds.…”

Section: Discussionmentioning

confidence: 60%

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The aberrantly expressed miR-372 partly impairs sensitivity to apoptosis in parathyroid tumor cells

Verdelli¹,

Forno²,

Morotti³

et al. 2018

Endocrine-Related Cancer

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Parathyroid tumors deregulate microRNAs belonging to the two clusters on the chromosome 19, the C19MC and miR-371-373 clusters. Here, we report that the embryonic miR-372 is aberrantly expressed in half of parathyroid adenomas (PAds) in most of atypical adenomas and carcinomas ( = 15). Through hybridization, we identified that miR-372-positive parathyroid tumor cells were scattered throughout the tumor parenchyma. In PAd-derived cells, ectopic miR-372 inhibited the expression of its targets/p21 and LATS2 at both mRNA and protein levels. Although the viability of parathyroid cells was not affected by miR-372 overexpression, the miRNA blunted camptothecin-induced apoptosis in primary PAd-derived cultures. miR-372 overexpression in parathyroid tumor cells increased parathormone () mRNA levels, and it positively correlated with circulating PTH levels. Conversely, the parathyroid-specific genes and were not affected by miR-372 mimic transfection. Finally, miR-372 dampened the Wnt pathway in parathyroid tumor cells through DKK1 upregulation. In conclusion, miR-372 is a novel mechanism exploited by a subset of parathyroid tumor cells to partially decrease sensitivity to apoptosis, to increase PTH synthesis and to deregulate Wnt signaling.

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Section: Discussionsupporting

confidence: 81%

Section: Discussionmentioning

confidence: 60%

The aberrantly expressed miR-372 partly impairs sensitivity to apoptosis in parathyroid tumor cells

Verdelli¹,

Forno²,

Morotti³

et al. 2018

Endocrine-Related Cancer

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“…MicroRNAs (miRs) have been widely accepted as a regulator of human cancers and it can be either cancer promoters or cancer suppressors. A plethora of studies have demonstrated that miR‐372 has a strong influence on some human cancers like gastric cancer, hepatocellular cancer, and colorectal cancer by regulating specific genes . MiR‐372‐3p, on the other hand, has not been reported to influence carcinogenesis too much, however, was discovered to suppress insulin‐like growth factor 2 mRNA‐binding protein 1 (IGF2BP1) therefore led to the decrease in proliferation and invasiveness in renal cell carcinoma .…”

Section: Discussionmentioning

confidence: 99%

MiR‐372‐3p promotes cell growth and metastasis by targeting FGF9 in lung squamous cell carcinoma

et al. 2017

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The aim of this study was to study the role of miR‐372‐3p in lung squamous cell carcinoma (LSCC) cell proliferation and invasion by suppressing FGF9. RT‐PCR was used to determine miR‐372‐3p and FGF9 mRNA expression in tissues and cells. Western blot was used to determine FGF9 expression in tissues and NCI‐H520 cell line. Dual luciferase reporter gene assay was conducted to confirm that FGF9 can be directly targeted by miR‐372‐3p. MTT, colony formation assays were conducted to investigate the effects of ectopic miR‐372‐3p and FGF9 expression on NCI‐H520 cell growth. Flow cytometry was used to analyze the influence of miR‐372‐3p and FGF9 expression on cell cycle distribution and apoptosis. Transwell assay was also conducted to see the effects of miR‐372‐3p and FGF9 expression on NCI‐H520 cell invasiveness. MiR‐372‐3p was found significantly overexpressed in both LSCC tissues and cell lines, whereas FGF9 mRNA was found underexpressed in LSCC tissues. MiR‐372‐3p directly bound to wild‐type FGF9 mRNA 3′UTR, therefore led to the reduction in FGF9 expression. The upregulation of FGF9 or the downregulation of miR‐372‐3p substantially retarded LSCC cell growth, mitosis, and invasion. MiR‐372‐3p enhanced LSCC cell proliferation and invasion through inhibiting FGF9.

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“…The upregulation of various genes like ferritin heavy polypeptide I (FTH1), urokinase plasminogen activator (uPA), ATP‐binding cassette (ABC) transporter, interleukin‐1 (IL‐1) receptor antagonist and keratin‐4 (K4) (Alevizos et al , ), keratin‐13 (K13) (Ida‐Yonemochi et al , ), keratin‐19 (K19) and keratin‐21 (K21) (Jiang et al , ), keratin‐15 (K15) (Khanom et al , ), interferon‐stimulated gene 15 (ISG‐15) (Sumino et al , ) miR‐372 and miR‐373 (Tu et al , ) have been implicated in oral cancer pathogenesis. All these findings suggest that the potential use of LCM could be considered as a forefront technology for early detection of OSCC (He et al , ; Khanom et al , ; Jensen et al , ; Xiao et al , ).…”

Section: Lcm For Integrated Oral Biosciencesmentioning

confidence: 99%

Exploring the potential of laser capture microdissection technology in integrated oral biosciences

et al. 2016

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Laser capture microdissection (LCM) is a high‐end research and diagnostic technology that helps in obtaining pure cell populations for the purpose of cell‐ or lesion‐specific genomic and proteomic analysis. Literature search on the application of LCM in oral tissues was made through PubMed. There is ample evidence to substantiate the utility of LCM in understanding the underlying molecular mechanism involving an array of oral physiological and pathological processes, including odontogenesis, taste perception, eruptive tooth movement, oral microbes, and cancers of the mouth and jaw tumors. This review is aimed at exploring the potential application of LCM in oral tissues as a high‐throughput tool for integrated oral sciences. The indispensable application of LCM in the construction of lesion‐specific genomic libraries with emphasis on some of the novel molecular markers thus discovered is also highlighted.

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Upregulation of miR‐372 and ‐373 associates with lymph node metastasis and poor prognosis of oral carcinomas

Abstract: N/A.

Cited by 42 publications

References 39 publications

The aberrantly expressed miR-372 partly impairs sensitivity to apoptosis in parathyroid tumor cells

The aberrantly expressed miR-372 partly impairs sensitivity to apoptosis in parathyroid tumor cells

MiR‐372‐3p promotes cell growth and metastasis by targeting FGF9 in lung squamous cell carcinoma

Exploring the potential of laser capture microdissection technology in integrated oral biosciences

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