<scp>LAMC</scp>2 is a predictive marker for the malignant progression of leukoplakia

Nguyen, Chi Thi Kim; Okamura, Takeshi; Morita, Keiichi; Yamaguchi, Satoshi; Harada, Hiroyuki; Miki, Yoshio; Izumo, Toshiyuki; Kayamori, Kou; Yamaguchi, Akira; Sakamoto, Kei

doi:10.1111/jop.12485

Cited by 32 publications

(21 citation statements)

References 19 publications

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“…Afterward, the anti‐tumor effects of miR‐765 and the oncogene role of LAMC2 were confirmed via CCK8, colony formation, and transwell assay. It has been widely reported as an oncogene and contributes to malignant progression and metastasis in several cancers . Silencing of LAMC2 was proved to significantly inhibit cell migration and invasion in HNSCC cells .…”

Section: Discussionmentioning

confidence: 99%

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LINC00511 interacts with miR‐765 and modulates tongue squamous cell carcinoma progression by targeting LAMC2

Ding

Yang

2018

J Oral Pathology Medicine

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Section: Discussionmentioning

confidence: 99%

“…LAMC2 is a subunit of the heterotrimeric glycoprotein laminin‐332, consisting of the α3, β3, and γ2 chains and located on chromosome 1q25‐q31. Overexpression of LAMC2 is regarded as a predictive marker for the poor prognosis and metastatic potential of colorectal cancer, leukoplakia, and lung adenocarcinoma …”

Section: Introductionmentioning

confidence: 99%

LINC00511 interacts with miR‐765 and modulates tongue squamous cell carcinoma progression by targeting LAMC2

Ding

Yang

2018

J Oral Pathology Medicine

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“…LAMC2 is a subunit of the heterotrimeric glycoprotein laminin‐332, consisting of the α3, β3 and ϒ2 chains; its coding gene is located on chromosome 1q25‐q31. Overexpression of LAMC2 has been demonstrated at the OSCC cancer‐stromal interface, and IHC studies in leukoplakia found that LAMC2‐positive foci were a significant predictive factor for malignant progression of leukoplakia, suggesting an imminent risk of cancer (Nguyen et al, ). Complementary base pairs for binding between miR‐765 and LINC00511 and between miR‐765 and LAMC2 mRNA were predicted in silico, thus identifying potential “target regions.” In vitro studies indicated that LINC00511 could regulate the expression of LAMC2 through sponging miR‐765 and also highlighted in Tca‐8113 cells that downregulation of LINC00511 significantly inhibited cell proliferation, impeded the colony formation ability and suppressed cell invasion capacity according to the invasion assay.…”

Section: The Endogenous Rna Networkmentioning

confidence: 99%

“…LAMC2 is a subunit of the heterotrimeric glycoprotein laminin-332, consisting of the α3, β3 and ϒ2 chains; its coding gene is located on chromosome 1q25-q31. Overexpression of LAMC2 has been demonstrated at the OSCC cancer-stromal interface, and IHC studies in leukoplakia found that LAMC2-positive foci w ere a significant predictive factor for malignant progression of leu koplakia, suggesting an imminent risk of cancer (Nguyen et al, 2017). Complementary base pairs for binding between miR-765 and LI NC00511 and between miR-765 and LAMC2 mRNA were predic ted in silico, thus identifying potential "target regions."…”

Section: Linc00511mentioning

confidence: 99%

World Workshop on Oral Medicine VII: Functional pathways involving differentially expressed lncRNAs in oral squamous cell carcinoma

et al. 2019

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Long non‐coding RNAs (lncRNA) modulate gene expression at the epigenetic, transcriptional and post‐transcriptional levels and are involved in tumorigenesis. They can form complex secondary and tertiary structures and have been shown to act as precursors, enhancers, reservoirs and decoys in the complex endogenous RNA network. They were first reported in relation to oral squamous cell carcinoma (OSCC) in 2013. Here, we summarise the functional roles and pathways of the most commonly studied lncRNAs in OSCC. Existing research demonstrates the involvement of lncRNA within pivotal pathways leading to the development and spread of OSCC, including interactions with key cancer‐associated microRNAs such as miR‐21. The number of studies on lncRNA and OSCC remains limited in this new field. As evidence grows, the tissue‐specific expression patterns of lncRNAs should further advance our understanding of the altered regulatory networks in OSCC and possibly reveal new biomarkers and therapeutic targets.

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“…Fifty one spots were fully evaluable after the loss of spots due to multiple sectioning. Histological evaluation was done as previously described [15]. Cancer-associated inflammation was scored based on the density of inflammatory cell infiltrates around tumor nests at the invasion front.…”

Section: Oscc Tissue Specimens and Immunohistochemistrymentioning

confidence: 99%

AIRE is induced in oral squamous cell carcinoma and promotes cancer gene expression

Sakamoto

Nguyen

Sawangarun

et al. 2019

Preprint

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Autoimmune regulator (AIRE) is a transcriptional regulator that is primarily expressed in medullary epithelial cells, where it induces tissue-specific antigen expression. Under pathological conditions, AIRE expression is induced in epidermal cells and promotes skin tumor development in association with stress-responsive keratin KRT17. This study aimed to clarify the role of AIRE in the pathogenesis of oral squamous cell carcinoma (OSCC). AIRE expression was evaluated in seven OSCC cell lines and in OSCC tissue specimens. Transient or constitutive expression of AIRE in 293A cells induced KRT17 expression. cDNA microarray analysis of 293A cells stably expressing AIRE revealed that STAT1 and ICAM1 were significantly upregulated by AIRE. Expression of KRT17, STAT1, ICAM1, MMP9, CXCL10, and CXCL11 was elevated in 293A cells stably expressing AIRE, and conversely, was decreased in AIRE-knockout HSC3 OSCC cells when compared to the respective controls. Upregulation of KRT17, STAT1, and ICAM in OSCC cells was confirmed in tissue specimens by immunohistochemistry. We provide evidence that AIRE exerts transcriptional control in cooperation with ETS1. Expression of STAT1, ICAM1, CXCL10, and MMP9 was increased in 293A cells upon Ets1 transfection, and coexpression of AIRE resulted in enhanced expression of STAT1. AIRE coprecipitated with ETS1 in a modified immunoprecipitation assay using formaldehyde crosslinking. Chromatin immunoprecipitation and quantitative PCR analysis revealed that promoter fragments of STAT1, ICAM1, CXCL10, and MMP9 were enriched in the AIRE precipitates. In oral cancer cells, ETS1 was diffusely located in the nucleus and partially overlapped with dot-like AIRE 4 accumulation sites. Nuclear translocation of AIRE was promoted by cotransfection with Ets1. These results indicate that AIRE is induced in OSCC and supports cancer-related gene expression in cooperation with ETS1. This is a novel function of AIRE in extrathymic tissues under the pathological condition.7 keratinocytes [8][9][10][11]. In the mouse epidermis, Aire is induced by inflammatory or tumorigenic stimuli concurrently with Krt17 and stimulates the transcription of several chemokine genes, such as Cxcl10and Cxcl11, and a gene encoding matrix-degrading enzyme, Mmp9, in keratinocytes [6]. The onset of genetically induced skin tumor is delayed in Aire-knockout mice, which mimic the phenotype of Krt17-knockout mice [6]. These results suggest a novel role of AIRE in extrathymic epithelial tissues under pathological conditions; however, the significance of AIRE in other cancers remains to be elucidated.The above findings inspired us to evaluate whether AIRE participates in the pathogenesis of OSCC. To this end, we first assessed the expression of AIRE in OSCC. Then, we explored the role of AIRE in the regulation of KRT17 and other genes associated with OSCC development. Materials and Methods Chemically induced mouse model of tongue and esophageal cancerCD-1 mice were obtained from Sankyo Labo Service Co. (Tokyo, Japan) and were housed in groups ...

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LAMC2 is a predictive marker for the malignant progression of leukoplakia

Abstract: The results of this study highlight the value of LAMC2 as a marker of cancer invasion. LAMC2-positive foci in leukoplakia suggest an imminent risk of cancer. LAMC2 immunostaining is expected to contribute to a more precise assessment of the malignancy of leukoplakia.

Cited by 32 publications

References 19 publications

LINC00511 interacts with miR‐765 and modulates tongue squamous cell carcinoma progression by targeting LAMC2

LINC00511 interacts with miR‐765 and modulates tongue squamous cell carcinoma progression by targeting LAMC2

World Workshop on Oral Medicine VII: Functional pathways involving differentially expressed lncRNAs in oral squamous cell carcinoma

AIRE is induced in oral squamous cell carcinoma and promotes cancer gene expression

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