Comparison of MMP2 and MMP9 expression levels between primary and metastatic regions of oral squamous cell carcinoma

Nishio, Kensuke; Motozawa, Keiko; Omagari, Daisuke; Gojoubori, Takahiro; Ikeda, Takayuki; Asano, Masaharu; Gionhaku, Nobuhito

doi:10.2334/josnusd.58.59

Cited by 28 publications

(24 citation statements)

References 36 publications

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“…and MMP9. Previous studies have shown that inhibition of the production and downregulation of MMP2 and MMP9 in colorectal cancer can play an anti-metastasis role [39]. We revealed that knockdown of KIFC1 resulted in a reduction of MMP2 and MMP9 of PTC cells, which agrees the results of previous studies [40,41].…”

Section: Discussionsupporting

confidence: 92%

KIFC1 accelerates the proliferation, migration and invasion of papillary thyroid cancer cells via MAPK signaling

Nie¹,

Han²,

Wen³

et al. 2020

Preprint

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Kinesin family member C1 (KIFC1) acts as a kind of minus end-directed motorized protein and is considered as an oncogene of some cancer types. However, no studies have fully elucidated its biological activity and molecular mechanisms in papillary thyroid cancer (PTC). The study focused on reporting the overexpression of KIFC1 in cell lines and tissues of PTC. Moreover, clinicopathological features analysis showed that KIFC overexpression is significantly correlated with extrathyroidal invasion and lymph node metastasis. Knockdown of KIFC1 significantly reduced cell growth, migration and invasion in PTC cells, and concomitant increased levels of differentiation markers, such as Tg and Nis. Knockdown of KIFC1 markedly increased the expression level of epithelial cell marker (E-cadherin), and decreased the expression levels of epithelial-mesenchymal transition (EMT) related transcriptional factor N-cadherin, Snail and ZEB1. Further study revealed that knockdown of KIFC1 downregulated stemness markers ALDH2 and SOX2, and inhibited the MAPK signaling cascades and downstream signaling, including p-ERK, ERK, p-JNK, JNK, MMP2, and MMP9, which can affect the expression of the EMT associated factors. Taken together, we reported that KIFC1 might promoted the proliferation, migration and invasion of PTC cells and offer a candidate molecular target for therapeutic intervention.

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Section: Discussionsupporting

confidence: 92%

KIFC1 accelerates the proliferation, migration and invasion of papillary thyroid cancer cells via MAPK signaling

Nie¹,

Han²,

Wen³

et al. 2020

Preprint

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show abstract

“…There are accumulating evidences that Bcl2 plays a pivotal role in chemoresistance and metastasis (Kallel‐Bayoudh et al ., ; Bold et al ., ), and also, MMPs are closely involved in metastasis (Deryugina and Quigley, ). Consistent with wound healing assay data, Dehydrocorydaline attenuated mRNA levels of MMP7 (Li et al ., ) and MMP9 (Nishio et al ., ) as metastasis biomarkers in H1299 cells by qRT‐PCR, and also, protein expression of Bcl2 was attenuated in a concentration‐dependent fashion in NSCLCs, implying the crucial roles of MMPs and Bcl‐2 signaling.…”

Section: Discussionmentioning

confidence: 91%

Anti-Metastatic Effect of Dehydrocorydaline on H1299 Non-Small Cell Lung Carcinoma Cells via Inhibition of Matrix Metalloproteinases and B Cell Lymphoma 2

et al. 2017

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Though Dehydrocorydaline, an alkaloid isolated from Corydalis turtschaninovii tuber, was known to have anti-coronary artery disease, anti-inflammatory, apoptotic, anti-allergic, anti-acetylcholinesterase, and antitumor effects, the underlying anti-metastatic mechanism of Dehydrocorydalin was never elucidated in lung cancer cells so far. Thus, in the present study, the anti-metastatic effect of Dehydrocorydaline was examined in non-small cell lung carcinoma (NSCLC) cells, mainly targeting matrix metalloproteinases (MMPs) and B cell lymphoma-2 (Bcl-2) signaling. Here, Dehydrocorydaline exerted weak cytotoxicity and attenuated the protein expression of Bcl-2 and activated Bax in a concentration-dependent manner in NSCLC cells, such as A549, H460, H1299, and H596 cells. Also, Dehydrocorydaline suppressed the migration of H1299 cells by wound healing assay and transwell migration assay. Consistently, Dehydrocorydaline attenuated mRNA and protein levels of MMP7 and MMP9 as metastasis biomarkers in H1299 cells by quantitative reverse transcription polymerase chain reaction. Of note, Bcl-2 overexpression reduced the cytotoxic and anti-metastatic effects of Dehydrocorydaline on pCDNA-Bcl-2 transfected H1299 cells. Overall, our findings provide scientific evidence that Dehydrocorydaline exerts anti-metastatic potential via suppression of MMPs and Bcl-2 signaling in NSCLC cells. Copyright © 2017 John Wiley & Sons, Ltd.

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“…An increased MMP1 expression level was detected in patients with OSCC compared with that in healthy controls and was related to metastasis . The expression levels of MMP2 were notably elevated in the metastatic regions of OSCC compared with those in the primary region . The epithelial‐mesenchymal transition related molecules, VIM and CDH1 , were significantly associated with lymph node metastasis and patient survival in OSCC .…”

Section: Discussionmentioning

confidence: 95%

Characterization of Copy Number Variations in Oral Cavity Squamous Cell Carcinoma Reveals a Novel Role for MLLT3 in Cell Invasiveness

et al. 2019

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Background. DNA copy number variations (CNVs) are a hallmark of cancer, and the current study aimed to demonstrate the profile of the CNVs for oral cavity squamous cell carcinoma (OSCC) and elucidate the clinicopathological associations and molecular mechanisms of a potential marker derived from CNVs, mixed-lineage leukemia translocated to chromosome 3 protein (MLLT3), in OSCC carcinogenesis. Materials and Methods. CNVs in 37 OSCC tissue specimens were analyzed using a high-resolution microarray, the OncoScan array. Gene expression was analyzed by real-time polymerase chain reaction in 127 OSCC and normal tissue samples. Cell function assays included cell cycle, migration, invasion and chromatin immunoprecipitation assays. Results. We found a novel copy number amplified region, chromosome 9p, encompassing MLLT3 via the comparison of our data set with six other OSCC genome-wide CNV data sets. MLLT3 overexpression was associated with

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Comparison of MMP2 and MMP9 expression levels between primary and metastatic regions of oral squamous cell carcinoma

Cited by 28 publications

References 36 publications

KIFC1 accelerates the proliferation, migration and invasion of papillary thyroid cancer cells via MAPK signaling

KIFC1 accelerates the proliferation, migration and invasion of papillary thyroid cancer cells via MAPK signaling

Anti-Metastatic Effect of Dehydrocorydaline on H1299 Non-Small Cell Lung Carcinoma Cells via Inhibition of Matrix Metalloproteinases and B Cell Lymphoma 2

Characterization of Copy Number Variations in Oral Cavity Squamous Cell Carcinoma Reveals a Novel Role for MLLT3 in Cell Invasiveness

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