scholarly journals SOX7 blocks vasculogenic mimicry in oral squamous cell carcinoma

2020 ◽  
Author(s):  
Kyoung-Ok Hong ◽  
Kyu-Young Oh ◽  
Hye-Jung Yoon ◽  
Neeti Swarup ◽  
Minjung Jung ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cell Lines ◽  
Squamous Cell ◽  
Vasculogenic Mimicry ◽  
Circulatory System ◽  
Migration And Invasion ◽  
Channel Formation

Abstract Background : Vasculogenic mimicry (VM) is the formation of an alternative circulatory system by aggressive tumor cells. The characteristics of VM and its underlying mechanism in oral squamous cell carcinoma (OSCC) remain unclear. This study aims to determine the relationship between VM channels in OSCC tissues and clinical outcomes and to investigate the biological role of SOX7 in VM in OSCC cells. Methods : CD31/PAS double staining was performed to evaluate VM status in OSCC tissue. The relationships between VM and clinicopathological variables, and VM and SOX7 levels were analyzed. VM channel formation was assay performed to observe VM channels in the OSCC cell lines. To investigate the role of SOX7 in VM channel formation, SOX7 was transiently over-expressed in SCC-9 cells. VM-modulating genes were identified by Western blotting. Results : We confirmed the presence of VM channels in OSCC tissue and several cell lines and found a positive correlation between VM and lymph node metastasis and patient survival in OSCC ( P = 0.003). We also found that the presence of VM channels in OSCC tissue was inversely associated with SOX7 expression ( P = 0.020). We observed that overexpression of SOX7 impaired VM channel formation by reducing the expression of VE-cadherin, thereby inhibiting cell migration and invasion. Conclusion : These results suggest that SOX7 plays an important role in the regulation of VM channel formation and may inhibit OSCC metastasis.

scholarly journals miR-195-5p Suppresses the Proliferation, Migration, and Invasion of Oral Squamous Cell Carcinoma by Targeting TRIM14

2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Tong Wang ◽  
Yipeng Ren ◽  
Ruixun Liu ◽  
Juntao Ma ◽  
Yueyi Shi ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cell Lines ◽  
Squamous Cell ◽  
Migration And Invasion ◽  
Specific Gene ◽  
Invasion And Migration ◽  
And Migration

MicroRNAs (miRNAs) play an essential role in tumor biological processes through interacting with specific gene targets. The involvement of miR-195-5p in cell proliferation, invasion, and migration has been demonstrated in several cancer cell lines, while its function in oral squamous cell carcinoma (OSCC) remains unclear. Here we find that miR-195-5p expression is lower in OSCC than in nontumor tissues, while its overexpression in cell lines can lead to the promotion of apoptosis and the reduction of cell growth, migration, and invasion. Moreover, we identify the tripartite motif-containing protein (TRIM14) as a target of miR-195-5p. Therefore, we reason that the tumor suppressor role of miR-195-5p in OSCC is dependent on the interaction with TRIM14.

scholarly journals SOX7 Blocks Vasculogenic Mimicry in Oral Squamous Cell Carcinoma

2020 ◽  
Author(s):  
Kyoung-Ok Hong ◽  
Kyu-Young Oh ◽  
Hye-Jung Yoon ◽  
Neeti Swarup ◽  
Minjung Jung ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Lymph Node ◽  
Lymph Node Metastasis ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Vasculogenic Mimicry ◽  
Channel Formation ◽  
Node Metastasis

Abstract Background: Vasculogenic mimicry (VM) is the formation of an alternative circulatory system by aggressive tumor cells. The characteristics of VM and its underlying mechanism in oral squamous cell carcinoma (OSCC) remain unclear. This study aims to determine the relationship between VM channels in OSCC tissues and clinical outcomes and to investigate the biological role of SOX7 in VM in OSCC cells.Methods: CD31/PAS double staining was performed to evaluate VM status in OSCC tissue. The relationships between VM and clinicopathological variables, and VM and SOX7 levels were analyzed. The correlation between SOX7 levels and head and Neck cancer corhorts were investigated using in silico analysis.VM channel formation assay was performed to observe VM channels in the OSCC cell lines. To investigate the role of SOX7 in VM channel formation, SOX7 was transiently over-expressed in SCC-9 cells. VM-modulating genes were identified by Western blotting.Results: We confirmed the presence of VM channels in OSCC tissue and several cell lines and found a positive correlation between VM and lymph node metastasis and patient survival in OSCC (P = 0.003). In silico analysis from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) database showed that down-regulation of SOX7 expression was significantly correlated with head and neck squamous cell carcinoma (HNSCC) patient cohorts (P = 0.0187) and lymph node metastasis (P = 0.0017). We also found that the presence of VM channels in OSCC tissue was inversely associated with SOX7 expression (P = 0.020). We observed that overexpression of SOX7 impaired VM channel formation by reducing the expression of VE-cadherin, thereby inhibiting cell migration and invasion.Conclusion: These results suggest that SOX7 plays an important role in the regulation of VM channel formation and may inhibit OSCC metastasis.

The role of tamoxifen in combination with cisplatin on oral squamous cell carcinoma cell lines

2007 ◽  
Vol 245 (1-2) ◽  
pp. 284-292 ◽  
Author(s):  
Myung-Jin Kim ◽  
Jong-Ho Lee ◽  
Young-Kyun Kim ◽  
Hoon Myoung ◽  
Pil-Young Yun
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cell Lines ◽  
Squamous Cell ◽  
Carcinoma Cell ◽  
Squamous Cell Carcinoma Cell ◽  
Carcinoma Cell Lines

Ral GTPase Activation by Downregulation of RalGAP Enhances Oral Squamous Cell Carcinoma Progression

2019 ◽  
Vol 98 (9) ◽  
pp. 1011-1019 ◽  
Author(s):  
P. Gao ◽  
S. Liu ◽  
R. Yoshida ◽  
C.Y. Shi ◽  
S. Yoshimachi ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cell Lines ◽  
Squamous Cell ◽  
Migration And Invasion ◽  
Activation Level ◽  
Ral Gtpase

Ral small GTPases, consisting of RalA and RalB, are members of the Ras family. Their activity is upregulated by RalGEFs. Since several RalGEFs are downstream effectors of Ras, Ral is activated by the oncogenic mutant Ras. Ral is negatively regulated by RalGAP complexes that consist of a catalytic α1 or α2 subunit and its common partner β subunit and similarly regulate the activity of RalA as well as RalB in vitro. Ral plays an important role in the formation and progression of pancreatic and lung cancers. However, the involvement of Ral in oral squamous cell carcinoma (OSCC) is unclear. In this study, we investigated OSCC by focusing on Ral. OSCC cell lines with high Ral activation exhibited higher motility. We showed that knockdown of RalGAPβ increased the activation level of RalA and promoted the migration and invasion of HSC-2 OSCC cells in vitro. In contrast, overexpression of wild-type RalGAPα2 in TSU OSCC cells attenuated the activation level of RalA and inhibited cell migration and invasion. Real-time quantitative polymerase chain reaction analysis of samples from patients with OSCC showed that RalGAPα2 was downregulated in oral cancer tissues as compared with normal epithelia. Among patients with OSCC, those with a lower expression of RalGAPα2 showed a worse overall survival rate. A comparison of DNA methylation and histone modifications of the RalGAPα2 gene in OSCC cell lines suggested that crosstalk among DNA methylation, histone H4Ac, and H3K27me2 was involved in the downregulation of RalGAPα2. Thus, activation of Ral GTPase by downregulation of RalGAP expression via a potential epigenetic mechanism may enhance OSCC progression.

Plasma miR-185 is decreased in patients with esophageal squamous cell carcinoma and might suppress tumor migration and invasion by targeting RAGE

2015 ◽  
Vol 309 (9) ◽  
pp. G719-G729 ◽  
Author(s):  
Rongrong Jing ◽  
Wen Chen ◽  
Huimin Wang ◽  
Shaoqing Ju ◽  
Hui Cong ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cell Lines ◽  
Squamous Cell ◽  
Biological Role ◽  
Migration And Invasion ◽  
High Level ◽  
Rage Expression

The receptor for advanced-glycation end products (RAGE) is upregulated in various cancers and has been associated with tumor progression, but little is known about its expression and regulation by microRNAs (miRNAs) in esophageal squamous cell carcinoma (ESCC). Here, we describe miR-185, which represses RAGE expression, and investigate the biological role of miR-185 in ESCC. In this study, we found that the high level of RAGE expression in 29 pairs of paraffin-embedded ESCC tissues was correlated positively with the depth of invasion by immunohistochemistry, suggesting that RAGE was involved in ESCC. We used bioinformatics searches and luciferase reporter assays to investigate the prediction that RAGE was regulated directly by miR-185. Besides, overexpression of miR-185 in ESCC cells was accompanied by 27% (TE-11) and 49% (Eca-109) reduced RAGE expression. The effect was further confirmed in RAGE protein by immunofluorescence in both cell lines. The effects were reversed following cotransfection with miR-185 and high-level expression of the RAGE vector. Furthermore, the biological role of miR-185 in ESCC cell lines was investigated using assays of cell viability, Ki-67 staining, and cell migration and invasion, as well as in a xenograft model. We found that overexpression of miR-185 inhibited migration and invasion by ESCC cells in vitro and reduced their capacity to develop distal pulmonary metastases in vivo partly through the RAGE/heat shock protein 27 pathway. Interestingly, in clinical specimens, the level of plasma miR-185 expression was decreased significantly ( P = 0.002) in patients with ESCC [0.500; 95% confidence interval (CI) 0.248–1.676] compared with healthy controls (2.410; 95% CI 0.612–5.671). The value of the area under the receiver-operating characteristic curve was 0.73 (95% CI 0.604–0.855). In conclusion, our findings shed novel light on the role of miR-185/RAGE in ESCC metastasis, and plasma miR-185 has potential as a novel diagnostic biomarker in ESCC.

scholarly journals Long Non-Coding RNA LINC01929 Accelerates Progression of Oral Squamous Cell Carcinoma by Targeting the miR-137-3p/FOXC1 Axis

2021 ◽  
Vol 11 ◽  
Author(s):  
Hongze Che ◽  
Yanhai Che ◽  
Zhimin Zhang ◽  
Qing Lu
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cell Lines ◽  
Squamous Cell ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Tissue Samples ◽  
Non Coding Rna ◽  
Luciferase Activity Assay

Recently, additional long noncoding RNAs (lncRNAs) have been identified and their possible roles were investigated in a variety of human tumors. One of these lncRNAs, LINC01929, promoted the progression of some cancers, whereas its expression and biological function in human oral squamous cell carcinoma (OSCC) remains still mostly uncertain. The LINC01929 expression in OSCC tissues or cell lines was identified via quantitative real-time polymerase chain reaction. The cell counting kit-8, transwell migration, wound-healing, and flow cytometry assays were utilized to characterize the functions of LINC01929 in OSCC cells. The interactive relationships between LINC01929 and miR-137-3p, miR-137-3p and Forkhead box C1 (FOXC1) were investigated by the dual-luciferase activity assay. Our findings demonstrated that LINC01929 was highly expressed in OSCC tissue samples and cell lines, whereas miR-137-3p expression was downregulated. LINC01929 acted as a carcinogenic lncRNA with accelerated OSCC cell proliferation, migration and invasion, and suppression of apoptosis. We further indicated that LINC01929 facilitated tumor growth in xenograft mouse models. Mechanistically, LINC01929 acted as a sponge for miR-137-3p to elevate FOXC1 expression, which is the target of miR-137-3p. In addition, downregulated miR-137-3p expression rescued the suppressive behaviors of LINC01929 knockdown on the biological behaviors of OSCC cells. Taken together, LINC01929 functioned as a tumor-promoting lncRNA via the miR-137-3p/FOXC1 axis in OSCC, suggesting novel targets for OSCC therapy.

scholarly journals Oct4 downregulation–induced inflammation increases the migration and invasion rate of oral squamous cell carcinoma

2021 ◽  
Author(s):  
Shuntao Sun ◽  
Hongyu Yang ◽  
Feng Wang ◽  
Shanshan Zhao
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Migration And Invasion ◽  
Invasion And Migration ◽  
Tnf Α ◽  
And Migration ◽  
Inflammatory Changes

Abstract Inflammatory changes are involved in tumor cell proliferation, migration, and invasion. Tumor necrosis factor-α (TNF-α) and lipopolysaccharide (LPS) play important roles in inflammatory regulation during tumor development. Oct4 acts as a transcription factor that modulates inflammatory changes in mesenchymal stem cells. In this study, we explored the role of Oct4 in the invasion and migration of oral squamous cell carcinoma (OSCC) cells. LPS and TNF-α were used to treat the OSCC cell lines HN4 and CAL27 to induce inflammation. The generation of inflammatory cytokines, including TNF-α, interleukin (IL)-1β, and IL-6, was evaluated by enzyme-linked immunosorbent assay and real-time quantitative PCR. Western blot analysis was employed to detect the expression and phosphorylation of JNK1, p65, and STAT3, which are key modulators of inflammation. Wound scratch healing and transwell invasion assays were further used to determine the role of inflammation in the invasion and migration of OSCC cells. Robust inflammation was observed in HN4 and CAL27 cells treated with LPS and TNF-α. A marked increase in JNK1, p65, and STAT3 phosphorylation levels in OSCC cells was also detected after LPS and TNF-α treatment. The migration and invasion of HN4 and CAL27 cells were significantly boosted by stimulation with LPS and TNF-α. Furthermore, Oct4 mRNA and protein levels were significantly upregulated by stimulation with LPS and TNF-α. Silencing of Oct4 led to reduced inflammation and decreased levels of phosphorylated JNK1, p65, and STAT3 and impaired invasion and migration in LPS- and TNF-α-stimulated OSCC cells. Overall, LPS- and TNF-α-induced inflammation suppressed the migration and invasion of OSCC cells by upregulating Oct4 expression.

scholarly journals Hsa_circ_0008309 May Be a Potential Biomarker for Oral Squamous Cell Carcinoma

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Bowen Li ◽  
Feng Wang ◽  
Xiang Li ◽  
Shuai Sun ◽  
Yuehong Shen ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cell Lines ◽  
High Throughput ◽  
Squamous Cell ◽  
High Throughput Sequencing ◽  
Potential Biomarker ◽  
Bioinformatics Databases

Objective. Oral squamous cell carcinoma (OSCC) is the most common cancer of the head and neck region. The circular RNA (circRNA) is known to serve an important role in the carcinogenesis of different types of cancer. However, the circRNA role of OSCC remains unclear. Methods. 8 pairs of OSCC tissues and adjacent normal tissues were obtained to detect circRNAs expression by high-throughput sequencing, and 45 pairs of OSCC tissues were selected to verify the differentially significant circRNAs by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). To further investigate the role of hsa_circ_0008309, the circRNA-microRNA (miR)-mRNA network was predicted using bioinformatics databases. The expression levels of hsa_circ_0008309, miR-1290, miR-136-5P, and miR-382-5P in SCC-15 and CAL27 cell lines were detected by RT-qPCR. Western blotting was performed to detect the protein level of Ataxin 1 (ATXN1). Results. The high-throughput sequencing results demonstrated that circRNAs were abundantly expressed in OSCC, and 16 circRNAs were significantly differentially expressed. Hsa_circ_0008309 was significantly downregulated in 45 pairs of OSCC tissue samples and was statistically correlated with pathological differentiation. The bioinformatics databases suggested that hsa_circ_0008309 could combine with miR-1290, miR-136-5P, and miR-382-5P, respectively, to regulate the expression of ATXN1. It was subsequently identified that hsa_circ_0008309 may inhibit miR-136-5P and miR-382-5P expression and increase ATXN1 expression in the OSCC cell lines. Conclusion. In summary, the results of the present study revealed that OSCC tissues have abundant circRNAs and, to the best of our knowledge, we firstly explore the regulatory role of the hsa_circ_0008309-miR-136-5P/hsa-miR-382-5P-ATXN1 network in OSCC. The results indicated that hsa_circ_0008309 may be a potential biomarker for OSCC.

scholarly journals Oncogenic role of MiR-130a in oral squamous cell carcinoma

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Karthik Mallela ◽  
Swamy Shivananda ◽  
Kodaganur S. Gopinath ◽  
Arun Kumar
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Therapeutic Strategy ◽  
Inverse Correlation ◽  
Migration And Invasion ◽  
Cellular Functions

AbstractAberrant activation of the PI3K/AKT/mTOR pathway is attributed to the pathogenesis of oral squamous cell carcinoma (OSCC). In recent years, increasing evidence suggests the involvement of microRNAs (miRNAs) in oral carcinogenesis by acting as tumor suppressors or oncogenes. TSC1, as a component of the above pathway, regulates several cellular functions such as cell proliferation, apoptosis, migration and invasion. Downregulation of TSC1 is reported in oral as well as several other cancers and is associated with an unfavourable clinical outcome in patients. Here we show that oncogenic miR-130a binds to the 3′UTR of TSC1 and represses its expression. MiR-130a-mediated repression of TSC1 increases cell proliferation, anchorage independent growth and invasion of OSCC cells, which is dependent on the presence of the 3′UTR in TSC1. We observe an inverse correlation between the expression levels of miR-130a and TSC1 in OSCC samples, suggesting that their interaction is physiologically relevant. Delivery of antagomiR-130a to OSCC cells results in a significant decrease in xenograft size. Taken together, the findings of the study indicate that miR-130a-mediated TSC1 downregulation is not only a novel mechanism in OSCC, but also the restoration of TSC1 levels by antagomiR-130a may be a potential therapeutic strategy for the treatment of OSCC.

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