scholarly journals Secernin 1 promotes cell invasion and migration by activating the TGF-β/Smad3 pathway in oral squamous cell carcinomas

2020 ◽  
Author(s):  
Li Xiao ◽  
Shuqiong Wen ◽  
Qianyu Zhang ◽  
Yanshuang Peng ◽  
Kaiyue Zheng ◽  
...  
Keyword(s):  
Cell Lines ◽  
Squamous Cell ◽  
Squamous Cell Carcinomas ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Enzyme Linked Immunosorbent Assay ◽  
Invasion And Metastasis ◽  
Tissue Samples ◽  
Invasion And Migration ◽  
And Migration

Abstract Background Secernin-1 (SCRN1) is a regulator of exocytosis in mast cells. Recently, SCRN1 has been reported to be correlated with the prognosis of colorectal cancer and gastric cancer but its functional effects on oral squamous cell carcinoma (OSCC) remains unclear. Our aim was to explore the expression pattern and the migration and invasion effects of the newly identified SCRN1 in OSCC. Methods Western blotting (WB) was used to measure SCRN1 expression in human OSCC tissue samples and OSCC cell lines. Then, the effects of SCRN1 on OSCC cell proliferation, invasion and metastasis were analyzed by cell counting kit-8 (CCK-8) and transwell assays. The secretion of matrix metalloproteinase (MMP)-2 and MMP-9 in SCRN1 knockdown OSCC cells and vector cells was investigated by enzyme-linked immunosorbent assay (ELISA). The expression levels of TGF-β, Smad3 and phosphorylated Smad3 (p-Smad3) in SCRN1 knockdown OSCC cells and vector cells were measured by WB. Results The expression of SCRN1 was significantly elevated in the OSCC tissues and cell lines. Furthermore, SCRN1 knockdown attenuated the proliferation, migration and invasion of SCC15 and HSC3 cells. SCRN1 knockdown reduced the secretion of MMP-9 from HSC3 and SCC15 cells, but the secretion of MMP-2 did not obviously change. Additionally, SCRN1 knockdown reduced the expression of TGF-β and p-Smad3 in HSC3 and SCC15 cells. Conclusions Our study demonstrated that SCRN1 is upregulated in OSCC. Further studies demonstrated that SCRN1 promotes proliferation, invasion and metastasis of OSCC cells via TGF-β/Smad3 signaling.

scholarly journals Melatonin Suppresses Oral Squamous Cell Carcinomas Migration and Invasion through Blocking FGF19/FGFR 4 Signaling Pathway

2021 ◽  
Vol 22 (18) ◽  
pp. 9907
Author(s):  
Leilei Wang ◽  
Yuxiong Su ◽  
Wing Shan Choi
Keyword(s):  
Squamous Cell ◽  
Squamous Cell Carcinomas ◽  
Migration And Invasion ◽  
Promising Alternative ◽  
Oral Squamous Cell Carcinomas ◽  
Invasion And Migration ◽  
Human Tongue ◽  
Underlying Mechanisms ◽  
And Migration ◽  
Fibroblast Growth Factor 19

Oral squamous cell carcinomas (OSCCs) are one of the most prevalent malignancies, with a low five-year survival rate, thus warranting more effective drugs or therapy to improve treatment outcomes. Melatonin has been demonstrated to exhibit oncostatic effects. In this study, we explored the anti-cancer effects of melatonin on OSCCs and the underlying mechanisms. A human tongue squamous cell carcinoma cell line (SCC-15) was treated with 2 mM melatonin, followed by transwell migration and invasion assays. Relative expression levels of Fibroblast Growth Factor 19 (FGF19) was identified by Cytokine Array and further verified by qPCR and Western blot. Overexpression and downregulation of FGF19 were obtained by adding exogenous hFGF19 and FGF19 shRNA lentivirus, respectively. Invasion and migration abilities of SCC-15 cells were suppressed by melatonin, in parallel with the decreased FGF19/FGFR4 expression level. Exogenous hFGF19 eliminated the inhibitory effects of melatonin on SCC-15 cells invasion and migration, while FGF19 knocking-down showed similar inhibitory activities with melatonin. This study proves that melatonin suppresses SCC-15 cells invasion and migration through blocking the FGF19/FGFR4 pathway, which enriches our knowledge on the anticancer effects of melatonin. Blocking the FGF19/FGFR4 pathway by melatonin could be a promising alternative for OSCCs prevention and management, which would facilitate further development of novel strategies to combat OSCCs.

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 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.

LncRNA PART1 promotes lung squamous cell carcinoma progression via miR-185-5p/Six1 axis

2020 ◽  
pp. 096032712097903
Author(s):  
Y Cao ◽  
R Zhang ◽  
X Luo ◽  
Y Yang
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cell Lines ◽  
Squamous Cell ◽  
Lung Squamous Cell Carcinoma ◽  
Loss Of Function ◽  
Tissue Samples ◽  
Invasion And Migration ◽  
Downstream Target ◽  
And Migration

Dysregulation of the long non-coding RNA prostate androgen regulated transcript 1 (lncRNA PART1) is involved in the tumorigenesis of various cancers. However, little is known about its function and molecular mechanism in the development of lung squamous cell carcinoma (LSCC). In this study, we examined the expression of PART1 in LSCC clinical tissue samples and cell lines, and gain- and loss-of-function experiments were performed to explore the function of PART1 in LSCC proliferation, invasion and migration. We found that PART1 was overexpressed in both LSCC tissues and cell lines. Functional studies revealed that PART1 knockdown significantly suppressed cell proliferation, invasion and migration but enhanced apoptosis in LSCC cells, whereas overexpression of PART1 showed the opposite results. Mechanistically, we identified that PART1 acted as a sponge of miR-185-5p, and sineoculis homeobox homolog 1 (Six1) was a direct downstream target of miR-185-5p. Moreover, restoration of miR-185-5p or silencing of Six1 partially abolished the oncogenic effect of PART1 in LSCC cells. Clinically, The areas under the receiver operating characteristic (ROC) curve of PART1, miR-185-5p, and Six1 were 0.7857, 0.7332, 0.8112, respectively. Notably, high PART1, low miR-185-5p, and high Six1 expressions were significantly associated with severe clinical parameters and were the independent risk factors for poor prognosis of LSCC patients. Thus, we concluded that the PART1/miR-185-5p/Six1 axis might serve as a novel biomarker for the diagnosis and treatment of LSCC.

scholarly journals Knowdown of lncRNA HOXA-AS2 inhibits proliferation, invasion and migration of oral squamous cell carcinoma

2020 ◽  
Author(s):  
Zhen Zhao ◽  
Yan Xing ◽  
Fei Yang ◽  
Zhijun Zhao ◽  
Yupeng Shen ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Viability ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Tunel Staining ◽  
Invasion And Migration ◽  
And Migration

Abstract Background Oral squamous cell carcinoma (OSSC) is one of the most common cancers in the world. The aim to the study was to evaluated the biological function and partly underlying regulatory mechanism of lncRNA homeobox A cluster antisense RNA2 (HOXA-AS2) on oral squamous cell carcinoma. Methods The expression of HOXA-AS2 in OSSC cells was detected by quantitative real time polymerase chain reaction (qRT-PCR). HOXA-AS2 expression was modified by transfection with HOXA-AS2 knockdown into TCA-8113 cells. The biological activity of TCA-8113 cells were detected by Cell Counting Kit-8 (CCK-8), EdU staining, Tunel staining, flow cytometry, wound healing, transwell assasy and western blot. The relationship between HOXA-AS2 and EZH2 was analyzed by RNA immunoprecipitation (RIP). Results At first, in this study, HOXA-AS2 expression in TCA-8113 cell line was increased compared with normal oral cells. Furthermore, HOXA-AS2 knockdown could inhibit cell viability, migration and invasion. Besides, EZH2 is the target of HOXA-AS2 in TCA-8113 cells. EZH2 expression was reduced by the HOXA-AS2 knockdown and the expression of P21 was negatively correlated to the expression of HOXA-AS2 in TCA-8113 cells. Conclusion In this study, silencing HOXA-AS2 reduced cell viability, invasion and migration capacity and EZH2, as an oncogene, could be downregulated by HOXA-AS2 knockdown in OSSC cells.

scholarly journals LncRNA CACS15 regulates tongue squamous cell carcinoma cell behaviors and predicts survival

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Xiao Wu ◽  
Jing Ma ◽  
Jian Chen ◽  
Han Huang
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Tongue Squamous Cell Carcinoma ◽  
Migration And Invasion ◽  
Tissue Samples ◽  
Cell Behaviors ◽  
Invasion And Migration ◽  
And Migration ◽  
High Level

Abstract Background The involvement of lncRNA CASC15 in several types of cancers has been reported, while its role in tongue squamous cell carcinoma (TSCC) is unknown. Our study aimed to investigate the clinical potentials of lncRNA CASC15 in TSCC. Methods The expression of CASC15 and miR-124 in tissue samples from TSCC patients and TSCC cell lines was analyzed by qPCR. Overexpression experiments were performed to analyze the interactions between CASC15 and miR-124. Survival analysis was performed to analyze the prognostic values of CASC15 and miR-124 for TSCC. Transwell assays were performed to analyze cell invasion and migration. Results We found that CASC15 was upregulated, while miR-124 was downregulated in TSCC tissues than in non-cancer tissues of TSCC patients. CASC15 and miR-125 expression was not significantly different among patients with different clinical stages, and patients with high level of CASC15 and low level of miR-125 showed low overall survival rate. CASC15 and miR-124 were inversely correlated in TSCC tissues, and CASC15 overexpression in TSCC cells resulted in downregulation of miR-124. In contrast, overexpression of miR-124 showed no significant effect on CASC15 expression. CASC15 overexpression resulted in the increased, while miR-124 overexpression resulted in the decreased migration and invasion rates of TSCC cells. Conclusion CASC15 and miR-124 predict TSCC patients’ survival and CASC15 may downregulate miR-124 to inhibit TSCC cell migration and invasion. The study was approved by Ethics Committee of The first Affiliated Hospital of Jinzhou Medical University (20103548FAHJMU).

miR-375 inhibits the proliferation, migration and invasion of esophageal squamous cell carcinoma by targeting XPR1

2020 ◽  
Vol 20 ◽  
Author(s):  
Wenbin Wu ◽  
Yangmei Zhang ◽  
Xiaowu Li ◽  
Xiang Wang ◽  
Yuan Yuan
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Luciferase Assay ◽  
Migration And Invasion ◽  
Promoting Effect ◽  
Dual Luciferase Assay ◽  
Invasion And Migration ◽  
And Migration

Objective: The purpose of this study was to explore the mechanism of the miR-375/XPR1 axis in esophageal squamous cell carcinoma (ESCC) and provide a new idea for targeted therapy of ESCC. Methods: Differentially expressed genes in GEO and TCGA databases were analyzed by bioinformatics. The expression levels of miR-375 and XPR1 mRNA were detected by qRT-PCR. Protein expression of XPR1 was detected by western blot. Bioinformatics analysis and dual luciferase assay were conducted to confirm the targeting relationship between miR-375 and XPR1. The viability, proliferation, migration and invasion of cells in each treatment group were detected by CCK-8, colony formation, wound healing and Transwell assays. Results: Significantly down-regulated miR-375 and remarkably up-regulated XPR1 were observed in ESCC tissue and cells. Overexpression of miR-375 inhibited proliferation, invasion and migration of ESCC cells, and greatly reduced the promoting effect of XPR1 overexpression on cell proliferation, migration and invasion. Dual luciferase assay confirmed that miR-375 targeted and inhibited XPR1 expression in ESCC. Conclusion: These results demonstrate the regulatory role of the miR-375/XPR1 axis in ESCC cells and provide a new potential target for the precise treatment of patients with ESCC.

LncRNA PCAT18/miR-301a/TP53INP1 axis is involved in gastric cancer cell viability, migration and invasion

2020 ◽  
Vol 168 (5) ◽  
pp. 547-555
Author(s):  
Jin Dou ◽  
Daoyuan Tu ◽  
Haijian Zhao ◽  
Xiaoyu Zhang
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cell Viability ◽  
Cell Lines ◽  
Underlying Mechanism ◽  
Migration And Invasion ◽  
Invasion And Migration ◽  
Proliferation And Metastasis ◽  
And Migration ◽  
Cell Proliferation And Metastasis

Abstract MiR-301a is as an oncogene involved in the regulation of gastric cancer (GC) progression, but the underlying mechanism is unclear. This study was to explore the lncRNA PCAT18/miR-301a/TP53INP1 axis in regulating the GC cell proliferation and metastasis. In the present study, GC tissues and cell lines were collected for the detection of PCAT18 expression. Herein, we found that PCAT18 is significantly decreases in human GC tissues and five GC cell lines. Overexpression of PCAT18 inhibits cell viability, invasion and migration of GC cells and tumour growth of GC xenograft tumours. PCAT18 negatively regulates the expression level of miR-301a. The interaction between PCAT18 and miR-301a is confirmed by RIP and RNA pull down. MiR-301a mimic increases cell viability and promotes cell migration and invasion and reverses the inhibitory action of PCAT18. TP53INP1 expression is negatively regulated by miR-301a and TP53INP1/miR-301a is involved in GC viability, migration and invasion. The promoting of PCAT18 on TP53INP1 expression is abolished by miR-301a overexpression. In conclusion, lncRNA PCAT18 acts as a tumour suppressor for GC and lncRNA PCAT18, miR-301a and TP53INP1 comprise a signal axis in regulating GC cell proliferation, migration and invasion.

Long Non-Coding Sprouty4-Intronic Transcript 1 (SPRY4-IT1) Regulates Cancer Biological Effects and Cisplatin Sensitivity in Cervical Cancer

2019 ◽  
Vol 9 (6) ◽  
pp. 789-796
Author(s):  
Hui Cai ◽  
Hongmei Deng
Keyword(s):  
Cervical Cancer ◽  
Cell Lines ◽  
Cancer Progression ◽  
Biological Effects ◽  
Scratch Test ◽  
Migration And Invasion ◽  
Invasion And Migration ◽  
Potential Biomarker ◽  
Cisplatin Sensitivity ◽  
And Migration

Background: Emerging evidences have revealed that Long noncoding RNAs (LncRNAs) is crucial for cancer progression. Previous studies have elucidated that patients with higher LncRNA SPRY4IT1 was more advanced. This study aims to investigate the biological effects of LncRNA SPRY4-IT1 and preliminary explore the effects of LncRNA SPRY4-IT1 on cisplatin sensitivity. Materials and methods: Quantitative reverse transcriptase PCR was used to validate the expression of SPRY4IT1. Cell migration and invasion were detected by scratch test and Transwell assay. Cell cytometry was performed for cell apoptosis. The expression of proteins was evaluated by immunoblotting. The drug sensitivity was measured by CCK-8. Results: LncRNA SPRY4-IT1 was significantly expressed in cervical cancer cell lines compared to normal cells. Downregulation of LncRNA SPRY4-IT1 in cervical cancer cells suppress the cell viability, cell invasion and migration and promoted apoptosis. In addition, decreases of LncRNA SPRY4-IT1 enhanced the cisplatin sensitivity in cervical cell lines. Conclusion: LncRNA SPRY4-IT1 is a potential biomarker and therapy target for cervical cancer.

scholarly journals CCR7 Regulates Cell Migration and Invasion through JAK2/STAT3 in Metastatic Squamous Cell Carcinoma of the Head and Neck

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Fa-Yu Liu ◽  
Jawad Safdar ◽  
Zhen-Ning Li ◽  
Qi-Gen Fang ◽  
Xu Zhang ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Migration ◽  
Cell Carcinoma ◽  
Head And Neck ◽  
Squamous Cell ◽  
Migration And Invasion ◽  
Signal Pathways ◽  
Invasion And Migration ◽  
Stat3 Phosphorylation ◽  
And Migration

Squamous cell carcinoma of the head and neck (SCCHN) frequently involves metastasis at diagnosis. Our previous research has demonstrated that CCR7 plays a key role in regulating SCCHN metastasis, and this process involves several molecules, such as PI3K/cdc42, pyk2, and Src. In this study, the goals are to identify whether JAK2/STAT3 also participates in CCR7’s signal network, its relationship with other signal pathways, and its role in SCCHN cell invasion and migration. The results showed that stimulation of CCL19 could induce JAK2/STAT3 phosphorylation, which can be blocked by Src and pyk2 inhibitors. After activation, STAT3 was able to promote low expression of E-cadherin and had no effect on vimentin. This JAk2/STAT3 pathway not only mediated CCR7-induced cell migration but also mediated invasion speed. The immunohistochemistry results also showed that the phosphorylation of STAT3 was correlated with CCR7 expression in SCCHN, and CCR7 and STAT3 phosphorylation were all associated with lymph node metastasis. In conclusion, JAk2/STAT3 plays a key role in CCR7 regulating SCCHN metastasis.

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