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.

Transcription factor EB influences invasion and migration in oral squamous cell carcinomas

Oral Diseases ◽  
2018 ◽  
Vol 24 (5) ◽  
pp. 741-748 ◽  
Author(s):  
H Sakamoto ◽  
K Yamashita ◽  
K Okamoto ◽  
T Kadowaki ◽  
E Sakai ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Squamous Cell ◽  
Squamous Cell Carcinomas ◽  
Oral Squamous Cell Carcinomas ◽  
Invasion And Migration ◽  
Transcription Factor Eb ◽  
And Migration

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.

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.

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.

scholarly journals LncRNA HOTAIR Influences the Growth, Migration, and Invasion of Papillary Thyroid Carcinoma via Affection on the miR-488-5p/NUP205 Axis

2020 ◽  
Vol 19 ◽  
pp. 153303382096212
Author(s):  
Feng Xia ◽  
Wei Xia ◽  
Xudong Yu
Keyword(s):  
Papillary Thyroid Carcinoma ◽  
Cell Growth ◽  
Thyroid Carcinoma ◽  
Migration And Invasion ◽  
Papillary Thyroid ◽  
Migration Ability ◽  
Invasion And Migration ◽  
Underlying Mechanisms ◽  
Well Assay ◽  
And Migration

Objective: The study was aim to investigate the effect of HOX transcript antisense RNA (HOTAIR) on the growth, migration, and invasion of papillary thyroid carcinoma (PTC) and its underlying mechanisms. Methods: Cell growth, invasion, and migration was respectively investigated using the MTT assay, trans-well assay, and wound healing assay. The expression of genes and proteins was respectively determined by Western blot analysis and RT-PCR experiments. Results: It was demonstrated that high expression of HOTAIR in PTC cells (BCPAP) and tissues resulted in fast tumor growth and poor survival time of the PTC-bearing mice models. Moreover, overexpression of HOTAIR leaded to markedly enhanced proliferation, migration, and invasion of BCPAP cells. Increase the levels of HOTAIR in BCPAP cells signally down-regulated the miR-488-5p levels which was able of inhibiting the growth rate, increasing the apoptosis rate, and decreasing the invasion/migration ability of BCPAP cells. Further studies indicated that HOTAIR promoted BCPAP cell growth, invasion, and migration mainly through regulating the miR-488-5p/NUP205 axis and the levels of Bcl-2 as well. Conclusion: HOTAIR promoted the growth, migration, and invasion of papillary thyroid carcinoma mainly through regulating the miR-488-5p/NUP205 axis.

scholarly journals TFE3 Regulates the Function of the Autophagy-Lysosome Pathway to Drive the Invasion and Metastasis of Papillary Thyroid Carcinoma

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Hongsheng Lu ◽  
Chumeng Zhu ◽  
Yanyun Ruan ◽  
Lilong Fan ◽  
Kena Wei ◽  
...  
Keyword(s):  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Cathepsin L ◽  
Clinicopathological Characteristics ◽  
Vital Role ◽  
Migration And Invasion ◽  
Papillary Thyroid ◽  
Invasion And Migration ◽  
Underlying Mechanisms ◽  
And Migration

Background. Accumulating evidence shows that autophagy plays a vital role in tumor occurrence, development, and metastasis and even determines tumor prognosis. However, little is known about its role in papillary thyroid carcinoma (PTC) or the potentially oncogenic role of TFE3 in regulating the autophagy-lysosome system. Methods. Immunohistochemistry and quantitative real-time PCR (qRT-PCR) were used to examine the expression of TFE3, P62/SQSTM1, and LC3 in PTC and paracancerous tissues. TFE3, P62/SQSTM1, LC3, cathepsin L (CTSL), and cathepsin B (CTSB) were evaluated using Western blot analysis. After inducing TFE3 overexpression by plasmid or TFE3 downregulation by small interfering RNA (siRNA) transfection, MTT, wound healing, and cell migration and invasion assays were used to verify the effects on invasion, migration, and the levels of autophagy-lysosome system-related proteins such as P62/SQSTM1, LC3, CTSL, and CTSB. Results. TFE3 was overexpressed in PTC tissues compared with paracancerous tissues. Analysis of the clinicopathological characteristics of PTC patients showed that high TFE3 expression was significantly correlated with lymph node metastasis. TFE3 overexpression in the PTC cell lines KTC-1 and BCPAP promoted proliferation, invasion, and migration, while TFE3 knockdown had the opposite effects. Furthermore, we identified a positive relationship among the expression levels of TFE3, P62/SQSTM1, LC3, CTSL, and CTSB. We found that silencing TFE3 inhibited the expression of P62/SQSTM1, LC3, CTSL, and CTSB in PTC cells. However, TFE3 overexpression had the opposite effects. Conclusions. The present study provided evidence for the underlying mechanisms by which TFE3 induces autophagy-lysosome system activity in PTC.

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 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 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.

Sign in / Sign up

Export Citation Format

Share Document