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 miR-223-5p Suppresses OTX1 to Mediate Malignant Progression of Lung Squamous Cell Carcinoma Cells

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Yunping Lu
Keyword(s):  
Squamous Cell Carcinoma ◽  
Western Blot ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Lung Squamous Cell Carcinoma ◽  
Luciferase Assay ◽  
Dual Luciferase Assay ◽  
Invasion And Migration ◽  
And Migration ◽  
The Relationship

Background. Lung squamous cell carcinoma (LUSC) features high morbidity and mortality as a worldwide malignant tumor. This study mainly explored a miR-223-5p-dependent mechanism that affected proliferation, invasion, and migration of LUSC cells. Methods. Expression data of mature miRNAs and sequencing data of total RNA of LUSC were downloaded from TCGA database. Differentially expressed mRNAs were obtained. Function of miR-223-5p in LUSC cells was detected by assays like qRT-PCR, MTT, wound healing assay, Western blot, and Transwell assay. Western blot was performed to analyze the relationship between OTX1 and JAK/STAT signaling pathways. Dual-luciferase assay detected the relationship between miR-223-5p and OTX1. The way how miR-223-5p regulated LUSC cell biological functions via OTX1 was further explored. Results. It was noted that miR-223-5p expression in LUSC tissue and cells was significantly reduced. Overexpression of miR-223-5p negatively regulated the proliferation, invasion, and migration of LUSC cells. The downstream target gene OTX1 was detected to be notably elevated in LUSC cells. A negative correlation between OTX1 and miR-223-5p was also found. As analyzed by GSEA, OTX1 was significantly enriched in the JAK/STAT signaling pathway and activated the pathway. Dual-luciferase assay demonstrated that OTX1 was a direct molecular target of miR-223-5p in LUSC cells. Rescue experiment verified that miR-223-5p regulated the malignant phenotypes of LUSC cells by pairing with OTX1. Conclusion. This study indicated that miR-223-5p was lowly expressed in LUSC cells. The impact of miR-223-5p on cell proliferation, invasion, and migration was realized by targeting OTX1. It is likely that miR-223-5p can be a novel target for LUSC treatment, which provides new ideas for future LUSC treatment.

scholarly journals Long noncoding RNA CASC2 suppresses esophageal squamous cell carcinoma progression by increasing SOCS1 expression

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Ke Sun ◽  
Guangping Zhang
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Noncoding Rna ◽  
Cancer Susceptibility ◽  
Underlying Mechanism ◽  
Luciferase Assay ◽  
Migration And Invasion ◽  
Cytokine Signaling

Abstract Objective Esophageal squamous cell carcinoma (ESCC) is one of the leading causes of cancer-related deaths worldwide. Emerging evidence suggests the involvement of long noncoding RNAs (lncRNAs) in tumorigenesis. LncRNA Cancer Susceptibility Candidate 2 (CASC2) has been demonstrated to act as a tumor suppressor contributing to the development and progression of several cancers. However, the functional significance and underlying mechanism of CASC2 in ESCC progression has not been well elucidated. Methods The expression levels of CASC2 in ESCC tissues were detected by qRT-PCR. CASC2 overexpression and knockdown models were established and used to investigate the functional role of CASC2 in ESCC cells. RIP, RNA pull-down and dual-luciferase assay was used to detect the association between CASC2 and miR-155. The interaction between CASC2 and Suppressor Of Cytokine Signaling 1 (SOCS1) was assessed by RIP and RNA pull-down assays. Results In the present study, we found that CASC2 was significantly downregulated in ESCC tissues and positively correlated with overall survival time of patients with ESCC. Functional assays demonstrated that CASC2 suppressed proliferation, migration and invasion, as well as enhanced drug sensitivity in ESCC cells. Mechanistically, CASC2 inhibited ESCC progression by upregulating the expression of SOCS1 via two different ways. CASC2 acted as competing endogenous RNA (ceRNA) for miR-155 to post-transcriptionally increase SOCS1 expression. On the other hand, CASC2 was capable of interacting with SOCS1 protein and suppressing its degradation. Conclusion Conclusively, these results demonstrated that CASC2 could exert as a tumor suppressive lncRNA in ESCC progression via regulating SOCS1.

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 HDAC2 enhances esophageal squamous cell carcinoma development through down-regulating microRNA-503-5p and promoting CXCL10

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Jindong Li ◽  
Chengyan Jin ◽  
Lihua Sun ◽  
Bin Wang ◽  
Peiyan Hua ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Invasion And Migration ◽  
Histone Deacetylase 2 ◽  
Mucosal Tissues ◽  
And Migration

Abstract Objective Although esophageal squamous cell carcinoma (ESCC)-oriented mechanism has been widely explored, the integrated action of histone deacetylase 2 (HDAC2), microRNA (miR)-503-5p and C-X-C motif chemokine 10 (CXCL10) in ESCC has not been thoroughly explored. Thus, we performed the research to study the role of HDAC2/miR-503-5p/CXCL10 axis in ESCC. Methods ESCC tissues and mucosal tissues (5 cm from cancer tissues) were collected, in which HDAC2, miR-503-5p and CXCL10 expression levels were tested. The mechanism of HDAC2, miR-503-5p and CXCL10 was interpreted. The viability, colony formation ability, apoptosis, invasion and migration abilities of ESCC cells were tested after HDAC2, miR-503-5p or CXCL10 expression was altered. Tumorigenesis in mice was observed to further verify the in vitro effects of HDAC2 and miR-503-5p. Results HDAC2 and CXCL10 were up-regulated while miR-503-5p was down-regulated in ESCC. HDAC2 bound to miR-503-5p and miR-503-5p targeted CXCL10. Silencing HDAC2 or restoring miR-503-5p depressed viability, colony-forming, invasion and migration abilities and enhanced apoptosis of ESCC cells in vitro, as well as suppressed ESCC tumorigenesis in vivo. Inhibition of miR-503-5p or elevation of CXCL10 negated HDAC2 knockout-induced effects on ESCC cells. Conclusion This work elucidates that HDAC2 knockdown retards the process of ESCC by elevating miR-503-5p and inhibiting CXCL10 expression, which may provide a guidance for ESCC management.

scholarly journals FLVCR1 Predicts Poor Prognosis and Promotes Malignant Phenotype in Esophageal Squamous Cell Carcinoma via Upregulating CSE1L

2021 ◽  
Vol 11 ◽  
Author(s):  
Suna Zhou ◽  
Mingxin Zhang ◽  
Chao Zhou ◽  
Yinnan Meng ◽  
Haihua Yang ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Colony Formation ◽  
Xenograft Model ◽  
Migration And Invasion ◽  
Node Metastasis ◽  
And Migration

ObjectiveDysregulation of feline leukemia virus subgroup C receptor 1(FLVCR1) expression has been investigated in several tumors. However, the expression and role of FLVCR1 in esophageal squamous cell carcinoma (ESCC) remain largely unknown.MethodsFLVCR1 expression in tissues was measured by immunohistochemical staining (IHC). Celigo assay, MTT assay, colony formation, caspase 3/7 activity analysis, wound healing assay, Transwell migration, and invasion assay were applied to assess the effects of FLVCR1 on ESCC tumorigenesis. Coimmunoprecipitation (Co-IP) and liquid chromatography-mass spectrometry (LC-MS) were used to identify protein interactions with FLVCR1. An in vivo imaging system (IVIS) was used to investigate the functions of FLVCR1 on the growth and metastatic capability of ESCC cells in a xenograft model and a tail vein metastasis model.ResultsElevated expression of FLVCR1 was detected in ESCC tissues and predicted poor survival. Upregulated FLVCR1 was positively correlated with lymph node metastasis (N stage) and late tumor-node-metastasis (TNM) stage. FLVCR1 knockdown inhibited cell proliferation and colony formation ability, induced cell apoptosis, and repressed cell migration and invasion of ESCC in vitro. Inhibition of FLVCR1 markedly repressed tumorigenicity and metastasis of ESCC cells in vivo. Mechanistically, chromosome segregation 1–like (CSE1L) was identified to interact with FLVCR1 using a Co-IP assay. Moreover, the inhibitory effect of FLVCR1 knockdown on proliferation and migration was counteracted by the exogenous expression of CSE1L.ConclusionFLVCR1 plays a pivotal role in ESCC cell survival, growth, and migration. These functions may be partially dependent upon the protein interaction between FLVCR1 and CSE1L. In addition, FLVCR1 can be applied as a clinical prognostic marker for patients with ESCC.

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.

Sign in / Sign up

Export Citation Format

Share Document