scholarly journals miR-182-5p Promotes Growth in Oral Squamous Cell Carcinoma by Inhibiting CAMK2N1

2018 ◽  
Vol 49 (4) ◽  
pp. 1329-1341 ◽  
Author(s):  
Nan Li ◽  
Chuan-Chuan Nan ◽  
Xue-Yun Zhong ◽  
Jun-Quan Weng ◽  
Hai-Dong Fan ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cell Lines ◽  
Squamous Cell ◽  
Colony Formation ◽  
Cell Counting ◽  
Control Group ◽  
Rt Pcr ◽  
Ki 67

Background/Aims: Emerging evidence suggests that the propagation of oral squamous cell carcinoma (OSCC) is influenced by the abnormal expression of microRNAs (miRNAs). This study aimed to characterize the involvement of miR-182-5p in OSCC by targeting the calcium/ calmodulin-dependent protein kinase II inhibitor CAMK2N1. Methods: miR-182-5p expression was quantified in OSCC tissues and cell lines with reverse transcription polymerase chain reaction (RT-PCR). Cell colony formation, Cell Counting Kit-8 (CCK-8), Ki-67, and nude mouse xenograft assays were used to characterize the role of miR-182-5p in the proliferation of OSCC. A miR-182-5p target gene was identified with western blotting, RT-PCR, and luciferase activity assays. OSCC patient survival based on CAMK2N1 expression was also analyzed. Results: miR-182-5p was up-regulated in in vitro cell lines and in vivo clinical OSCC samples. CCK-8, colony formation, and Ki-67 assays revealed that miR-182-5p promoted the growth and proliferation of OSCC cells. miR-182-5p directly targeted CAMK2N1, as evidenced by luciferase assays and target prediction algorithms. CAMK2N1 operated as a tumor suppressor gene in patients with OSCC. Down-regulating miR-182-5p expression in the CAL-27 cell line restored CAMK2N1-mediated OSCC cell proliferation. miR-182-5p expression inhibited the activation of AKT, ERK1/2, and NF-κB. Mice injected with CAL-27 cells transfected with miR-182-5p-inhibitor demonstrated a significant increase in tumor size and weight and increased CAMK2N1 mRNA and protein expression compared with the miR-negative control group. Conclusion: The miR-182-5p-CAMK2N1 pathway can be potentially targeted to regulate the proliferation of OSCC cells.

scholarly journals Anti-tumor effect of cisplatin in human oral squamous cell carcinoma was enhanced by andrographolide via upregulation of phospho-p53 in vitro and in vivo

Tumor Biology ◽  
2017 ◽  
Vol 39 (5) ◽  
pp. 101042831770533 ◽  
Author(s):  
Songjie Chen ◽  
Hui Hu ◽  
Shushu Miao ◽  
Jiayong Zheng ◽  
Zhijian Xie ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Tumor Regression ◽  
Cell Counting ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Ki 67

Oral squamous cell carcinoma is one of the most common neoplasm in the world. Despite the improvements in diagnosis and treatment, the outcome is still poor now. Thus, the development of novel therapeuticapproaches is needed. The aim of this study is to assess the synergistic anti-tumor effect of andrographolide with cisplatin (DDP) in oral squamous cell carcinoma CAL-27 cells in vitro and in vivo. We performed Cell Counting Kit-8 proliferation assay, apoptosis assay, and western blotting on CAL-27 cells treated with andrographolide, DDP or the combination in vitro. In vivo, we also treated CAL-27 xenografts with andrographolide or the combination, and performed terminal deoxynucleotidyl transferase–mediated deoxyuridine triphosphate nick-end labeling assay and immunohistochemical analysis of Ki-67. The results showed the combination of andrographolide and DDP synergistically inhibited CAL-27 cell proliferation in vitro and caused tumor regression in vivo in the CAL-27 xenografts. In addition, the synergistic anti-tumor effect of andrographolide with synergistic was due to an enhanced apoptosis. Moreover, the combination therapy upregulated the expression level of p-p53 in vitro and decreased Ki-67 expression in vivo. Our data indicate that the combination treatment of andrographolide and DDP results in synergistic anti-tumor growth activity against oral squamous cell carcinoma CAL-27 in vitro and in vivo. These results demonstrated that combination of andrographolide with DDP was likely to represent a potential therapeutic strategy for oral squamous cell carcinoma.

scholarly journals As a Novel Tumor Suppressor, LHPP Promotes Apoptosis by Inhibiting the PI3K/AKT Signaling Pathway in Oral Squamous Cell Carcinoma

2021 ◽  
Author(s):  
Shanshan Liu ◽  
Wenzhen Gao ◽  
Yupu Lu ◽  
Qin Zhou ◽  
Rongjian Su ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Tumor Suppressor ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Signaling Pathway ◽  
Cell Lines ◽  
Squamous Cell ◽  
Akt Signaling ◽  
Cell Counting ◽  
Akt Signaling Pathway

Abstract Background: Oral squamous cell carcinoma (OSCC) refers to the malignant tumor of the head and neck with a highest morbidity. It exhibits a poor prognosis and unsatisfactory treatment, which is partially attributed to delayed diagnosis. As indicated from existing reports, the protein histidine phosphatase LHPP acts as a vital factor in tumorigenesis in liver, lung, bladder, breast and pancreatic tumor tissues. Thus far, the expression level of LHPP in OSCC has been rarely studied, and its functional mechanism remains unclear. Methods: DEG analysis, OSCC cell lines and OSCC samples were used to detect the expression of LHPP in adjacent normal and cancerous tissues and its relationship with OSCC differentiation. Immunofluorescence staining was used to detect the over-expressed LHPP in OSCC cell lines. The cell counting kit 8 test, EdU proliferation test, scratch test, invasion test, single clone formation test, mouse xenograft tumor model HE staining and immunohistochemistry were used to estimate the biological characteristics of LHPP in OSCC in vivo and in vitro. GO and KEGG enrichment analysis and LHPP transcription factor analysis were used to further predict the role of LHPP and its related genes. The Western blotting assay, real-time PCR analysis and flow cytometry determined the inhibitory mechanism of LHPP in OSCC cells.Results: LHPP was down-regulated in OSCC tissues and cells than that in normal oral mucosa tissues and cells, LHPP expressing also displays a close association with the degree differentiation of OSCC. LHPP is capable of significantly inhibiting OSCC cells from proliferating, migrating and invading. The increase in LHPP expression facilitated OSCC cell apoptosis through PI3K/AKT signaling pathway.Conclusion: LHPP is a novel tumor suppressor which promotes apoptosis by inhibiting the PI3K/AKT signaling pathway in OSCC, indicating that LHPP is a new diagnostic marker and therapeutic target for OSCC.

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 LncRNA HOXA-AS3 promotes the progression of oral squamous cell carcinoma through sponging miR-218-5p

2020 ◽  
Author(s):  
Yue Zhao ◽  
Rui Yao
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Colony Formation ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Proliferative Potential ◽  
Binding Condition ◽  
Gene Assay

Abstract Objective The aim of the present study was to investigate the roles and molecular mechanism of long non-coding RNA (lncRNA) HOXA-AS3 in the progression of oral squamous cell carcinoma (OSCC). Methods The expression of HOXA-AS3 and miR-218-5p was detected in OSCC tissues and cells using quantitative real-time polymerase chain reaction (qRT-PCR). Cell Counting Kit-8 (CCK-8) and colony formation assays were used to examine the effects of HOXA-AS3 and miR-218-5p on the proliferation of OSCC cells. Luciferase reporter gene assay was used to confirm the directly binding condition between lncRNA HOXA-AS3 and miR-218-5p in OSCC cells. RNA immunoprecipitation assay was employed to verify the interaction between HOXA-AS3 and miR-218-5p. Results The relative expression of lncRNA HOXA-AS3 was observably upregulated in OSCC tissues and cell lines compared with the para-cancerous tissues and normal human oral keratinocyte (NHOK), respectively. Knockdown of HOXA-AS3 significantly inhibited the proliferation and colony formation of OSCC cells. Bioinformatics analysis and luciferase reporter assay showed that HOXA-AS3 directly bound to miR-218-5p. Moreover, the expression of miR-218-5p was negatively regulated by HOXA-AS3, and there was an inverse correlation between them. Silencing miR-218-5p reversed the inhibitory effect of lncRNA HOXA-AS3 knockdown on the proliferative potential of OSCC cells. Conclusion In summary, our study illustrated lncRNA HOXA-AS3 promoted cancer cell proliferation in OSCC possibly by sponging miR-218-5p for the first time, which provides a new target or a potential diagnostic biomarker of the treatment for OSCC.

scholarly journals MicroRNA-99a-5p suppresses cell proliferation, migration, and invasion by targeting isoprenylcysteine carboxylmethyltransferase in oral squamous cell carcinoma

2021 ◽  
Vol 49 (5) ◽  
pp. 030006052093903
Author(s):  
Xiang Sun ◽  
Huixin Yan
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cell Lines ◽  
Squamous Cell ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Isoprenylcysteine Carboxylmethyltransferase

Background MicroRNA (miR)-99a-5p acts as a tumor suppressor in several tumors, including bladder cancer and breast cancer, but its biological function in oral squamous cell carcinoma (OSCC) is poorly understood. Methods miR-99a-5p expression was determined in OSCC tissues and cell lines using quantitative reverse transcription polymerase chain reaction (RT-qPCR). Cell proliferation was assessed by the Cell Counting Kit-8 assay and colony formation assay. Wound healing and Transwell assays were used to analyze migration and invasion abilities, respectively, in OSCC cells. The luciferase reporter assay, RT-qPCR, and western blotting were used to determine the relationship between miR-99a-5p and isoprenylcysteine carboxylmethyltransferase (ICMT). Results miR-99a-5p expression in OSCC tissues and cell lines was significantly decreased compared with corresponding controls, and was significantly associated with clinical stage and lymph node metastasis in OSCC. Functional assays revealed that miR-99a-5p overexpression significantly inhibited the proliferation, migration, and invasion abilities of CAL-27 and TCA-8113 OSCC cells. miR-99a-5p was found to directly target ICMT, while ICMT restoration reversed the role of miR-99a-5p in OSCC cells. Conclusions Our results indicate that miR-99a-5p-mediates the down-regulation of ICMT, which could be used as a novel potential therapeutic target for OSCC treatment.

scholarly journals LncRNA HOXA-AS3 promotes the progression of oral squamous cell carcinoma via inhibiting miR-218-5p

2020 ◽  
Author(s):  
Yue Zhao ◽  
Rui Yao
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Colony Formation ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Gene Assay

Abstract Objective: The aim of the present study was to investigate the roles and molecular mechanism of long non-coding RNA (lncRNA) HOXA-AS3 in the progression of oral squamous cell carcinoma (OSCC). Methods : The expression of HOXA-AS3 and miR-218-5p was detected in OSCC tissues and cells using quantitative real-time polymerase chain reaction (qRT-PCR). Cell Counting Kit-8 (CCK-8) and colony formation assays were used to examine the effects of HOXA-AS3 and miR-218-5p on the proliferation of OSCC cells. Luciferase reporter gene assay was used to confirm the directly binding condition between lncRNA HOXA-AS3 and miR-218-5p in OSCC cells. Subsequently, a tumor xenograft model was used to determine the function of HOXA-AS3 in OSCC growth in vivo . Results: The relative expression of lncRNA HOXA-AS3 was observably upregulated in OSCC tissues and cell lines compared with the para-cancerous tissues and normal human oral keratinocyte (NHOK), respectively. Knockdown of HOXA-AS3 significantly inhibited the cell proliferation and colony formation of OSCC in vitro and in vivo . Bioinformatics and luciferase reporter assays showed that HOXA-AS3 directly bound to miR-218-5p. Moreover, the expression of miR-218-5p was negatively regulated by HOXA-AS3, and there was an inverse correlation between them. Silencing miR-218-5p reversed the inhibitory effect of lncRNA HOXA-AS3 knockdown on the proliferative potential of OSCC cells. Conclusion: In summary, our study illustrated lncRNA HOXA-AS3 promoted cancer cell proliferation in OSCC possibly by inhibiting miR-218-5p for the first time, which provides a new target or a potential diagnostic biomarker of the treatment for OSCC.

scholarly journals The Effect of Aflibercept and Arsenic Trioxide on the Proliferation, Migration and Apoptosis of Oral Squamous Cell Carcinoma in Vitro

2021 ◽  
Author(s):  
Samira Derakhshan ◽  
Pouyan Aminishakib ◽  
Fatemeh Pirzadeh ◽  
Sedigheh Rahrotaban ◽  
Parvaneh Farzaneh ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Squamous Cell Carcinoma ◽  
Cell Growth ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Arsenic Trioxide ◽  
Cell Lines ◽  
Squamous Cell ◽  
Colony Formation ◽  
Cytotoxic Effect

Abstract Aflibercept and arsenic trioxide drugs apply a cytotoxic effect on some human cancer cell lines. However, no more study has followed the effects of both drugs, especially arsenic trioxide, on oral squamous cell carcinoma (OCC). We used three OCC lines as a model to show the effect of these drugs on the genetically complex disease and investigate its targeted therapy.In this study, three human OCC cell lines were used from different patients. We treated cell lines with both medications to detect the effect and relevant molecular basis. First, methyl thiazolyl tetrazolium (MTT) assay was performed to detect the cytotoxicity effect and cell growth. Second, western blot and flow cytometry were performed to evaluate the anti-angiogenic effect on OCC lines. Next apoptosis was analyzed by flow cytometry. Finally, clonogenesis capacity and cell migration were assessed by colony formation assay and wound healing, respectively.Aflibercept had no cytotoxic effect on the three OCC cell lines but decreased cell growth rate. Arsenic trioxide had a significant cytotoxic effect on three cell lines. Our results demonstrated that both drugs significantly decreased endoglin and VEGF expression. In addition, Migration and colony formation assays confirmed that these drugs have significant anti-proliferative and anti-migration effect on oral carcinoma cells.These results revealed that both medications might be a potential drug for the management of oral cancer patients.

scholarly journals PDIA6 contributes to aerobic glycolysis and cancer progression in oral squamous cell carcinoma

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Ling Mao ◽  
Xiaoweng Wu ◽  
Zhengpeng Gong ◽  
Ming Yu ◽  
Zhi Huang
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Growth ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Expression Pattern ◽  
Cancer Progression ◽  
Squamous Cell ◽  
Aerobic Glycolysis ◽  
Lactate Production ◽  
Control Group

Abstract Background/objective Accumulated evidence has demonstrated that aerobic glycolysis serves as a regulator of tumor cell growth, invasion, and angiogenesis. Herein, we explored the role of protein disulfide isomerase family 6 (PDIA6) in the aerobic glycolysis and the progression of oral squamous cell carcinoma (OSCC). Methods The expression pattern of PDIA6 in OSCC tissues was determined by qPCR and western blotting. Lentivirus and small interfering RNAs (siRNAs) were introduced into cells to upregulate and downregulate PDIA6 expression. CCK-8, flow cytometry, transwell, and xenotransplantation models were applied to detect cell proliferation, apoptosis, migration, invasion, and tumorigenesis, respectively. Results A high expression pattern of PDIA6 was observed in OSCC tissues, which was closely associated with lower overall survival and malignant clinical features in OSCC. Compared with the control group, overexpression of PDIA6 induced significant enhancements in cell growth, migration, invasiveness, and tumorigenesis and decreased cell apoptosis, while knockdown of PDIA6 caused opposite results. In addition, overexpression of PDIA6 increased glucose consumption, lactate production, and ATP level in OSCC cells. Conclusion This study demonstrated that PDIA6 expression was elevated in OSCC tissues, and overexpression of it promoted aerobic glycolysis and OSCC progression.

scholarly journals Identification of E2F transcription factor 7 as a novel potential biomarker for oral squamous cell carcinoma

2021 ◽  
Vol 17 (1) ◽  
Author(s):  
Ping Zhou ◽  
Lei Xiao ◽  
Xiaonan Xu
Keyword(s):  
Squamous Cell Carcinoma ◽  
Transcription Factor ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cell Lines ◽  
Squamous Cell ◽  
Loss Function ◽  
High Expression ◽  
E2f Transcription Factor ◽  
Gain And Loss

Abstract Background As a tumor-accelerating transcriptional factor, E2F transcription factor 7 (E2F7) was up-regulated in many forms of cancers. Nevertheless, little has been reported about the impacts of E2F7 on oral squamous cell carcinoma (OSCC). Here, we aimed to probe whether E2F7 had influences on OSCC and its potential mechanism. Methods The expression of E2F7 in OSCC tissues was analyzed using the data acquired from TCGA and ONCOMINE databases. E2F7 prognostic value in OSCC patients was analyzed utilizing TCGA database. The expression of E2F7 in OSCC cell lines was detected by qRT-PCR. Gain-and loss-function of E2F7 assays in TCA-83 and CAL27 cells were performed respectively to inquire the function of E2F7. Western blotting was applied to test the alternations of EMT-related markers. Results In OSCC tissues, E2F7 was highly expressed. Besides, high expression of E2F7 predicted worse prognosis in OSCC patients. Moreover, E2F7 was over-expressed in TCA-83, HSC-4 and CAL27 (all OSCC cell lines) cells relative to that in HNOK (a normal cell line) cells. Gain-and loss-function assays displayed that deficiency of E2F7 suppresses CAL27 cell growth, migration, invasion and E2F7 high-expression resulted in inverse outcomes in TCA-83 cells. Finally, we found that silencing of E2F7 facilitated E-cadherin protein expression level and reduced N-cadherin, Vimentin and Snail protein levels in CAL27 cells, whilst E2F7 high-expression exhibited the opposite effects in TCA-83 cells. Conclusions These outcomes indicated that E2F7 performs a carcinogenic role in OSCC, which provides a theoretical basis for the therapeutic strategies of OSCC.

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