Specific cellular accumulation of photofrin-II in EC cells promotes photodynamic treatment efficacy in esophageal cancer

2016 ◽  
Vol 14 ◽  
pp. 27-33 ◽  
Author(s):  
Shegan Gao ◽  
Shuo Liang ◽  
Kaili Ding ◽  
Zhifeng Qu ◽  
Ying Wang ◽  
...  
Keyword(s):  
Esophageal Cancer ◽  
Treatment Efficacy ◽  
Photodynamic Treatment ◽  
Cellular Accumulation ◽  
Photofrin Ii ◽  
Ec Cells

FAM196B promotes proliferation and migration via regulating epithelial-mesenchymal transition in esophageal cancer

2021 ◽  
pp. 1-8
Author(s):  
Haifeng Xia ◽  
Fang Hu ◽  
Liangbin Pan ◽  
Chengcheng Xu ◽  
Haitao Huang ◽  
...  
Keyword(s):  
Esophageal Cancer ◽  
Western Blot ◽  
Cox Regression ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Cox Regression Analysis ◽  
Ec Cells ◽  
And Migration ◽  
Proliferation And Migration

BACKGROUND: EC (esophageal cancer) is a common cancer among people in the world. The molecular mechanism of FAM196B (family with sequence similarity 196 member B) in EC is still unclear. This article aimed to clarify the role of FAM196B in EC. METHODS: The expression of FAM196B in EC tissues was detected using qRT-PCR. The prognosis of FAM196B in EC patients was determined by log-rank kaplan-Meier survival analysis and Cox regression analysis. Furthermore, shRNA was used to knockdown the expression of FAM196B in EC cell lines. MTT, wound healing assays and western blot were used to determine the role of FAM196B in EC cells. RESULTS: In our research, we found that the expression of FAM196B was up-regulated in EC tissues. The increased expression of FAM196B was significantly correlated with differentiation, lymph node metastasis, stage, and poor survival. The proliferation and migration of EC cells were inhibited after FAM196B-shRNA transfection in vitro and vivo. The western blot result showed that FAM196B could regulate EMT. CONCLUSION: These results suggested that FAM196B severs as an oncogene and promotes cell proliferation and migration in EC. In addition, FAM196B may be a potential therapeutic target for EC patients.

scholarly journals Simultaneous Photodiagnosis and Photodynamic Treatment of Metastatic Melanoma

Molecules ◽  
2019 ◽  
Vol 24 (17) ◽  
pp. 3153 ◽  
Author(s):  
Channay Naidoo ◽  
Cherie Ann Kruger ◽  
Heidi Abrahamse
Keyword(s):  
Metastatic Melanoma ◽  
Drug Absorption ◽  
Treatment Efficacy ◽  
Poor Prognosis ◽  
Needle Aspiration ◽  
Diagnostic Tools ◽  
Photodynamic Diagnosis ◽  
Photodynamic Treatment ◽  
Irradiation Therapy ◽  
Non Destructive

Metastatic melanoma (MM) has a poor prognosis and is attributed to late diagnoses only when metastases has already occurred. Thus, early diagnosis is crucial to improve its overall treatment efficacy. The standard diagnostic tools for MM are incisional biopsies and/or fine needle aspiration biopsies, while standard treatments involve surgery, chemotherapy, or irradiation therapy. The combination of photodynamic diagnosis (PDD) and therapy (PDT) utilizes a photosensitizer (PS) that, when excited by light of a low wavelength, can be used for fluorescent non-destructive diagnosis. However, when the same PS is activated at a higher wavelength of light, it can be cytotoxic and induce tumor destruction. This paper focuses on PS drugs that have been used for PDD as well as PDT treatment of MM. Furthermore, it emphasizes the need for continued investigation into enhanced PS delivery via active biomarkers and passive nanoparticle systems. This should improve PS drug absorption in MM cells and increase effectiveness of combinative photodynamic methods for the enhanced diagnosis and treatment of MM can become a reality.

scholarly journals Circ-SFMBT2 drives the malignant phenotypes of esophageal cancer by the miR-107-dependent regulation of SLC1A5

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Zhiwei Chang ◽  
Yang Fu ◽  
Yongxu Jia ◽  
Ming Gao ◽  
Lijie Song ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Esophageal Cancer ◽  
Protein Detection ◽  
Protein Quantification ◽  
Glutamine Metabolism ◽  
Luciferase Reporter ◽  
Morphological Observation ◽  
Circular Rnas ◽  
Ec Cells

Abstract Background Increasing studies focused on the regulatory roles of circular RNAs (circRNAs) in diverse cancers. This study was to evaluate the function and mechanism of circRNA Scm-like with four malignant brain tumor domains 2 (circ-SFMBT2) in esophageal cancer (EC). Methods The circ-SFMBT2, microRNA-107 (miR-107) and solute-linked carrier family A1 member 5 (SLC1A5) levels were analyzed by quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation was evaluated by 3-(4, 5-dimethylthiazol-2-y1)-2, 5-diphenyl tetrazolium bromide (MTT) assay, colony formation assay and EdU assay. Cell apoptosis and invasion were detected by flow cytometry and transwell assay. Glutamine metabolism was assessed by the corresponding kits for glutamine consumption, α-ketoglutarate production and glutamate production. Western blot was used for protein quantification. The binding analysis was performed using dual-luciferase reporter assay, RNA immunoprecipitation (RIP) and pull-down assays. The functional research of circ-SFMBT2 in vivo was performed by xenograft tumor assay. Exosomes were identified by morphological observation and protein detection. Results Circ-SFMBT2 was overexpressed in EC samples and cells. Circ-SFMBT2 downregulation inhibited EC cell proliferation, invasion and glutamine metabolism. Circ-SFMBT2 targeted miR-107 and the regulation of circ-SFMBT2 was achieved by sponging miR-107. SLC1A5 was a target of miR-107, and it worked as an oncogene in EC cells. MiR-107 retarded the EC progression by downregulating SLC1A5. Circ-SFMBT2 could affect the SLC1A5 expression by targeting miR-107. Circ-SFMBT2 regulated EC progression in vivo by miR-107/SLC1A5 axis. Circ-SFMBT2 was transferred by exosomes in EC cells. Conclusion These results suggested that circ-SFMBT2 upregulated the SLC1A5 expression to promote the malignant development of EC by serving as a miR-107 sponge.

scholarly journals EGFL6 Modulates WNT Signaling to Drive Esophageal Cancer Metastasis and Proliferation

2020 ◽  
Author(s):  
Yanhong Wang ◽  
Jing Kang ◽  
Jihua Tian ◽  
Hongyan Jia ◽  
Juanjuan Wang ◽  
...  
Keyword(s):  
Esophageal Cancer ◽  
Western Blot ◽  
Real Time ◽  
Real Time Pcr ◽  
Expression Level ◽  
Marker Genes ◽  
Invasion And Migration ◽  
Ec Cells

Abstract Background Esophageal cancer (EC) is the sixth deadliest cancer in the world. There has been no breakthrough in the research on EC in the past few decades. Epidermal growth factor-like protein 6 (EGFL6), as a member of the epidermal growth factor superfamily, plays an important role in the occurrence and development of some tumors. However, the role of EGFL6 in the EC has never explored. Methods Immunohistochemical staining was used to evaluate the expression level of EGEC6 protein in human EC and its adjacent non-tumor tissues, and analyzed the correlation between the expression level of EGFL6 protein and clinical pathological indexes and survival rate. In vitro, by constructing EGFL6 silence and overexpressed EC cells,used CCK-8, clone formation, wound healing assays, transwell experiment and flow cytometry to explore the effects of EGFL6 on the proliferation, invasion, migration and apoptosis of EC. By using real-time PCR or western blot to detect the related marker genes of epithelial-mesenchymal transformation (EMT), tumor stem cells (TSCs) and Wnt/β-catenin. In vivo, established a nude mouse EC transplantation tumor model. Results The results showed that the expression level of EGFL6 in EC is significantly higher than that in adjacent non-tumor tissues, and is related to poor prognosis of patients. In vitro, CCK-8, clone formation, wound healing assays, transwell experiment and flow cytometry results show that EGFL6 overexpression can promotes proliferation, invasion and migration of EC cells and inhibits apoptosis. EGFL6 silencing inhibits proliferation, invasion and migration of EC cells and promotes apoptosis. Real-time PCR and Western-blot detection of EMT-related markers found that EGFL6 can induce EC cells EMT. Real-time PCR detection of esophageal cancer stem cell-related genes showed that EGFL6 may maintain the expression of esophageal cancer stem cell-like cell population. Western-blot detection of Wnt/β-catenin signaling marker genes showed that EGFL6 participated in the expression of Wnt/β-catenin signaling pathway. In vivo experiments found that knockout of EGFL6 could inhibit the formation of subcutaneous tumors in nude mice. Conclusion Taken together, our study identified a novel role and mechanism of EGFL6 in EC and provided epigenetic therapeutic strategies for the treatment of EC.

scholarly journals m6A Demethylase FTO Promotes Tumor Progression via Regulation of Lipid Metabolism in Esophageal Cancer

2021 ◽  
Author(s):  
Xiaoran Duan ◽  
Li Yang ◽  
Liuya Wang ◽  
Qinghua Liu ◽  
Kai Zhang ◽  
...  
Keyword(s):  
Esophageal Cancer ◽  
Cancer Progression ◽  
Poor Prognosis ◽  
Lipid Droplets ◽  
Target Gene ◽  
Potential Role ◽  
Theoretical Foundation ◽  
Rna Modification ◽  
Ec Cells

Abstract BackgroundEpitranscriptomics studies have contributed greatly to the development of research on human cancers. In recent years, N6-methyladenosine (m6A), an RNA modification on the N-6 position of adenosine, has been found to play a potential role in epigenetic regulation. Therefore, we aimed to evaluate the regulation of cancer progression properties by m6A. ResultsWe found that m6A demethylase fat mass and obesity-associated protein (FTO) was highly expressed in esophageal cancer (EC) stem-like cells, and that its level was also substantially increased in EC tissues, which was closely correlated with a poor prognosis in EC patients. FTO knockdown significantly inhibited the proliferation, invasion, stemness, and tumorigenicity of EC cells, whereas FTO overexpression promoted these characteristics. Furthermore, integrated transcriptome and meRIP-seq analyses revealed that HSD17B11 may be a target gene regulated by FTO. Moreover, FTO promoted the formation of lipid droplets in EC cells by enhancing HSD17B11 expression. Furthermore, depleting YTHDF1 increased the protein level of HSD17B11. ConclusionsThese data indicate that FTO may rely on the reading protein YTHDF1 to affect the translation pathway of the HSD17B11 gene to regulate the formation of lipid droplets in EC cells, thereby promoting the development of EC. The understanding of the role of epitranscriptomics in the development of EC will lay a theoretical foundation for seeking new anticancer therapies.

scholarly journals LINC00261 Inhibits Esophageal Cancer Radioresistance By Downregulating microRNA-552-3p And Promoting DIRAS1

2021 ◽  
Author(s):  
Baolong Yang ◽  
Hongbing Ma ◽  
Yan Bian
Keyword(s):  
Esophageal Cancer ◽  
Survival Fraction ◽  
Protein Coding ◽  
X Ray ◽  
Normal Tissues ◽  
Competing Endogenous Rna Network ◽  
Life Threatening ◽  
Ec Cells

Abstract Background: Esophageal cancer (EC) is a life-threatening tumor with a high increasing incidence rate. Long intergenic non-protein coding RNAs (LINCs) are widely researched in EC. This study set out to investigate the role of LINC00261 in EC radioresistance.Methods: Radioresistant EC cell lines TE-1-R and TE-5-R were established using TE-1 and TE-5 cells. LINC00261, microRNA (miR)-552-3p, and DIRAS1 expression in EC tissues and adjacent normal tissues and EC cells was evaluated. Then, survival fraction (SF), colony formation, apoptosis, and γ-H2AX expression were analyzed. The binding relation between LINC00261 and miR-552-3p and between miR-552-3p and DIRAS1 were detected. Eventually, xenograft transplantation was applied to confirm the effect of LINC00261 on EC radioresistance in vivo.Results: LINC00261 and DIRAS1 were weakly expressed in EC tissues and cells, but miR-552-3p was overexpressed. For EC cells with X-ray radiation, overexpression of LINC00261 reduced SF and cell viability, strengthened γ-H2AX expression, and promoted apoptosis, which were all counteracted by miR-522-3p overexpression or DIRAS1 silencing. Mechanically, the binding relation between LINC00261 and miR-552-3p and between miR-552-3p and DIRAS1 were verified. In addition, LINC00261 overexpression suppressed tumor growth and reduced EC radioresistance in vivo.Conclusion: LINC00261 could suppress EC radioresistance via the competing endogenous RNA network to sponge miR-552-3p and upregulate DIRAS1 transcription.

Flash Photolysis and ESR Studies on Hematoporphyrin and Photofrin II in Polar and Microheterogeneous Environment

1989 ◽  
Vol 44 (4) ◽  
pp. 283-290 ◽  
Author(s):  
Raimund Quint ◽  
Ruth Maria Quint ◽  
Nikola Getoff ◽  
Tsvetan Gantchev ◽  
Maria Shopova
Keyword(s):  
Triplet State ◽  
Singlet Oxygen ◽  
Absorption Spectra ◽  
Flash Photolysis ◽  
Reducing Agent ◽  
Photodynamic Treatment ◽  
Photofrin Ii

Hematoporphyrin (HP) and its derivatives (HPD; e.g. photofrin II) are used as efficient sensitizers in the photodynamic treatment of tumors. The photoinduced formation of various transients resulting from these substrates at pH 12 and 7.4 were studied by conventional flash photolysis and by ESR techniques in the presence of various additives. EDTA is acting as an efficient reducing agent for the triplet state of the substrates. The absorption spectra of some transients (HP·-, HP -OH, HPD·-, HPD -OH) were obtained. Further, ESR studies (pH 4-7) showed that 3HP is mostly converted into HP·- - in the presence of EDTA, but this is not the case with 3HPD. In airfree HPD solutions a longlived transient was registered, which was attributed to HPD·+ species. In aerated substrate solutions the singlet oxygen ( 1O2) and peroxyradicals are formed. The discussed transients very likely are involved in the photodynamic treatment of tumors in man.

scholarly journals MiR-25-3p targets PTEN to regulate the migration, invasion, and apoptosis of esophageal cancer cells via the PI3K/AKT pathway

2020 ◽  
Vol 40 (10) ◽  
Author(s):  
Liang Zhang ◽  
Zhuang Tong ◽  
Zhe Sun ◽  
Guolian Zhu ◽  
Erdong Shen ◽  
...  
Keyword(s):  
Esophageal Cancer ◽  
Target Gene ◽  
Opposite Effect ◽  
Caspase 3 ◽  
Malignant Tumors ◽  
Luciferase Reporter ◽  
Akt Pathway ◽  
Migration And Invasion ◽  
Ec Cells ◽  
Esophageal Cancer Cells

Abstract Background: Esophageal cancer (EC) is one of the most common malignant tumors of the digestive system. MiR-25-3p was proved to be a biomarker for the diagnosis and treatment of many cancers. MiR-25-3p was found to be high expressed in the blood of EC patients. The aim of the present study was to explore the effect of miR-25-3p and its target gene on EC. Methods: miR-25-3p expression in the blood of EC patients and EC cells was detected by RT-qPCR. The target of miR-25-3p was identified by bioinformatics and luciferase reporter assay. After transfection, cell viability, apoptosis, migration, and invasion were detected by MTT, flow cytometry, wound healing, and transwell assays, respectively. The expressions of PTEN, Bax, Bcl-2, cleaved Caspase-3, p-PI3K, PI3K, p-AKT, and AKT were detected by Western blot. Results: MiR-25-3p was high expressed in the blood of EC patients and EC cells. MiR-25-3p targeted PTEN and inhibited the expression of PTEN. MiR-25-3p mimic increased the viability, migration, invasion and the expressions of Bcl-2, and inhibited the apoptosis and the expression of Bax and cleaved caspase-3 in EC cells. MiR-25-3p mimic also enhanced the expressions of p-PI3K and p-AKT and the ratios of p-PI3K/PI3K and p-AKT/AKT in EC cells. PTEN overexpression not only had an opposite effect of miR-25-3p mimic, but also reversed the effect of miR-25-3p mimic on EC cells. Conclusion: MiR-25-3p targeted PTEN to promote the migration and invasion, and inhibit apoptosis of EC cells via the PI3K/AKT pathway, which might provide a new therapeutic target for EC treatment.

scholarly journals LINC00657/miR-26a-5p/CKS2 ceRNA network promotes the growth of esophageal cancer cells via the MDM2/p53/Bcl2/Bax pathway

2020 ◽  
Vol 40 (6) ◽  
Author(s):  
Xiao-Mei Zhang ◽  
Jian Wang ◽  
Zhu-Long Liu ◽  
Hong Liu ◽  
Yu-Feng Cheng ◽  
...  
Keyword(s):  
Esophageal Cancer ◽  
Molecular Mechanism ◽  
Migration And Invasion ◽  
Cerna Network ◽  
Transwell Invasion Assay ◽  
Tumorigenesis And Progression ◽  
Novel Biomarkers ◽  
Ec Cells ◽  
Induced Apoptosis ◽  
Esophageal Cancer Cells

Abstract LncRNA LINC00657 has oncogenic or anti-carcinoma roles in different cancers, and yet its detailed molecular mechanism in esophageal cancer (EC) remains unclear. In addition, competitive endogenous RNA (ceRNA) regulatory lncRNA–miRNA–mRNA networks are critical for tumorigenesis and progression. Hence, the present study explored the roles of LINC00657 in EC and identified its relevant ceRNA network. We first detected the expression of LINC00657 in EC. Then, we applied starBase and TargetScan websites to find miR-26a-5p binding to LINC00657 and obtain CKS2 as a target of miR-26a-5p. The roles of LINC00657, miR-26a-5p or CKS2 in the proliferation, migration, invasion, and apoptosis of EC cells were respectively assessed by CCK-8, wound healing assay, transwell invasion assay, and flow cytometry. The changes of the MDM2/p53/Bcl2/Bax pathway were measured via Western blot. The results revealed that LINC00657 showed an aberrant high expression in EC cells, which promoted the growth of EC cells. Additionally, LINC00657 functioned as a sponge of miR-26a-5p, and LINC00657 negatively mediated miR-26a-5p to regulate the growth of EC cells. Furthermore, CKS2 was observed as a direct target of miR-26a-5p, and CKS2 controlled the growth of EC cells via the MDM2/p53/Bcl2/Bax pathway. Moreover, there was a positive correlation between LINC00657 and CKS2. LINC00657 knockdown inhibited CKS2 expression to suppress the proliferation, migration, and invasion of EC cells and induced apoptosis via regulating the MDM2/p53/Bcl2/Bax pathway. Collectively, LINC00657/miR-26a-5p/CKS2 ceRNA network could promote the progression of EC, which is good for understanding the molecular mechanism of EC and offers novel biomarkers for EC diagnosis and therapy.

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