Utilizing ICG Spectroscopical Properties for Real-Time Nanoparticle Release Quantification In vitro and In vivo in Imaging Setups

2020 ◽  
Vol 26 (31) ◽  
pp. 3828-3833 ◽  
Author(s):  
Tuula Peñate-Medina ◽  
Eike Kraas ◽  
Kunliang Luo ◽  
Jana Humbert ◽  
Hanwen Zhu ◽  
...  
Keyword(s):  
Release Kinetics ◽  
Pure Water ◽  
Squamous Carcinoma ◽  
Peak Shift ◽  
Intensity Increase ◽  
Nude Mouse Model ◽  
Absorption And Emission ◽  
Squamous Carcinoma Cells

Background: Nanoparticle imaging and tracking the release of the loaded material from the nanoparticle system have attracted significant attention in recent years. If the release of the loaded molecules could be monitored reliably in vivo, it would speed up the development of drug delivery systems remarkably. Methods: Here, we test a system that uses indocyanine green (ICG) as a fluorescent agent for studying release kinetics in vitro and in vivo from the lipid iron nanoparticle delivery system. The ICG spectral properties like its concentration dependence, sensitivity and the fluctuation of the absorption and emission wavelengths can be utilized for gathering information about the change of the ICG surrounding. Results: We have found that the absorption, fluorescence, and photoacoustic spectra of ICG in lipid iron nanoparticles differ from the spectra of ICG in pure water and plasma. We followed the ICG containing liposomal nanoparticle uptake into squamous carcinoma cells (SCC) by fluorescence microscopy and the in vivo uptake into SCC tumors in an orthotopic xenograft nude mouse model under a surgical microscope. Conclusion: Absorption and emission properties of ICG in the different solvent environment, like in plasma and human serum albumin, differ from those in aqueous solution. Photoacoustic spectral imaging confirmed a peak shift towards longer wavelengths and an intensity increase of ICG when bound to the lipids. The SCC cells showed that the ICG containing liposomes bind to the cell surface but are not internalized in the SCC-9 cells after 60 minutes of incubation. We also showed here that ICG containing liposomal nanoparticles can be traced under a surgical camera in vivo in orthotopic SCC xenografts in mice.

SASS6 promotes proliferation of esophageal squamous carcinoma cells by inhibiting the p53 signaling pathway

2020 ◽  
Author(s):  
Yuanji Xu ◽  
Kunshou Zhu ◽  
Junqiang Chen ◽  
Liyan Lin ◽  
Zhengrong Huang ◽  
...  
Keyword(s):  
Esophageal Cancer ◽  
Protein Expression ◽  
Signaling Pathway ◽  
Squamous Carcinoma ◽  
Tumor Formation ◽  
Squamous Carcinoma Cells ◽  
P53 Signaling ◽  
P53 Signaling Pathway

Abstract SASS6 encodes for the Homo sapiens SAS-6 centriolar assembly protein and is important for proper centrosome formation. Although centrosomes are amplified in a wide variety of tumor types, abnormally high SASS6 expression had previously only been identified in colon cancer. Moreover, the role of SASS6 in esophageal squamous cell carcinoma (ESCC) pathogenesis has not yet been elucidated. The aim of this study was to investigate the role and mechanisms of SASS6 in ESCC. In this study, we found that the mRNA and protein levels of SASS6 were increased in human ESCC samples. In addition, SASS6 protein expression was associated with the esophageal cancer stage and negatively affected survival of patients with ESCC. Furthermore, silencing of SASS6 inhibited cell growth and promoted apoptosis of ESCC cells in vitro and inhibited xenograft tumor formation in vivo. A genetic cluster and pathway analysis showed that SASS6 regulated the p53 signaling pathway. Western blot demonstrated that CCND2, GADD45A and EIF4EBP1 protein expression decreased and that TP53 protein expression increased after the knockdown of SASS6 in ESCC cells. Therefore, SASS6 promoted the proliferation of esophageal cancer by inhibiting the p53 signaling pathway. SASS6 has potential as a novel tumor marker and a therapeutic target for ESCC.

scholarly journals Tumor protein D52 is upregulated in oral squamous carcinoma cells under hypoxia in a hypoxia-inducible-factor-independent manner and is involved in cell death resistance

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yuzo Abe ◽  
Yoshiki Mukudai ◽  
Mai Kurihara ◽  
Asami Houri ◽  
Junichiro Chikuda ◽  
...  
Keyword(s):  
Hypoxia Inducible Factor ◽  
Squamous Carcinoma ◽  
Cancer Therapeutics ◽  
Tumor Xenograft ◽  
Independent Manner ◽  
Protein Levels ◽  
Squamous Carcinoma Cells ◽  
Oral Squamous Carcinoma

Abstract Background Tumor protein D52 (TPD52) reportedly plays an important role in the proliferation and metastasis of various cancer cells, including oral squamous cell carcinoma (OSCC) cells, and is expressed strongly at the center of the tumor, where the microenvironment is hypoxic. Thus, the present study investigated the roles of TPD52 in the survival and death of OSCC cells under hypoxia, and the relationship with hypoxia-inducible factor (HIF). We examined the expression of TPD52 in OSCC cells under hypoxic conditions and analyzed the effects of HIF on the modulation of TPD52 expression. Finally, the combinational effects of TPD52 knockdown and HIF inhibition were investigated both in vitro and in vivo. Results The mRNA and protein levels of TPD52 increased in OSCC cells under hypoxia. However, the increase was independent of HIF transcription. Importantly, the observation was due to upregulation of mRNA stability by binding of mRNA to T-cell intercellular antigen (TIA) 1 and TIA-related protein (TIAR). Simultaneous knockdown of TPD52 and inhibition of HIF significantly reduced cell viability. In addition, the in vivo tumor-xenograft experiments showed that TPD52 acts as an autophagy inhibitor caused by a decrease in p62. Conclusions This study showed that the expression of TPD52 increases in OSCC cells under hypoxia in a HIF-independent manner and plays an important role in the proliferation and survival of the cells in concordance with HIF, suggesting that novel cancer therapeutics might be led by TPD52 suppression.

scholarly journals Tumor Protein D52 Is Upregulated in Oral Squamous Carcinoma Cells Under Hypoxia in a Hypoxia-inducible-factor-independent Manner and Is Involved in Cell Death Resistance

2021 ◽  
Author(s):  
Yuzo Abe ◽  
Yoshiki Mukudai ◽  
Mai Kurihara ◽  
Asami Houri ◽  
Junichiro Chikuda ◽  
...  
Keyword(s):  
Hypoxia Inducible Factor ◽  
Squamous Carcinoma ◽  
Cancer Therapeutics ◽  
Tumor Xenograft ◽  
Independent Manner ◽  
Protein Levels ◽  
Squamous Carcinoma Cells ◽  
Oral Squamous Carcinoma

Abstract Background. Tumor protein D52 (TPD52) reportedly plays an important role in the proliferation and metastasis of various cancer cells, including oral squamous cell carcinoma (OSCC) cells, and is expressed strongly at the center of the tumor, where the microenvironment is hypoxic. Thus, the present study investigated the roles of TPD52 in the survival and death of OSCC cells under hypoxia, and the relationship with hypoxia-inducible factor (HIF). We examined the expression of TPD52 in OSCC cells under hypoxic conditions and analyzed the effects of HIF on the modulation of TPD52 expression. Finally, the combinational effects of TPD52 knockdown and HIF inhibition were investigated both in vitro and in vivo.Results. The mRNA and protein levels of TPD52 increased in OSCC cells under hypoxia. However, the increase was independent of HIF transcription. Importantly, the observation was due to upregulation of mRNA stability by binding of mRNA to T-cell intercellular antigen (TIA) 1 and TIA-related protein (TIAR). Simultaneous knockdown of TPD52 and inhibition of HIF significantly reduced cell viability. In addition, the in vivo tumor-xenograft experiments showed that TPD52 acts as an autophagy inhibitor caused by a decrease in p62.Conclusions. This study showed that the expression of TPD52 increases in OSCC cells under hypoxia in a HIF-independent manner and plays an important role in the proliferation and survival of the cells in concordance with HIF, suggesting that novel cancer therapeutics might be led by TPD52 suppression.

Anti-PD-L1-modified and ATRA-loaded nanoparticles for immuno-treatment of oral dysplasia and oral squamous cell carcinoma

Nanomedicine ◽  
2020 ◽  
Vol 15 (10) ◽  
pp. 951-968 ◽  
Author(s):  
Xiao-Jie Chen ◽  
Xue-Qiong Zhang ◽  
Ming-Xiu Tang ◽  
Qi Liu ◽  
Gang Zhou
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Squamous Carcinoma ◽  
Oral Dysplasia ◽  
Squamous Carcinoma Cells ◽  
Induced Apoptosis

Aim: To develop nanomedicines for immuno-therapy of oral dysplasia and oral squamous cell carcinoma. Materials & methods: All-trans retinoic acid (ATRA)-poly(lactide-co-glycolide acid) (PLGA)-poly(ethylene glycol) (PEG)-programmed death-ligand 1 (PD-L1) nanomedicines were fabricated by loading ATRA into PLGA-PEG nanocarriers and modification using an anti-PD-L1 antibody. Results: ATRA-PLGA-PEG-PD-L1 nanoparticles showed fast cellular uptake, significantly inhibited proliferation and induced apoptosis in DOK and CAL27 cells. Moreover, in C3H tumor-bearing mice, ATRA-PLGA-PEG-PD-L1 nanoparticles more specifically targeted tumor cells, enhanced anticancer activity and reduced side effects when compared with free ATRA. Furthermore, CD8+ T cells were activated around PD-L1 positive cells in the tumor microenvironment after treatment. Conclusion: ATRA-PLGA-PEG-PD-L1 nanoparticles had low toxicity, high biocompatibility and specifically targeted oral dysplasia and squamous carcinoma cells both in vitro and in vivo.

MicroRNA-378-3p/5p suppresses the migration and invasiveness of oral squamous carcinoma cells by inhibiting KLK4 expression

2020 ◽  
Vol 98 (2) ◽  
pp. 154-163
Author(s):  
Zhi Cui ◽  
Shiqun Sun ◽  
Qilin Liu ◽  
Xuechun Zhou ◽  
Siyu Gao ◽  
...  
Keyword(s):  
Epithelial Mesenchymal Transition ◽  
Squamous Carcinoma ◽  
Effective Measure ◽  
Mesenchymal Transition ◽  
Squamous Carcinoma Cells ◽  
Oral Squamous Carcinoma ◽  
In Cells

Distant metastasis frequently occurs in oral squamous cell carcinoma (OSCC) and contributes to the adverse prognosis for patients with OSCC. However, the potential mechanisms behind the metastasis have not yet been clarified. This study investigated the role of miR-378 in the migration and invasiveness of OSCC in vitro and in vivo. According to our results, the migration and invasiveness of OSCC cells were increased in cells overexpressing miR-378, and reduced in cells where miR-378-3p/5p was silenced. In addition, overexpression of miR-378 suppressed the expressions and activities of matrix metalloproteinase 9 (MMP-9) and MMP-2. Epithelial–mesenchymal transition (EMT) was restrained by overexpression of miR-378, as evidenced by an increase in E-cadherin expression and decrease in N-cadherin and uPA expression. However, knockdown of miR-378-3p/5p produced the opposite results. Moreover, kallikrein-related peptidase 4 (KLK4) was confirmed to be a target gene of miR-378. Overexpression of KLK4 reversed the induced decrease in migration and invasiveness of cells overexpressing miR-378 by upregulating the levels of MMP-9, MMP-2, and N-cadherin, and downregulating the level of E-cadhrin. Finally, the number of metastasis nodules in the lung tissues of nude mice was reduced by overexpression of miR-378, whereas the number of metastases increased with knockdown of miR-378. Taken together, our results suggest that the miR-378–KLK4 axis is involved in the mechanisms behind the migration and invasiveness of OSCC cells. Targeting the miR-378–KLK4 axis may be an effective measure for treating OSCC.

Flavokawain B inhibits growth of human squamous carcinoma cells: Involvement of apoptosis and cell cycle dysregulation in vitro and in vivo

2012 ◽  
Vol 23 (4) ◽  
pp. 368-378 ◽  
Author(s):  
Elong Lin ◽  
Wen-Hsin Lin ◽  
Sheng-Yang Wang ◽  
Chih-Sheng Chen ◽  
Jiuun-Wang Liao ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Squamous Carcinoma ◽  
Carcinoma Cells ◽  
Squamous Carcinoma Cells

scholarly journals Apoptotic Effects of Diosgeninlactoside on Oral Squamous Carcinoma Cells in Vitro and in Vivo

2014 ◽  
Vol 37 (9) ◽  
pp. 1450-1459 ◽  
Author(s):  
Xu Wang ◽  
Chongkui Sun ◽  
Shiliang He ◽  
Xiurong Guo ◽  
Hao Xu ◽  
...  
Keyword(s):  
Squamous Carcinoma ◽  
Carcinoma Cells ◽  
Squamous Carcinoma Cells ◽  
Oral Squamous Carcinoma ◽  
Apoptotic Effects

scholarly journals Interplay between Podoplanin, CD44s and CD44v in Squamous Carcinoma Cells

Cells ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 2200 ◽  
Author(s):  
Lucía Montero-Montero ◽  
Jaime Renart ◽  
Andrés Ramírez ◽  
Carmen Ramos ◽  
Mariam Shamhood ◽  
...  
Keyword(s):  
Cell Lines ◽  
Carcinoma Cell ◽  
Mouse Skin ◽  
Squamous Carcinoma ◽  
Chemical Carcinogenesis ◽  
Cd44 Variant ◽  
Variant Isoforms ◽  
Squamous Carcinoma Cells

Podoplanin and CD44 are transmembrane glycoproteins involved in inflammation and cancer. In this paper, we report that podoplanin is coordinately expressed with the CD44 standard (CD44s) and variant (CD44v) isoforms in vivo—in hyperplastic skin after a pro-inflammatory stimulus with 12-O-tetradecanoylphorbol-13-acetate (TPA)—and in vitro—in cell lines representative of different stages of mouse-skin chemical carcinogenesis, as well as in human squamous carcinoma cell (SCC) lines. Moreover, we identify CD44v10 in the mouse-skin carcinogenesis model as the only CD44 variant isoform expressed in highly aggressive spindle carcinoma cell lines together with CD44s and podoplanin. We also characterized CD44v3-10, CD44v6-10 and CD44v8-10 as the major variant isoforms co-expressed with CD44s and podoplanin in human SCC cell lines. Immunofluorescence confocal microscopy experiments show that these CD44v isoforms colocalize with podoplanin at plasma membrane protrusions and cell–cell contacts of SCC cells, as previously reported for CD44s. Furthermore, CD44v isoforms colocalize with podoplanin in chemically induced mouse-skin SCCs in vivo. Co-immunoprecipitation experiments indicate that podoplanin physically binds to CD44v3-10, CD44v6-10 and CD44v8-10 isoforms, as well as to CD44s. Podoplanin–CD44 interaction is mediated by the transmembrane and cytosolic regions and is negatively modulated by glycosylation of the extracellular domain. These results point to a functional interplay of podoplanin with both CD44v and CD44s isoforms in SCCs and give insight into the regulation of the podoplanin–CD44 association.

Phototherapy with Argon Lasers and Rhodamine-123 for Tumor Eradication

1988 ◽  
Vol 98 (6) ◽  
pp. 581-588 ◽  
Author(s):  
Dan J. Castro ◽  
Romaine E. Saxton ◽  
Harold R. Fetterman ◽  
Donna J. Castro ◽  
Paul H. Ward
Keyword(s):  
Laser Treatment ◽  
Test Group ◽  
Squamous Carcinoma ◽  
Argon Laser ◽  
Carcinoma Cells ◽  
Rhodamine 123 ◽  
Complete Regression ◽  
Squamous Carcinoma Cells

The effectiveness of Rhodamine-123 (Rh-123) as a new photochemosensitizing agent for the argon laser treatment of human melanoma and squamous carcinoma cells in vitro was recently demonstrated. In this study, a new technique of “rosette” treatment with the argon laser was developed to completely eradicate human squamous carcinoma (P3) tumor transplants in nude mice after chemosensitization with Rh-123. Each group included four nu/nu mice injected subcutaneously with 107 P3 carcinoma cells/site for a total of 48 sites. Tumor take was >95% at one week, with >10 mm3 tumor volume at each site. Test groups were sensitized with Rh-123 (1 μg/ml for 1 hour) by intratumor or intraperitoneal injection at 1 week and then treated with the argon laser at 514.5 nm. To allow uniform delivery of energies to the tumor and its edges, a new “rosette” technique was developed. The tumors were then exposed to nonthermal levels of 700 J/cm2 (36°C) or 950 J/cm2 (40°C) as determined by a new and reproducible method of dosimetry. All 16 tumors in this test group showed complete regression with excellent wound healing at 2 weeks and no recurrences, even after an 8 week followup. These results demonstrate that effective eradication of tumors can be achieved in vivo only after sensitization with Rh-123 and specific argon laser treatment (“rosette”), even at nonthermal levels of energies. The high effectiveness of this technique and low toxicity of Rh-123 may render its clinical use very attractive for the treatment of superficial malignancies.

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