Therapeutic effect of quantum dots for cancer treatment

RSC Advances ◽  
2016 ◽  
Vol 6 (114) ◽  
pp. 113791-113795 ◽  
Author(s):  
Mei-Xia Zhao ◽  
Bing-Jie Zhu ◽  
Wen-Jing Yao ◽  
Di-Feng Chen
Keyword(s):  
Quantum Dots ◽  
Tumor Growth ◽  
Cancer Treatment ◽  
Therapeutic Effect ◽  
Cell Apoptosis

The therapeutic effect of Qdots for cancer treatment arises from ROS-induced cell apoptosis and inhibited tumor growth in vivo.

scholarly journals A New Nanomaterial Based on Extracellular Vesicles Containing Chrysin-Induced Cell Apoptosis Through Let-7a in Tongue Squamous Cell Carcinoma

2021 ◽  
Vol 9 ◽  
Author(s):  
Zhijing Yang ◽  
Da Liu ◽  
Hengzong Zhou ◽  
Boqiang Tao ◽  
Lu Chang ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Tumor Growth ◽  
Cell Carcinoma ◽  
Therapeutic Effect ◽  
Extracellular Vesicles ◽  
Squamous Cell ◽  
Cell Apoptosis ◽  
Tongue Squamous Cell Carcinoma ◽  
Apoptosis Pathway

Although the therapeutic strategy showed significant improvement, the therapeutic effect was poor on metastases in tongue squamous cell carcinoma (TSCC) which is the most malignant tumor found in the head and neck. Chrysin, similar to the flavonoids, plays an antitumor role by regulating the expression of ncRNAs in many kinds of cancers. Compared to flavonoids, gold nanoparticles (AuNPs) provide a novel insight into inhibiting cancer cell growth via photothermal therapy (PPT) which is irradiated by near-infrared radiation (NIR). However, most flavonoids and AuNPs lack specificity of tumor in vivo. The extracellular vesicles (EVs) which were abundant with ncRNAs are isolated from the cellular supernatant fluid and have the ability to carry drugs or nanoparticles to improve specificity. In the present study, we aimed to synthesize a new nanomaterial based on EVs containing chrysin and analyzed cell apoptosis in TSCC cells. Our results demonstrated that EVs-chrysin were isolated from SCC9 cells that were treated with chrysin. To improve the therapeutic effect, AuNPs were carried by EVs-chrysin (Au-EVs). Compared to BGC823 and HCC-LM3 cells, the uptake of Au-EVs was specific in SCC9 cells. Moreover, Au-EVs combined with NIR enhanced cell apoptosis in TSCC cells. To confirm the role of miRNAs in cell apoptosis, the differentially expressed miRNAs between EVs-Con and EVs-chrysin were screened by RNA-seq. The results revealed that the let-7a-3p family, which acts as the tumor suppressor, was upregulated in EVs-chrysin compared to EVs-Con. Thus, let-7a-3p was screened in the apoptosis pathway that was associated with the p53 protein. Furthermore, compared to the Con group, Au-EVs combined with the NIR group effectively inhibited tumor growth in vivo via increasing the expression of let-7a-3p. Together, as a new nanomaterial, Au-EVs induced cell apoptosis and inhibited tumor growth by regulating let-7a-3p expression in TSCC.

Glial-specific retrovirally mediated gas1 gene expression induces glioma cell apoptosis and inhibits tumor growth in vivo

2004 ◽  
Vol 15 (3) ◽  
pp. 483-491 ◽  
Author(s):  
Absalom Zamorano ◽  
Britt Mellström ◽  
Paula Vergara ◽  
José R Naranjo ◽  
José Segovia
Keyword(s):  
Gene Expression ◽  
Tumor Growth ◽  
Cell Apoptosis ◽  
Glioma Cell

scholarly journals Artesunate induces mitochondria-mediated apoptosis of human retinoblastoma cells by upregulating Kruppel-like factor 6

2019 ◽  
Vol 10 (11) ◽  
Author(s):  
Ying Yang ◽  
Nandan Wu ◽  
Yihui Wu ◽  
Haoting Chen ◽  
Jin Qiu ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Cell Apoptosis ◽  
Underlying Mechanism ◽  
Dependent Manner ◽  
Chemotherapeutic Drug ◽  
Sprague Dawley ◽  
Fundus Fluorescein Angiography ◽  
Intravitreal Chemotherapy ◽  
Vitreous Seeds

Abstract Retinoblastoma (RB) is the most common primary intraocular malignancy in children. Intravitreal chemotherapy achieves favorable clinical outcomes in controlling RB vitreous seeds, which are a common reason for treatment failure. Thus, a novel, effective and safe intravitreal chemotherapeutic drug is urgently required. The malaria drug artesunate (ART) recently demonstrated remarkable anticancer effects with mild side effects. The purpose of this study is to investigate the anti-RB efficacy, the underlying mechanism and the intraocular safety of ART. Herein, we verified that ART inhibits RB cell viability and induces cell apoptosis in a dose- and time-dependent manner. Microarray analysis revealed that Kruppel-like factor 6 (KLF6) was upregulated after ART treatment, and this was further confirmed by real-time PCR and western blot assays. Silencing of KLF6 expression significantly reversed ART-induced RB cell growth inhibition and apoptosis. Furthermore, ART activated mitochondria-mediated apoptosis of RB cells, while silencing KLF6 expression significantly inhibited this effect. In murine xenotransplantation models of RB, we further confirmed that ART inhibits RB tumor growth, induces tumor cell apoptosis and upregulates KLF6 expression. In addition, KLF6 silencing attenuates ART-mediated inhibition of tumor growth in vivo. Furthermore, we proved that intravitreal injection of ART in Sprague-Dawley (SD) rats is safe, with no obvious retinal function damage or structural disorders observed by electrophysiology (ERG), fundal photographs, fundus fluorescein angiography (FFA) or optical coherence tomography (OCT) examinations. Collectively, our study revealed that ART induces mitochondrial apoptosis of RB cells via upregulating KLF6, and our results may extend the application of ART to the clinic as an effective and safe intravitreal chemotherapeutic drug to treat RB, especially RB with vitreous seeds.

scholarly journals MicroRNA-140-5p inhibits salivary adenoid cystic carcinoma progression and metastasis via targeting survivin

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Zhu Qiao ◽  
Yue Zou ◽  
Hu Zhao
Keyword(s):  
Cell Proliferation ◽  
Tumor Growth ◽  
Cell Apoptosis ◽  
Luciferase Reporter ◽  
Survivin Mrna ◽  
Reporter Assay ◽  
Salivary Adenoid Cystic Carcinoma ◽  
Adenoid Cystic ◽  
Proliferation And Invasion

Abstract Background Salivary adenoid cystic carcinoma (SACC) is one of the most frequent carcinomas derived from the salivary gland. Growing evidence implied the involvement of microRNAs (miRNAs) in SACC progression and metastasis. This study aimed to determine the regulatory role of miR-140-5p in SACC progression and metastasis and to explore the underlying mechanisms. Materials and methods MiR-140-5p and survivin mRNA expression levels were determined by quantitative real-time PCR; protein levels were evaluated by western blot assay; cell proliferation, growth, invasion, apoptosis and caspase-3 activity were evaluated by respective in vitro functional assays; xenograft nude mice model was used to assess the in vivo tumor growth; a luciferase reporter assay determined the interaction between miR-140-5p and survivin. Results MiR-140-5p overexpression suppressed SACC cell proliferation and invasion, induced cell apoptosis and inhibited in vivo tumor growth of SACC cells. The loss-of-function studies showed that miR-140-5p knockdown enhanced SACC cell proliferation and invasion, inhibited cell apoptosis and led to an accelerated in vivo tumor growth. The bioinformatics prediction and luciferase reporter assay revealed that miR-140-5p directly targeted survivin 3′ untranslated region, and survivin was inversely regulated by miR-140-5p. Knockdown of survivin exerted tumor-suppressive effects on SACC cells, while enforced expression of survivin counteracted the tumor-suppressive actions of miR-140-5p overexpression in SACC cells. Mechanistically, miR-140-5p modulated the protein expression levels of apoptosis- and epithelial-mesenchymal transition-related mediators as well as matrix metallopeptidase-2/-9 via targeting survivin. More importantly, the down-regulation of miR-140-5p and the up-regulation of survivin were detected in the SACC clinical tissues, and miR-140-5 expression was inversely correlated with survivin mRNA expression level in SACC tissues. Conclusion Our data indicated that miR-140-5p suppressed SACC cell proliferation and invasion, induced cell apoptosis via regulating survivin expression. The present study provide evidence that that miR-140-5p could be a promising target for treating SACC, which requires further investigations.

The Application of CRISPR/Cas9 System in Cervical Precancerous Lesions

2020 ◽  
Author(s):  
Chun Gao ◽  
Ping Wu ◽  
Lan Yu ◽  
Liting Liu ◽  
Hong Liu ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Transgenic Mice ◽  
Therapeutic Effect ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cell Apoptosis ◽  
Precancerous Lesions ◽  
Cervical Carcinogenesis ◽  
Cervical Precancerous Lesions

Abstract Background : The clustered regularly interspaced short palindromic repeat (CRISPR)/Cas9 system is becoming a promising gene therapy method. Herein, we evaluated the therapeutic effect of CRISPR/Cas9 system in cervical carcinogenesis, especially cervical precancerous lesions. Methods : In cervical cancer/pre-cancer cell lines, we transfected the CRISPR/Cas9, transcription activator–like effector nuclease (TALEN), and zinc finger nuclease (ZFN) plasmids, respectively. We used the cell apoptosis, cell viability, and colony formation assays to examine the efficiency and specificity of inhibition of cell apoptosis and growth between the different gene editing tools. Western blotting was used to estimate the related protein expression. We used xenograft formation assays to examine the ability of inhibition of cell growth in vivo. In the K14-HPV16 transgenic mice model of HPV-driven cervical carcinogenesis, we investigated the therapeutic effect by vaginal administration. Results : Compared to ZFN and TALEN, CRISPR/Cas9 has shown comparable efficiency and specificity of inhibition of cell apoptosis and growth in cervical cancer cell lines, which seem to be more pronounced in the S12 cell line derived from the low-grade cervical lesion. In xenograft formation assays, CRISPR/Cas9 could inhibit tumor formation in vivo and affects the expression of the corresponding protein. In the K14-HPV16 transgenic mice, CRISPR/Cas9 treatment caused mutations of the E7 gene and restored the expression of RB, E2F1, and CDK2, thereby reversing the cervical carcinogenesis phenotype. Conclusion : In this study, we have demonstrated that CRISPR/Cas9 targeting HPV16 E7 could effectively reduce the expression of E7 protein in vitro. Additionally, it could revert the HPV-related cervical carcinogenesis in K14-HPV16 transgenic mice, which has shown great potential in clinical treatment.

scholarly journals Overcoming chemotherapy resistance using pH-sensitive hollow MnO2 nanoshells that target the hypoxic tumor microenvironment of metastasized oral squamous cell carcinoma

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Zhi-hang Zhou ◽  
Si-yuan Liang ◽  
Tong-chao Zhao ◽  
Xu-zhuo Chen ◽  
Xian-kun Cao ◽  
...  
Keyword(s):  
Controlled Release ◽  
Therapeutic Effect ◽  
Cell Apoptosis ◽  
Metastatic Cancer ◽  
Hypoxia Inducible Factor ◽  
Tumor Hypoxia ◽  
Control Group ◽  
Hypoxia Inducible Factor 1Α

Abstract Background Smart nanoscale drug delivery systems that target acidic tumor microenvironments (TME) could offer controlled release of drugs and modulate the hypoxic TME to enhance cancer therapy. The majority of previously reported MnO2 nanostructures are nanoparticles, nanosheets, or nanocomposites incorporated with other types of nanoparticles, which may not offer the most effective method for drug loading or for the controlled release of therapeutic payloads. Previous studies have designed MnO2 nanoshells that achieve tumor-specific and enhanced combination therapy for localized advanced cancer. However, the therapeutic effect of MnO2 nanoshells on metastatic cancer is still uncertain. Result Here, intelligent “theranostic” platforms were synthesized based on hollow mesoporous MnO2 (H-MnO2) nanoshells that were loaded with chemotherapy agents docetaxel and cisplatin (TP) to form H-MnO2-PEG/TP nanoshells, which were designed to alleviate tumor hypoxia, attenuate angiogenesis, trigger the dissolution of Mn2+, and synergize the efficacy of first-class anticancer chemotherapy. The obtained H-MnO2-PEG/TP nanoshells decomposed in the acidic TME, releasing the loaded drugs (TP) and simultaneously attenuated tumor hypoxia and hypoxia-inducible factor-1α (HIF-1α) expression by inducing endogenous tumor hydrogen peroxide (H2O2) decomposition. In vitro experiments showed that compared with the control group, the proliferation, colony formation and migration ability of CAL27 and SCC7 cells were significantly reduced in H-MnO2-PEG/TP group, while cell apoptosis was enhanced, and the expression of hypoxia-inducible factor-1α(HIF-1α) was down-regulated. In vivo experiments showed that tumor to normal organ uptake ratio (T/N ratio) of mice in H-MnO2-PEG/TP group was significantly higher than that in TP group alone (without the nanoparticle), and tumor growth was partially delayed. In the H-MnO2-PEG/TP treatment group, HE staining showed that most of the tumor cells were severely damaged, and TUNEL assay showed cell apoptosis was up-regulated. He staining of renal and liver sections showed no obvious fibrosis, necrosis or hypertrophy, indicating good biosafety. Fluorescence staining showed that HIF-1α expression was decreased, suggesting that the accumulation of MnO2 in the tumor caused the decomposition of H2O2 into O2 and alleviated the hypoxia of the tumor. Conclusion In conclusion, a remarkable in vivo and in vitro synergistic therapeutic effect is achieved through the combination of TP chemotherapy, which simultaneously triggered a series of antiangiogenic and oxidative antitumor reactions. Graphic abstract

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