scholarly journals Anti-EGFR-Coated Gold Nanoparticles In Vitro Carry 5-Fluorouracil to Colorectal Cancer Cells

Materials ◽  
2020 ◽  
Vol 13 (2) ◽  
pp. 375 ◽  
Author(s):  
Raquel B. Liszbinski ◽  
Graziela G. Romagnoli ◽  
Carolina M. Gorgulho ◽  
Caroline R. Basso ◽  
Valber A. Pedrosa ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Gold Nanoparticles ◽  
Cancer Cells ◽  
Cell Lines ◽  
Antineoplastic Agent ◽  
Physicochemical Characterization ◽  
Colorectal Cancer Cells ◽  
Induced Apoptosis ◽  
20 Nm

The aim of the current study is to present a strategy to improve the efficiency of 5-fluorouracil (5-FU), which is widely used as antineoplastic agent against solid tumors-based on the use of gold nanocarriers to overcome the resistance of colorectal cancer cells. 5-FU was loaded on gold nanoparticles (AuNP) coated with anti-EGFR antibodies in order to target them towards colorectal cancer cells that overexpress epidermal growth factor receptors (EGFR). Physicochemical characterization has shown that AuNP size was approximately 20 nm and that AuNP functionalization led to spherical nanoparticles. Flow cytometry allowed observing that some compounds synthesized by our research group have induced apoptosis/necrosis and impaired the proliferation of colon cancer cell lines ‘HCT-116′ and ‘HT-29′. The antibody/drug combination in AuNP (AuNP 5FU EGFR) has improved the apoptosis rate and impaired cell proliferation in both cell lines, regardless of the exposure time. Overall, these results have shown that AuNP functionalization with monoclonal antibodies focused on delivering 5-FU to tumor cells is an exciting strategy against colorectal cancer.

Transfection of PDCD5 sensitizes colorectal cancer cells to cisplatin-induced apoptosis in vitro and in vivo

2010 ◽  
Vol 649 (1-3) ◽  
pp. 120-126 ◽  
Author(s):  
Anning Yin ◽  
Yingan Jiang ◽  
Xianfeng Zhang ◽  
Juan Zhao ◽  
Hesheng Luo
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Colorectal Cancer Cells ◽  
Induced Apoptosis

scholarly journals IL-24-armed oncolytic vaccinia virus exerts potent antitumor effects via multiple pathways in colorectal cancer

2020 ◽  
Author(s):  
Lili Deng ◽  
Xue Yang ◽  
Jun Fan ◽  
Yuedi Ding ◽  
Ying Peng ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Vaccinia Virus ◽  
Cancer Cells ◽  
Treatment Options ◽  
Antitumor Effects ◽  
Colorectal Cancer Cells ◽  
Cancer Tumor ◽  
Induced Apoptosis

Colorectal cancer is an aggressive malignancy for which there are limited treatment options. Oncolytic vaccinia virus isbeing developed as a novel strategy for cancer therapy. Arming vaccinia virus with immunostimulatory cytokines can enhance the tumor cell-specific replication and antitumor efficacy. Interleukin-24 (IL-24) is an important immune mediator, as well as a broad-spectrum tumor suppressor. Here, we constructed a targeted vaccinia virus of Guang9 strain harbored IL-24 (VG9-IL-24) to evaluate its antitumor effects. In vitro, VG9-IL-24 induced increased number of apoptotic cells and blocked colorectal cancer cells in the G2/M phase of the cell cycle. VG9-IL-24 induced apoptosis in colorectal cancer cells via multiple apoptotic signaling pathways. In vivo,VG9-IL-24 significantly inhibited the tumor growth and prolonged the survival both in human and murine colorectal cancer models. Besides, VG9-IL-24 stimulated multiple antitumor immune responses and direct bystander antitumor activity. Our results indicate that VG9-IL-24 can inhibit the growth of colorectal cancer tumor by inducing oncolysis and apoptosis as well as stimulating the anti-tumor immune effects. These findings indicate that VG9-IL-24 may exert a potential therapeutic strategy for combating colorectal cancer

scholarly journals Exploiting the Efficacy of Tyro3 and Folate Receptors to Enhance the Delivery of Gold Nanoparticles into Colorectal Cancer Cells In Vitro

2020 ◽  
Author(s):  
Nakul Nautam Patel ◽  
Lucy Ghali ◽  
Ivan Roitt ◽  
Leonardo Pantoja Munoz ◽  
Richard Bayford
Keyword(s):  
Colorectal Cancer ◽  
Gold Nanoparticles ◽  
Cancer Cells ◽  
Folate Receptor ◽  
Tyrosine Kinase Receptor ◽  
Folate Receptors ◽  
Common Cancer ◽  
Colorectal Cancer Cells ◽  
Different Types

Abstract Colorectal cancer (CRC) is the fourth most common cancer in the world. Due to its asymptomatic nature, CRC is diagnosed at an advanced stage where the survival rate is <5%. Besides, prognosis from CRC treatment using chemotherapy, radiotherapy and surgery often causes undesirable side-effects. As such, gold nanoparticles (GNPs) are envisaged in the field for the diagnosis and treatment of CRC. GNPs have unique physical, chemical and electrical properties at nanoscale which makes them suitable for application in biomedicine. However, for GNPs to become clinically effective, its internalisation efficiency in the cancer cells must be enhanced. Folate receptor-α (FR) are overexpressed in CRC wherein FR helps in uptake of folic acid within the cell. Tyro3, a novel tyrosine kinase receptor, drives cell proliferation and its overexpression is correlated with poor prognosis in CRC. Their upregulated expression in CRC cells relative to normal cells makes them an ideal target for GNPs using active targeting. Therefore, in this study receptors FR and Tyro3 were simultaneously targeted using specific antibody-coated GNPs in order to enhance uptake and internalisation of GNPs in CRC cells in vitro. Four different types of coated-GNPs were synthesised GNPs-PEG, GNPs-anti-FR, GNPs-anti-Tyro3 and GNPs-anti-(FR+Tyro3) and incubated (0ng – 50ng) with three CRC cell lines including CRL1790, CRL2159 and HCT116. Simultaneous targeting of these receptors by GNPs-anti-(FR+Tyro3) was found to be the most effective in internalisation in CRC cells compared with GNPs targeted singly to FR or Tyro3 (p<0.05). Besides this, results show that Tyro3 mediated similar internalisation efficacy as FR (p<0.05) in CRC using ICP-OES.

scholarly journals Preparation and Characterization of Self Nano-Emulsifying Drug Delivery System Loaded with Citraland Its Antiproliferative Effect on Colorectal Cells In Vitro

Nanomaterials ◽  
2019 ◽  
Vol 9 (7) ◽  
pp. 1028 ◽  
Author(s):  
Mira Nadiah Mohd Izham ◽  
Yazmin Hussin ◽  
Muhammad Nazirul Mubin Aziz ◽  
Swee Keong Yeap ◽  
Heshu Sulaiman Rahman ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Drug Delivery ◽  
Cancer Cells ◽  
Drug Delivery System ◽  
Delivery System ◽  
Average Particle Size ◽  
Physicochemical Characterization ◽  
Average Particle ◽  
Colorectal Cancer Cells

Citral is an active compound naturally found in lemongrass, lemon, and lime. Although this pale-yellow liquid confers low water solubility, the compound has been reported to possess good therapeutic features including antiproliferative and anticancer modalities. The self nano-emulsifying drug delivery system (SNEDDS) is a type of liquid-lipid nanocarrier that is suitable for the loading of insolubilized oil-based compound such as Citral. This study reports the design and optimization of a SNEDDS formulation, synthesis and characterization as well as loading with Citral (CIT-SNEDDS). Further assessment of theantiproliferative effects of CIT-SNEDDS towards colorectal cancer cells was also conducted. SNEDDS composed of coconut oil, dimethyl sulfoxide (DMSO) and Tween 80. CIT-SNEDDS was prepared via gentle agitation of SNEDDS with 0.5% Citral for 72 h at room temperature. Physicochemical characterization was performed using several physicochemical analyses. The average particle size of CIT-SNEDDS was16.86 ± 0.15 nm, zeta potential of 0.58 ± 0.19 mV, and polydispersity index (PDI) of 0.23 ± 0.01. In vitro drug release of Citral from CIT-SNEDDS was 79.25% of release, and for Citral the release percentage was 93.56% over 72 h. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was done to determine the cytotoxicity effect of CIT-SNEDDS in human colorectal cancer cell lines HT29 and SW620. The half maximal inhibitory concentrations (IC50) for 72 hof CIT-SNEDDS and Citral on SW620 were 16.50 ± 0.87 µg/mL and 22.50 ± 2.50 µg/mL, respectively. The IC50 values of CIT-SNEDDS and Citral after 72 h of treatment on HT29 were 34.10 ± 0.30 µg/mL and 21.77 ± 0.23 µg/mL, respectively. This study strongly suggests that CIT-SNEDDS has permitted the sustained release of Citral and that CIT-SNEDDS constitutes a potential soluble drug nanocarrier that is effective against colorectal cancer cells.

N,N-Ru(ii)-p-cymene-poly(N-vinylpyrrolidone) surface functionalized gold nanoparticles: from organoruthenium complex to nanomaterial for antiproliferative activity

2021 ◽  
Author(s):  
Durairaj Gopalakrishnan ◽  
S. Saravanan ◽  
Ronald Merckx ◽  
Arumugam Madan Kumar ◽  
Themmila Khamrang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Gold Nanoparticles ◽  
Anticancer Activity ◽  
Cancer Cells ◽  
Antiproliferative Activity ◽  
First Report ◽  
Functionalized Gold Nanoparticles ◽  
Arene Complex ◽  
Colorectal Cancer Cells

The first report of a Ru(arene)metallopolymer–gold nanoconjugate to enhance the in vitro anticancer activity of Ru–arene complex in colorectal cancer cells.

scholarly journals Knockdown of Mir-135b Sensitizes Colorectal Cancer Cells to Oxaliplatin-Induced Apoptosis Through Increase of FOXO1

2018 ◽  
Vol 48 (4) ◽  
pp. 1628-1637 ◽  
Author(s):  
Yan Qin ◽  
Longhai Li ◽  
Fang Wang ◽  
Xinyi Zhou ◽  
Yankui Liu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Cell Lines ◽  
Luciferase Reporter ◽  
Pcr Analysis ◽  
Aberrant Expression ◽  
Colorectal Cancer Cells ◽  
Novel Strategy ◽  
Induced Apoptosis

Background/Aims: Aberrant expression of microRNAs (miRNAs) is found to be responsible for tumorigenesis, cancer development and chemoresistance. Although oxaliplatin is an effective chemotherapeutic drug for treatment of colorectal cancer (CRC), CRC cells can develop some mechanisms to evade oxaliplatin-induced cell death. It is urgent to explore the novel strategies to increase the chemosensitivity of CRC cells. Methods: QRT-PCR analysis was performed to detect the expression of miR-135b in CRC patients’ serum and CRC cell lines. MTT assays were used to evaluate the effect of anti-miR-135b on oxaliplatin-induced cell death in CRC cell lines. Western blot, flow cytometry and luciferase reporter assays were performed to evaluate the potential mechanism and pathway of anti-miR-135b-promoted apoptosis in oxaliplatin-treated CRC cells. Results: Significant upregulation of miR-135b was observed in CRC cell lines and CRC patients’ serum. Knockdown of miR-135b was found to sensitize colorectal cancer cells to oxaliplatin-induced cytotoxicity. Mechanically, knockdown of miR-135b increased the expression level of FOXO1 in CRC. As the downstream, the increased FOXO1 induced by anti-miR-135b promoted the expression of Bim and Noxa. Since Bim and Noxa act as key pro-apoptotic proteins in mitochondrial apoptosis, anti-miR-135b was able to enhance the oxaliplatin-induced apoptosis dependent on the anti-miR-135b/FOXO1 axis. Conclusions: Anti-miR-135b enhanced the anti-tumor effect of oxaliplatin on CRC. Combination with miR-135b antisense nucleotides may represent a novel strategy to sensitize CRC to oxaliplatin-based treatment.

scholarly journals Downregulation of miR-423-5p Contributes to the Radioresistance in Colorectal Cancer Cells

2021 ◽  
Vol 10 ◽  
Author(s):  
Yuanyuan Shang ◽  
Lingfei Wang ◽  
Zhe Zhu ◽  
Wei Gao ◽  
Dan Li ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Rectal Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Radiation Treatment ◽  
Locally Advanced ◽  
Altered Expression ◽  
Colorectal Cancer Cells ◽  
Radiation Induced ◽  
Induced Apoptosis

Resistance to radiotherapy is the main reason causing treatment failure in locally advanced rectal cancer. MicroRNAs (miRNAs) have been well demonstrated to regulate cancer development and progression. However, how miRNAs regulate radiotherapy resistance in colorectal cancer remains unknown. Herein, we established two human colorectal cancer cell lines resistant to radiotherapy, named HCT116-R and RKO-R, using the strategy of fractionated irradiation. The radioresistant phenotypical changes of the two cell lines were validated by cell viability assay, colony formation assay and apoptosis assay. The miRNA expression profilings of HCT116-R and RKO-R were determined using RNA-seq analyses, and further confirmed by quantitative real-time PCR. Multiple miRNAs, including miR-423-5p, miR-7-5p, miR-522-3p, miR-3184-3p, and miR-3529-3p, were identified with altered expression in both of the radiotherapy-resistant cells, compared to the parental cells. The downregulation of miR-423-5p was further validated in the rectal cancer tissues from radiotherapy-resistant patients. Silencing of miR-423-5p in parental HCT116 and RKO cells decreased the sensitivity to radiation treatment, and inhibited the radiation-induced apoptosis. In consistence, overexpression of miR-423-5p in HCT116-R and RKO-R cells partially rescued their sensitivity to radiotherapy, and promoted the radiation-induced apoptosis. Bcl-xL (Bcl-2-like protein 1) was predicted to be a potential target gene for miR-423-5p, and miR-423-5p/Bcl-xL axis could be a critical mediator of radiosensitivity in colorectal cancer cells. The current finding not only revealed a novel role of miR-423-5p in regulating the radiosensitivity in colorectal cancer, but also suggested miR-423-5p as a molecular candidate for combination therapy with radiation to treat colorectal cancer.

scholarly journals Exploiting the efficacy of Tyro3 and Folate receptors to enhance the delivery of Gold Nanoparticles into Colorectal Cancer cells in vitro

2021 ◽  
Author(s):  
Nakul Nautam Patel ◽  
Lucy Ghali ◽  
Ivan Roitt ◽  
Leonardo Pantoja Munoz ◽  
Richard Bayford
Keyword(s):  
Colorectal Cancer ◽  
Gold Nanoparticles ◽  
Survival Rate ◽  
Cancer Cells ◽  
Advanced Stage ◽  
Folate Receptors ◽  
Common Cancer ◽  
Colorectal Cancer Cells ◽  
The World

Colorectal cancer (CRC) is the fourth most common cancer in the world. Due to its asymptomatic nature, CRC is diagnosed at an advanced stage where the survival rate is <5%....

scholarly journals Knockdown of MiR-20a Enhances Sensitivity of Colorectal Cancer Cells to Cisplatin by Increasing ASK1 Expression

2018 ◽  
Vol 47 (4) ◽  
pp. 1432-1441 ◽  
Author(s):  
Luyao Zhang ◽  
Liang He ◽  
Hua Zhang ◽  
Yan Chen
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Western Blotting ◽  
Luciferase Reporter ◽  
Mirna Regulation ◽  
Platinum Based Chemotherapy ◽  
Colorectal Cancer Cells

Background/Aims: Platinum-based chemotherapy is one of the most important strategies for treatment of colorectal cancer. To improve the therapeutic efficiency, adjuvant drugs were sought to sensitize colorectal cancer cells to platinum-based agents such as cisplatin. As previous research has shown that miRNAs are associated with chemosensitivity, we aimed to alter miRNA regulation in colorectal cancer cells to increase their chemosensitivity. Methods: MTT assays were performed to determine the viability of HT29, SW480, and LoVo cells. Quantitative real time polymerase chain reaction (qRT-PCR) was performed to examine the expression of miR-20a in these cell lines. Regulation of the miR-20a/ASK1 axis was confirmed by western blotting and luciferase reporter assays. After treatment with miR-20a inhibitor (anti-miR-20a) and cisplatin, production of reactive oxygen species (ROS), mitochondrial membrane potential, and apoptosis were measured by flow cytometry. Activation of ASK1, Bcl-xl, JNK, and caspase-9, -7, and -3 was detected by western blotting. Results: miR-20a was overexpressed in colorectal cancer cell lines. Furthermore, knockdown of miR-20a increased the sensitivity of colorectal cancer cells to cisplatin treatment in vitro and in vivo. We demonstrated that the ASK1 gene was the target of miR-20a, and knockdown of miR-20a increased the expression of ASK1 in colorectal cancer cells. As cisplatin treatment induced production of ROS, knockdown of miR-20a enhanced ROS signaling through promoting the phosphorylation of ASK1. Phosphorylation of JNK and the subsequent mitochondrial apoptosis were triggered by the combination of cisplatin and anti-miR-20a. Conclusions: Knockdown of miR-20a enhanced sensitivity of colorectal cancer cells to cisplatin through the ROS/ASK1/JNK pathway.

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