Hyaluronic acid co-functionalized gold nanoparticle complex for the targeted delivery of metformin in the treatment of liver cancer (HepG2 cells)

2015 ◽  
Vol 128 ◽  
pp. 63-74 ◽  
Author(s):  
C. Senthil Kumar ◽  
M.D. Raja ◽  
D. Sathish Sundar ◽  
M. Gover Antoniraj ◽  
K. Ruckmani
Keyword(s):  
Hyaluronic Acid ◽  
Liver Cancer ◽  
Gold Nanoparticle ◽  
Targeted Delivery ◽  
Hepg2 Cells ◽  
Nanoparticle Complex

scholarly journals Targeted Delivery of Paclitaxel in Liver Cancer Using Hyaluronic Acid Functionalized Mesoporous Hollow Alumina Nanoparticles

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Yu Gao ◽  
Lili Hu ◽  
Ying Liu ◽  
Xiaoyan Xu ◽  
Chao Wu
Keyword(s):  
Hyaluronic Acid ◽  
Cancer Therapy ◽  
Liver Cancer ◽  
Drug Release ◽  
Targeted Delivery ◽  
Amorphous State ◽  
Alumina Nanoparticles ◽  
Sustained Drug Release ◽  
Scanning Calorimetry ◽  
Adsorption Method

Hyaluronic acid functionalized mesoporous hollow alumina nanoparticles (HMHA) were used as a tumor-targeted delivery carrier for liver cancer therapy. Paclitaxel (PAC) incorporated in the carrier by the adsorption method was analyzed by X-ray diffraction and differential scanning calorimetry. PAC was found to be in an amorphous state. The hyaluronic acid coated on the surface of mesoporous hollow alumina nanoparticles (MHA) regulated the drug release rate and the loaded samples obtained a sustained drug release. In vitro experiments demonstrated that paclitaxel-hyaluronic acid functionalized mesoporous hollow alumina nanoparticles (PAC-HMHA) had a high cellular uptake, which increased the drug level in tumor tissues and was beneficial to promote apoptosis. An in vivo tumor inhibition rate study demonstrated that PAC-HMHA (64.633 ± 4.389%) had a better antitumor effect than that of paclitaxel-mesoporous alumina nanoparticles (PAC-MHA, 56.019 ± 6.207%) and pure PAC (25.593 ± 4.115%). Therefore it can be concluded that PAC-HMHA are a prospective tumor-targeted delivery medium and can be useful for future cancer therapy.

scholarly journals Preparation of DNA/Gold Nanoparticle Encapsulated in Calcium Phosphate

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Tomoko Ito ◽  
Koyuki Ibe ◽  
Tomohiro Uchino ◽  
Hiroyuki Ohshima ◽  
Makoto Otsuka
Keyword(s):  
Gene Therapy ◽  
Hyaluronic Acid ◽  
Calcium Phosphate ◽  
Simulated Body Fluid ◽  
Gold Nanoparticle ◽  
Body Fluid ◽  
Enzymatic Degradation ◽  
Dna Complexes ◽  
Dna Complex ◽  
Nanoparticle Complex

Biocompatible DNA/gold nanoparticle complex with a protective calcium phosphate (CaP) coating was prepared by incubating DNA/gold nanoparticle complex coated by hyaluronic acid in SBF (simulated body fluid) with a Ca concentration above 2 mM. The CaP-coated DNA complex was revealed to have high compatibility with cells and resistance against enzymatic degradation. By immersion in acetate buffer (pH 4.5), the CaP capsule released the contained DNA complex. This CaP capsule including a DNA complex is promising as a sustained-release system of DNA complexes for gene therapy.

scholarly journals Possible Role of IRS-4 in the Origin of Multifocal Hepatocellular Carcinoma

Cancers ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 2560
Author(s):  
Luis G. Guijarro ◽  
Patricia Sanmartin-Salinas ◽  
Eva Pérez-Cuevas ◽  
M. Val Toledo-Lobo ◽  
Jorge Monserrat ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Cancer ◽  
Hepg2 Cells ◽  
Cellular Polarity ◽  
Ki 67 ◽  
Tissue Samples ◽  
Vitro Analysis ◽  
Tumoral Cells

New evidence suggests that insulin receptor substrate 4 (IRS-4) may play an important role in the promotion of tumoral growth. In this investigation, we have evaluated the role of IRS-4 in a pilot study performed on patients with liver cancer. We used immunohistochemistry to examine IRS-4 expression in biopsies of tumoral tissue from a cohort of 31 patient suffering of hepatocellular carcinoma (HCC). We simultaneously analyzed the expression of the cancer biomarkers PCNA, Ki-67, and pH3 in the same tissue samples. The in vitro analysis was conducted by studying the behavior of HepG2 cells following IRS-4 overexpression/silencing. IRS-4 was expressed mainly in the nuclei of tumoral cells from HCC patients. In contrast, in healthy cells involved in portal triads, canaliculi, and parenchymal tissue, IRS-4 was observed in the cytosol and the membrane. Nuclear IRS-4 in the tumoral region was found in 69.9 ± 3.2%, whereas in the surrounding healthy hepatocytes, nuclear IRS-4 was rarely observed. The percentage of tumoral cells that exhibited nuclear PCNA and Ki-67 were 52.1 ± 7%, 6.1 ± 1.1% and 1.3 ± 0.2%, respectively. Furthermore, we observed a significant positive linear correlation between nuclear IRS-4 and PCNA (r = 0.989; p < 0.001). However, when we correlated the nuclear expression of IRS-4 and Ki-67, we observed a significant positive curvilinear correlation (r = 0.758; p < 0.010). This allowed us to define two populations, (IRS-4 + Ki-67 ≤ 69%) and (IRS-4 + Ki-67 > 70%). The population with lower levels of IRS-4 and Ki-67 had a higher risk of suffering from multifocal liver cancer (OR = 16.66; CI = 1.68–164.8 (95%); p < 0.05). Immunoblot analyses showed that IRS-4 in normal human liver biopsies was lower than in HepG2, Huh7, and Chang cells. Treatment of HepG2 with IGF-1 and EGF induced IRS-4 translocation to the nucleus. Regulation of IRS-4 levels via HepG2 transfection experiments revealed the protein’s role in proliferation, cell migration, and cell-collagen adhesion. Nuclear IRS-4 is increased in the tumoral region of HCC. IRS-4 and Ki-67 levels are significantly correlated with the presence of multifocal HCC. Moreover, upregulation of IRS-4 in HepG2 cells induced proliferation by a β-catenin/Rb/cyclin D mechanism, whereas downregulation of IRS-4 caused a loss in cellular polarity and in its adherence to collagen as well as a gain in migratory and invasive capacities, probably via an integrin α2 and focal adhesion cascade (FAK) mechanism.

scholarly journals Echinacoside exerts anti-tumor activity via the miR-503-3p/TGF-β1/Smad aixs in liver cancer

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Wen Li ◽  
Jing Zhou ◽  
Yajie Zhang ◽  
Jing Zhang ◽  
Xue Li ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Hepg2 Cells ◽  
Luciferase Reporter ◽  
Therapeutic Effects ◽  
Dependent Manner ◽  
Expression Levels ◽  
Liver Cancer Cells ◽  
Anti Tumor Activity ◽  
Tgf Β1

Abstract Background Echinacoside (ECH) is the main active ingredient of Cistanches Herba, which is known to have therapeutic effects on metastatic tumors. However, the effects of ECH on liver cancer are still unclear. This study was to investigate the effects of ECH on the aggression of liver cancer cells. Methods Two types of liver cancer cells Huh7 and HepG2 were treated with different doses of ECH at different times and gradients. MTT and colony formation assays were used to determine the effects of ECH on the viability of Huh7 and HepG2 cells. Transwell assays and flow cytometry assays were used to detect the effects of ECH treatment on the invasion, migration, apoptosis and cell cycle of Huh7 and HepG2 cells. Western blot analysis was used to detect the effects of ECH on the expression levels of TGF-β1, smad3, smad7, apoptosis-related proteins (Caspase-3, Caspase-8), and Cyto C in liver cancer cells. The relationship between miR-503-3p and TGF-β1 was detected using bioinformatics analysis and Luciferase reporter assay. Results The results showed that ECH inhibited the proliferation, invasion and migration of Huh7 and HepG2 cells in a dose- and time-dependent manner. Moreover, we found that ECH caused Huh7 and HepG2 cell apoptosis by blocking cells in S phase. Furthermore, the expression of miR-503-3p was found to be reduced in liver tumor tissues, but ECH treatment increased the expression of miR-503-3p in Huh7 and HepG2 cells. In addition, we found that TGF-β1 was identified as a potential target of miR-503-3p. ECH promoted the activation of the TGF-β1/Smad signaling pathway and increased the expression levels of Bax/Bcl-2. Moreover, ECH could trigger the release of mitochondrial Cyto C, and cause the reaction Caspases grade. Conclusions This study demonstrates that ECH exerts anti-tumor activity via the miR-503-3p/TGF-β1/Smad aixs in liver cancer, and provides a safe and effective anti-tumor agent for liver cancer.

scholarly journals Assessment of Chemopreventive Potential of the Plant Extracts against Liver Cancer Using Hepg2 Cell Line

Molecules ◽  
2021 ◽  
Vol 26 (15) ◽  
pp. 4593
Author(s):  
Deepthi Venkatachalapathy ◽  
Chandan Shivamallu ◽  
Shashanka Prasad ◽  
Gopenath Thangaraj Saradha ◽  
Parthiban Rudrapathy ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Vitis Vinifera ◽  
Bioactive Compounds ◽  
Camellia Sinensis ◽  
Hepg2 Cells ◽  
Human Liver ◽  
Withania Somnifera ◽  
Antioxidant Properties ◽  
Annexin V ◽  
Human Liver Cancer

The edible parts of the plants Camellia sinensis, Vitis vinifera and Withania somnifera were extensively used in ancient practices such as Ayurveda, owing to their potent biomedical significance. They are very rich in secondary metabolites such as polyphenols, which are very good antioxidants and exhibit anti-carcinogenic properties. This study aims to evaluate the anti-cancerous properties of these plant crude extracts on human liver cancer HepG2 cells. The leaves of Camellia sinensis, Withania somnifera and the seeds of Vitis vinifera were collected and methanolic extracts were prepared. Then, these extracts were subjected to DPPH, α- amylase assays to determine the antioxidant properties. A MTT assay was performed to investigate the viability of the extracts of HepG2 cells, and the mode of cell death was detected by Ao/EtBr staining and flow cytometry with PI Annexin- V FITC dual staining. Then, the protein expression of BAX and BCl2 was studied using fluorescent dye to determine the regulation of the BAX and BCl2 genes. We observed that all the three extracts showed the presence of bioactive compounds such as polyphenols or phytochemicals. The W. somnifera bioactive compounds were found to have the highest anti-proliferative activity on human liver cancer cells.

scholarly journals Hyaluronic Acid-Coated MTX-PEI Nanoparticles for Targeted Rheumatoid Arthritis Therapy

Crystals ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 321
Author(s):  
Shenghui Zhong ◽  
Peng Liu ◽  
Jinsong Ding ◽  
Wenhu Zhou
Keyword(s):  
Rheumatoid Arthritis ◽  
Hyaluronic Acid ◽  
Targeted Delivery ◽  
High Dose ◽  
One Pot ◽  
Inflammatory Site ◽  
Pei Nanoparticles ◽  
Toxic Reactions

Methotrexate (MTX) is an anchor drug for the treatment of rheumatoid arthritis (RA); however, long-term and high-dose usage of MTX for patients can cause many side effects and toxic reactions. To address these difficulties, selectively delivering MTX to the inflammatory site of a joint is promising in the treatment of RA. In this study, we prepared MTX-PEI@HA nanoparticles (NPs), composed of hyaluronic acid (HA) as the hydrophilic negative electrical shell, and MTX-linked branched polyethyleneimine (MTX-PEI) NPs as the core. MTX-PEI@HA NPs were prepared in the water phase by a one-pot method. The polymeric NPs were selectively internalized via CD44 receptor-mediated endocytosis in the activated macrophages. In the in vivo mice mode study, treatment with MTX-PEI@HA NPs mitigated inflammatory arthritis with notable safety at a high dose of MTX. We highlight the distinct advantages of aqueous-synthesized NPs coated with HA for arthritis-selective targeted delivery, thus verifying MTX-PEI@HA NPs as a promising MTX-based nanoplatform for treatment of RA.

scholarly journals Galangin, a novel dietary flavonoid, attenuates metastatic feature via PKC/ERK signaling pathway in TPA-treated liver cancer HepG2 cells

2015 ◽  
Vol 15 (1) ◽  
pp. 15 ◽  
Author(s):  
Shang-Tao Chien ◽  
Ming-Der Shi ◽  
Yi-Chieh Lee ◽  
Chou-Chia Te ◽  
Yuan-Wei Shih
Keyword(s):  
Liver Cancer ◽  
Signaling Pathway ◽  
Hepg2 Cells ◽  
Erk Signaling ◽  
Dietary Flavonoid

scholarly journals Kaempferol inhibits proliferation, migration, and invasion of liver cancer HepG2 cells by down-regulation of microRNA-21

2018 ◽  
Vol 32 ◽  
pp. 205873841881434 ◽  
Author(s):  
Genglong Zhu ◽  
Xialei Liu ◽  
Haijing Li ◽  
Yang Yan ◽  
Xiaopeng Hong ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Liver Cancer ◽  
Signaling Pathway ◽  
Hepg2 Cell ◽  
Cell Apoptosis ◽  
Hepg2 Cells ◽  
Mtor Signaling ◽  
Brdu Incorporation ◽  
Migration And Invasion ◽  
Mtor Signaling Pathway

Liver cancer is one of the most common and lethal cancers in human digestive system, which kills more than half a million people every year worldwide. This study aimed to investigate the effects of kaempferol, a flavonoid compound isolated from vegetables and fruits, on hepatic cancer HepG2 cell proliferation, migration, invasion, and apoptosis, as well as microRNA-21 (miR-21) expression. Cell viability was detected using cell counting kit-8 (CCK-8) assay. Cell proliferation was measured using 5-bromo-2′-deoxyuridine (BrdU) incorporation assay. Cell apoptosis was assessed using Guava Nexin assay. Cell migration and invasion were determined using two-chamber migration (invasion) assay. Cell transfection was used to change the expression of miR-21. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was performed to analyze the expressions of miR-21 and phosphatase and tensin homologue (PTEN). Expression of key proteins involved in proliferation, apoptosis, migration, invasion, and phosphatidylinositol 3-kinase/protein kinase 3/mammalian target of rapamycin (PI3K/AKT/mTOR) pathway were evaluated using western blotting. Results showed that kaempferol significantly inhibited HepG2 cell proliferation, migration, and invasion, and induced cell apoptosis. Kaempferol remarkably reduce the expression of miR-21 in HepG2 cells. Overexpression of miR-21 obviously reversed the effects of kaempferol on HepG2 cell proliferation, migration, invasion, and apoptosis. Moreover, miR-21 negatively regulated the expression of PTEN in HepG2 cells. Kaempferol enhanced the expression of PTEN and inactivated PI3K/AKT/mTOR signaling pathway in HepG2 cells. In conclusion, kaempferol inhibited proliferation, migration, and invasion of HepG2 cells by down-regulating miR-21 and up-regulating PTEN, as well as inactivating PI3K/AKT/mTOR signaling pathway.

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