RETRACTED ARTICLE: A convergent synthetic platform for dual anticancer drugs functionalized by reduced graphene nanocomposite delivery for hepatocellular cancer
Abstract:Hepatocellular carcinoma (HCC) is widespread cancer with a high degree of morbidity and mortality in individuals worldwide and a serious concern for its resistance to present chemotherapy drugs. In this investigation, the combination of cisplatin (CPT) and metformin (MET) to kill the HepG2 and caco-2 cells was developed into a new pH-responding magnetic nanocomposite based on reduced graphene oxide. Polyhydroxyethyl methacrylic (PHEA) was then linked employing grafting from approach to the reduced graphene oxi… Show more
“…5 . These findings align with the work of Amaral et al 67 , who have suggested that p53 triggers apoptosis by activating pro-apoptotic proteins bcl-2-like protein 4 (Bax and Bak) and suppressing anti-apoptotic genes such as BCl2 and surviving, thus activating the caspase pathway 68 . Figure 5 The gene expression of p53, BCl2, and NF-kB after RGOH100 treatment in cells HepG2.…”
In this study, a novel method for the fabrication of hesperidin/reduced graphene oxide nanocomposite (RGOH) with the assistance of gamma rays is reported. The different RGOHs were obtained by varying hesperidin concentrations (25, 50, 100, and 200 wt.%) in graphene oxide (GO) solution. Hesperidin concentrations (25, 50, 100, and 200 wt.%) in graphene oxide (GO) were varied to produce the various RGOHs. Upon irradiation with 80 kGy from γ-Ray, the successful reduction of GO occurred in the presence of hesperidin. The reduction process was confirmed by different characterization techniques such as FTIR, XRD, HRTEM, and Raman Spectroscopy. A cytotoxicity study using the MTT method was performed to evaluate the cytotoxic-anticancer effects of arbitrary RGOH on Wi38, CaCo2, and HepG2 cell lines. The assessment of RGOH’s anti-inflammatory activity, including the monitoring of IL-1B and IL-6 activities as well as NF-kB gene expression was done. In addition, the anti-invasive and antimetastatic properties of RGOH, ICAM, and VCAM were assessed. Additionally, the expression of the MMP2-9 gene was quantified. The assessment of apoptotic activity was conducted by the detection of gene expressions related to BCl2 and P53. The documentation of the JNK/SMAD4/MMP2 signaling pathway was ultimately accomplished. The findings of our study indicate that RGOH therapy has significant inhibitory effects on the JNK/SMAD4/MMP2 pathway. This suggests that it could be a potential therapeutic option for cancer.
“…5 . These findings align with the work of Amaral et al 67 , who have suggested that p53 triggers apoptosis by activating pro-apoptotic proteins bcl-2-like protein 4 (Bax and Bak) and suppressing anti-apoptotic genes such as BCl2 and surviving, thus activating the caspase pathway 68 . Figure 5 The gene expression of p53, BCl2, and NF-kB after RGOH100 treatment in cells HepG2.…”
In this study, a novel method for the fabrication of hesperidin/reduced graphene oxide nanocomposite (RGOH) with the assistance of gamma rays is reported. The different RGOHs were obtained by varying hesperidin concentrations (25, 50, 100, and 200 wt.%) in graphene oxide (GO) solution. Hesperidin concentrations (25, 50, 100, and 200 wt.%) in graphene oxide (GO) were varied to produce the various RGOHs. Upon irradiation with 80 kGy from γ-Ray, the successful reduction of GO occurred in the presence of hesperidin. The reduction process was confirmed by different characterization techniques such as FTIR, XRD, HRTEM, and Raman Spectroscopy. A cytotoxicity study using the MTT method was performed to evaluate the cytotoxic-anticancer effects of arbitrary RGOH on Wi38, CaCo2, and HepG2 cell lines. The assessment of RGOH’s anti-inflammatory activity, including the monitoring of IL-1B and IL-6 activities as well as NF-kB gene expression was done. In addition, the anti-invasive and antimetastatic properties of RGOH, ICAM, and VCAM were assessed. Additionally, the expression of the MMP2-9 gene was quantified. The assessment of apoptotic activity was conducted by the detection of gene expressions related to BCl2 and P53. The documentation of the JNK/SMAD4/MMP2 signaling pathway was ultimately accomplished. The findings of our study indicate that RGOH therapy has significant inhibitory effects on the JNK/SMAD4/MMP2 pathway. This suggests that it could be a potential therapeutic option for cancer.
“…Another evidence of the greater interaction of graphene-based NPs with biological membranes was derived from the confocal microscopy studies: graphene-based nanocarriers comparatively required a longer time to gain access in the HeLa cells, which is a strong indication of its improved interaction with the membrane lipid layer. In the study of nuclear apoptosis of HepG2 cells with stronger internalized Fe 3 O 4 -rGO-based drug NPs, condensed and disintegrated nuclei and chromatin were observed from the apoptotic nuclei at the membrane boundaries . The study on the interaction of GO with mammalian HT-29 cells reveals that GO promotes cell attachment and proliferation .…”
Section: Resultsmentioning
confidence: 96%
“…In the study of nuclear apoptosis of HepG2 cells with stronger internalized Fe 3 O 4 -rGO-based drug NPs, condensed and disintegrated nuclei and chromatin were observed from the apoptotic nuclei at the membrane boundaries. 61 The study on the interaction of GO with mammalian HT-29 cells reveals that GO promotes cell attachment and proliferation. 62 The complex based on the drug−GO−Fe 3 O 4 structure advantageously reduced the viability of HT29 cells in comparison with bare drug−GO NPs and free drug.…”
We
demonstrate a single-step ultrasonic in situ complexation of
salicylic acid during the growth of Fe3O4-reduced
graphene oxide nanoparticles (∼10 nm) to improve the antioxidant
and antiproliferative effects of pristine drug molecules. These nanoparticles
have a precisely defined electronic molecular structure with salicylic
acid ligands specifically complexed to Fe(III)/Fe(II) sites, four
orders of magnitude larger electric surface potential, and enzymatic
activity modulated by ascorbic acid molecules. The diminishing efficiency
of hydroxyl radicals by Fe3O4-rGO-SA nanoparticles
is tenfold higher than that by pristine salicylic acid in the electro-Fenton
process. The H+ production of these nanoparticles can be
switched by the interaction with ascorbic acid ligands and cause the
redox deactivation of iron or enhanced antioxidation, where rGO plays
an important role in enhanced charge transfer catalysis. Fe3O4-rGO-SA nanoparticles are nontoxic to erythrocytes,
i.e., human peripheral blood mononuclear cells, but surpassingly inhibit
the growth of three cancer cell lines, HeLa, HepG2, and HT29, with
respect to pristine salicylic acid molecules.
“…They documented that the nanoparticles loaded with metformin/cisplatin exhibited the lowest concentration rate of HepG2 and Caco-2 cells compared to the drug-loaded single nanocomposite groups and free drugs by promoting an apoptotic response. Moreover, Fe3O4@rGO-G-PSEA demonstrated robust effectiveness against tumors in vivo while causing minimal harm to healthy tissues [ 95 ].…”
Section: Preclinical Evidence About Metformin Influence On Hcc Hallmarksmentioning
Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related deaths worldwide. There has been significant progress in understanding the risk factors and epidemiology of HCC during the last few decades, resulting in efficient preventative, diagnostic and treatment strategies. Type 2 diabetes mellitus (T2DM) has been demonstrated to be a major risk factor for developing HCC. Metformin is a widely used hypoglycemic agent for patients with T2DM and has been shown to play a potentially beneficial role in improving the survival of patients with HCC. Experimental and clinical studies evaluating the outcomes of metformin as an antineoplastic drug in the setting of HCC were reviewed. Pre-clinical evidence suggests that metformin may enhance the antitumor effects of immune checkpoint inhibitors (ICIs) and reverse the effector T cells’ exhaustion. However, there is still limited clinical evidence regarding the efficacy of metformin in combination with ICIs for the treatment of HCC. We appraised and analyzed in vitro and animal studies that aimed to elucidate the mechanisms of action of metformin, as well as clinical studies that assessed its impact on the survival of HCC patients.
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