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Cell Banking
Published in Anthony S. Lubiniecki, Large-Scale Mammalian Cell Culture Technology, 2018
Michael E. Wiebe, Laurie H. May
The use of serially passaged cultured cells to produce biologicals has its origins in the early 1960s when Hayflick and Moorhead (21) described the establishment of human diploid cell strains derived from several normal fetal tissues and suggested that they might be useful for the preparation of human virus vaccines. One of these cell strains, WI-38, was carefully characterized by karyological studies and by a thorough search for viral contaminants, and was found to be normal and free of exogenous infectious agents. Despite this, there was great reluctance to use WI-38 cells during the 1960s largely due to fears that unknown "cancer-causing" viruses or other "cancer-causing" components would be transmitted to vaccine recipients. The controversy over the use of human diploid cells raged on for 10 years before the first diploid cell product, poliomyelitis vaccine, was approved for use in the United States. The history of the acceptance of human diploid cell strains has been documented in a number of recent reviews (22–24). Human diploid cells (WI-38 or MRC-5) have been used to produce licensed vaccines against poliovirus, adenovirus types 4 and 7, rubella virus, rubeola virus, and rabies. Recipients of these vaccines number in the tens of millions and there are no reports of untoward effects that are due to the cell substrate.
Nanostructured assemblies of liquid-crystalline supermolecules: from display to medicine
Published in Liquid Crystals, 2019
We evaluated the cytotoxicity of 3-ring heterocyclic derivatives possessing a phenol unit against A549 human lung cancer cells as well as WI-38 normal human fibroblast cells [96]. Molecular structures under investigation are shown in Figure 41. Compounds A–E exhibited marked cytotoxic effects on A549 cells as shown in Table 2. A 3-ring heterocyclic unit possessing a hydroxyl group plays an important role in cytotoxicity. Furthermore, compounds A–E were found to induce apoptosis. Compounds D and E induced G2/M arrest, while compounds A, B and C caused G1 arrest. Interestingly, compounds A, B and C showed no significant growth-suppressive effects against the normal human fibroblast WI-38 as shown in Figure 42, which is promising for cancer-specific agents. Analyses of the cell cycle and cell-death induction reveal that compounds A, B and C induce cell death through DNA damage-signalling pathway. The response to DNA damage varies depending on the cell type, and it is mentioned that fibroblasts are relatively resistant to DNA damage-induced apoptosis [97,98]. That is why cytotoxic effect by compounds A, B and C through the DNA damage-signalling pathway might not be effective in human fibroblast WI-38 cells.
Recent advances and therapeutic journey of pyridine-based Cu(II) complexes as potent anticancer agents: a review (2015–2022)
Published in Journal of Coordination Chemistry, 2023
Notably, the IC50 values of CP7 against two cancer cell lines, A549 (IC50 = 5.5 ± 0.5 µM) and HepG2 (IC50 = 3.6 ± 0.2 µM), as well as those of the CP8 against HepG2 (IC50 = 2.8 ± 0.3 µM) are lower than those of the cisplatin (IC50 for HepG2 and A549 is 5 ± 1 and for 7.3 ± 0.2 µM, respectively). Both complexes have two times greater IC50 value than cisplatin values against normal human cell lines [57]. Borges et al. investigated the antineoplastic activities of pyridine-based Cu(II) complexes CP9 and CP10 (Figure 3) using different cellular models of human colon cancer (COLO 205), human leukemia (JURKAT, THP-1, HL60, U937, Molt-4) and murine highly metastatic melanoma (B16-F10) cell lines. Both complexes showed excellent potency against the tested cell lines and induced cell death [58]. Koley Seth et al. synthesized Cu(II) complexes CP11 and CP12. The structure-dependent influence of CP11 and CP12 on their in vitro apoptosis, cytotoxicity, and DNA binding were performed. The SAR studies of CP11 and CP12 towards in vitro cytotoxicity and apoptosis against WI-38 and HeLa cell lines were studied by MTT assay and FACS techniques. Both complexes showed a high cytotoxic effects against WI-38 and HeLa cell lines. The acidic hydrogen in CP11 enhances its activity more than the methyl group in CP12. The results of FACS experiments and MTT assay showed selective inhibition of cell growth (cell viability 85% (WI-38) versus 39% (HeLa)) and occurrence of apoptosis rather than necrosis [59]. Three Cu(II) complexes (CP13-CP15) with tridentate N2O ligand were synthesized and characterized by magnetochemical measurements, XRD, UV–Vis spectroscopy, FTIR, and electrochemical analyses. The anticancer activities of CP13-CP15 were evaluated against MDA-MB-231, A549, HeLa, K562, and LS174 by MTT assay.
Structure characterization and antitumor activity of palladium pseudo halide complexes with 4-acetylpyridine
Published in Journal of Coordination Chemistry, 2019
Mohamed M. El-bendary, Muhammad N. Arshad, Abdullah M. Asiri
Using MTT-based assays, the in vitro cytotoxicities of 1 and 2 were examined on mammary gland breast cancer MCF-7 and hepatocellular carcinoma HePG-2; the data are listed in Table 6. The cytotoxicity screening results are expressed as IC50, the concentration needed to inhibit the cancer cells by 50% as compared to control untreated cells (Table 6). Doxorubicin (DOX) was utilized as standard anticancer medication for comparison [41–44]. The data showed that 1 and 2 decrease the growth of tumor cancer cells under investigation in a dose-dependent manner (Figures 6 and 7). The cytotoxicities of 1 and 2 were screened against normal cell line WI-38 (non-tumorigenic) derived from human lung fibroblast cell lines as a positive cancer cell lines control (Figure 8). Complexes 1 and 2 showed IC50 > 30 (± 3) and IC50 > 19(± 2) µM, respectively, against WI-38 (Figure 8, Table 6). Complex 1 is more active than 2 (IC50 = 11 ± 1 µM for 1 and 44 ± 3 µM for 2) against HePG2 cell line. Also, 1 has more activity (IC50 = 8.3 ± 0.9 µM) than 2 (IC50 = 33 ± 2 µM) against MCF-7 cell line (Table 6). Complex 1 showed a sigmoidal dose-response inhibition of the investigated cell viabilities giving good IC50 values (Table 6). The significant difference in the IC50 values of 1 and 2 may be due to the different pseudo halides ligands (thiocyanate and azide). The examined complexes 1 and 2 at IC50 concentration inhibit the growth of tumor cell lines MCF-7 and HePG-2 compared to the control group (Figures 6 and 7). Furthermore, the data indicate that 1 and 2 exhibit weak cytotoxic effects on normal cell line WI-38 (non-tumorigenic) compared to the screened tumor cells (Figure 8). The data (Table 6 and Figures 6–8) indicated selectivity of 1 and 2 with lower toxicity against non-tumorigenic cells (normal cells). These results encourage more investigation in vitro and in vivo on 1 and 2.