Human oral squamous carcinoma

The anticancer properties of a series of dibenzoyl dihydropyrimidines have recently been reported [40]. In particular, compound 73 (Fig. 10) showed cytotoxic activity against human oral squamous carcinoma (HSC-2) cells and also inhibited the Pgp-mediated drug efflux in (multidmg resistant) MDR cells. 

Fujita, M. et al., Okadaic acid stimulates expression of Fas receptor and Fas ligand by activation of nuclear factor kappa-B in human oral squamous carcinoma cells. Oral Oncol, 40, 199, 2004. 

Nikitakis,N.G., Hebert, C., Lopes, M.A., Reynolds, M.A., and Sauk, J.J. (2002) PPAR gamma-Mediated Antineoplastic Effect of NS AID Sulindac on Human Oral Squamous Carcinoma Cells, Int. J. Cancer 98, 817-823. 

In a p53 null human oral squamous carcinoma cell line curcumin (5 pM and (10 pM) arrested growth in S/G2 which was confirmed with an increased bromodeoxyuridine labelling (Weir and Hague 2002). Treated cells showed increased... 

Pinus densifiora Sieb. et Zucc. (Pinaceae) EO inhibited proliferation and induced apoptosis in YD 8 cells (human oral squamous carcinoma). Cell proliferation was inhibited by 30% and 60% at concentrations of 40 and 60 pg/mL EO. The EO reduced cancer cells by 70% when treated with 60 pg/mL EO. Apoptosis was induced by activation of caspase-9 (Jo et al., 2012). Soeur et al. (2011) found ihdXAniba rosaeodora Ducke (Lauraceae) had cytotoxic effects against A431 (human epidermoid carcinoma cell line) and on HaCaT (human keratinocytes) cells. At a concentration... 

Scheper MA, Shirtliff ME, Meiller TF, Peters BM, Jabra-Rizk MA (2008) Famesol, a fungal quorum sensing molecule triggers apoptosis in human oral squamous carcinoma cells. Neoplasia 10 954... 

Shalinsky DR, Bischoff ED, Gregory ML, Lamph WW, Heyman RA, Hayes JS, Thomazy V, Davies PJA (1996) Enhanced antitumor efficacy of cisplatin in combination with ALRT 1057 i -cis retinoic acid) in human oral squamous carcinoma xenografts in nude mice. Clin Cancer Res 2 511-520... 

KeUey, E. E., Domann, E. E., Buettner, G. R., Oberley, L. W., and Bums, C. P., 1997, Increased efficacy of in vitro Photofrin photosensitization of human oral squamous ceU carcinoma by iron and ascorbate, 7. Photochem. Photobiol. B 40 273-277. 

Mallery SR, Shenderova A, Pei P, Begum S, Giminieri JR, Wilson RF, Gasto BG, Schuller DE, Morse MA, Effects of 10-hydroxycamptothecin, delivered from locally injectable poly(lactide-co-glycolide) microspheres, in a murine human oral squamous cell carcinoma regression model, Anticancer Res 21 1713-1722, 2001. 

Cytotoxic activity against human oral squamous cell carcinoma (HSC-2)... 

Nakayama S, Sasaki A, Mese H, Alcalde RE, Tsuji T, Matsumura T. The E-cadherin gene is silenced by CpG methylation in human oral squamous cell carcinomas. Int J Cancer 2001 93 667-673. 

Kelley EE, Domann FE, Buettner GR, Oberley LW, Burns CP. Increased efficacy in vitro Photofrin photosensitization of human oral squamous cell carcinoma by iron and ascorbate. / Photochem Photobiol B Biol 1997 40 273-77. 

The mitomycins are a family of aziridine-containing antibiotics isolated from Streptomyces lavendulae. One of these antibiotics, mitomycin C (MMC), is an antitumor antibiotic frequently used for the treatment of breast, lung, stomach, intestinal, testicular, cholioepithelial, seminal and oral carcinoma [18-20]. When human oral squamous cell carcinoma cell lines (HSC-2, HSC-4) were treated with MMC, the viable cell number was dose-dependently reduced (CC50 of MMC against HSC-2, HSC-3 and HSC-4 cells 3.5, 9.7 and 18 xM, respectively, determined 24 hours after treatment). The rapid decline of polyamines (measured at 3 hours after MMC treatment) was observed prior to the expression of early apoptosis markers such as the production of annexin-positive cells and caspase activation (Table 1) [21]. The interactions... 

Cells treated with 5-FU undergo cell cycle arrest or apoptosis by inhibition of DNA synthesis. When human oral squamous cell carcinomas (HSC-2, HSC-3, HSC-4) were treated with 5-FU, viable cell numbers declined dose-dependently (CC50 determined after 24 hours treatment 3.4,6.9 and 1.7 p,M, respectively). The intracellular putrescine concentration slightly declined (Table 2) [29]. The combination treatment of 5-FU with N(l),N(ll)-diethylnorspermine (DEN-SPM), which is an inducer of spermidine/spermine N(l)-acetyltransferase (SSAT) that depletes polyamine, has been reported to augment the cytotoxic activity of 5-FU, suggesting possible clinical application [30]. 

Considerable difference in the sensitivity to MK-2 and GG was found among the tumor cell lines used, with human leukemic cell lines (HL-60, ML-1, KG-1, K-562) the most sensitive and the human glioblastoma cell lines (T98G, U87MG) the most resistant. The sensitivity of the human oral squamous cell carcinoma cell lines (HSC-2, HSC-3, HSC-4) was intermediate. Consistent with previous reports [60,61], GG induced apoptosis in the most sensitive HL-60 cells, but not in the less sensitive HSC-4 cells. This suggested that the type of cell death induced (either apoptosis or non-apoptosis) may depend on the target cells. 

Heterocycles such as 4-trifluoromethylimidazole, phenoxazine, 3-formyl-chromone, coumarin derivatives, and vitamin K2 derivatives were investigated for their cytotoxicity against human normal and tumor cells. These compounds induced moderate tumor-specific cytotoxicity. VitaminK2 derivatives and prenylalcohols displayed disappointingly low tumor-specific cytotoxicity, although they have been reported to induce apoptosis-inducing activity. Human oral squamous cell carcinoma cell lines showed considerable variation in drug sensitivity. The type of cell death induced depended both on which types of cells and which inducers were used. 

Twelve 4-trifluoromethylimidazoles (1-12) were synthesized by the method of Kawase et al. [24,25]. Compound 13 was purchased from Aldrich, USA. Cytotoxicity assays and determination of 50% cytotoxic concentration (CC50) against human promyelocytic leukaemia HL-60 and human oral squamous cell carcinoma HSC-3 cell lines were performed as described elsewhere [23]. 

Vitamin K2 (menaquinone) represents a series of compounds in which the phytyl side chain of phytonadione has been replaced by a side chain built up of 1-14 isoprenyl units. It has been reported that vitamin K2 with four isoprenyl units (4) induced the monocytic differentiation of human myeloid leukemia cell lines [58], or apoptosis in isolated osteoclast [59] and human ovary cancer cells [60]. We have recently found that vitamin K2 derivatives (1-3) induced some tumor-specific cytotoxicity and non-apoptotic cell death in oral carcinoma [61]. As an extension of the search for tumor-specific substances targeted against human oral squamous, hepatocellular carcinoma, and promyelocytic leukemia cell lines, we investigated the QSAR of seven vitamin K2 derivatives (1-7) (Fig. 18), by conventional and recent techniques of computation chemistry, such as the concept of absolute hardness [ 16-18]. 

Uchida D., Begum N. M., Tomizuka Y., et al. (2004) Acquisition of lymph node, but not distant metastatic potentials, by the overexpression of CXCR4 in human oral squamous cell carcinoma. Lab Invest, b, 1538 46. 

Uchida D, Onoue T, Tomizuka Y, et al. (2007) Involvement of an autocrine stromal cell derived factor-1/CXCR4 system on the distant metastasis of human oral squamous cell carcinoma. Mol Cancer Res 7 685-694... 

Cestrum noctumum spirostane (36) HSC-2 (oral squamous carcinoma), HGF (human gingival fibroblast) LD50 2.0-2.8 lig/ml [29]... 

It has been shown that tannic acid (TA) exerts cancer chemopreventive activity in various animal models (61). TA induced either growth arrest or apoptotic death (62). TA induced apoptosis more in human oral squamous cell carcinoma and salivary gland tumor cell lines than in normal human gingival fibroblasts, whereas gallic acid, a component unit of TA, showed much weaker selective cytotoxicity (63). Recently, it was shown that inhibition of the proteosome of living Jurkat cells results in accumulation of two natural proteosome substrates, the cyclin-dependent kinase inhibitor p27 and the proapoptotic protein Bax, followed growth arrest in G1 and induction of apoptotic cell death (d ). 

Elango, N., Samuel, S., Chinnakkannii, P. (2006). Enzymatic and non-enzymatic antioxidant sta-ms in stage (III) human oral squamous cell carcinoma and treated with radical radio therapy influence of selenium supplementation. Clin. Chim. Acta 373(1-2), 92-98. 

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