scholarly journals In vitro cell proliferation inhibition activity and antibody activity of immunoconjugates consist of monoclonal antibodies and carboplatin.

1994 ◽  
Vol 9 (6) ◽  
pp. 413-416
Author(s):  
Yoriko Ota ◽  
Akihiko Takeda ◽  
Ichio Fukasawa ◽  
Noriyuki Inaba
Author(s):  
Yunqiu Pu ◽  
Fengxia Sun ◽  
Rongli Sun ◽  
Zhaodi Man ◽  
Shuangbin Ji ◽  
...  

Benzene, a commonly used chemical, has been confirmed to specifically affect the hematopoietic system as well as overall human health. PTP4A3 is overexpressed in leukemia cells and is related to cell proliferation. We previously found that HIF-1alpha was involved in benzene toxicity and PTP4A3 may be the target gene of HIF-1alpha via ChIP-seq. The aim of this study is to confirm the relationship between HIF-1alpha and PTP4A3 in benzene toxicity, as well as the function of PTP4A3 on cell toxicity induced by 1,4-benzoquinone (1,4-BQ). Our results indicate that HIF-1alpha could regulate PTP4A3 with in vivo and in vitro experiments. A cell line with suppressed PTP4A3 was established to investigate the function of PTP4A3 in 1,4-BQ toxicity in vitro. The results revealed that cell proliferation inhibition was more aggravated in PTP4A3 low-expression cells than in the control cells after 1,4-BQ treatment. The relative oxygen species (ROS) significantly increased in cells with inhibited PTP4A3, while the rise was inferior to the control cells at the 20 μM 1,4-BQ group. An increase in DNA damage was seen in PTP4A3 down-regulated cells at the 10 μM 1,4-BQ group, whereas the results reversed at the concentration of 20 μM. Moreover, the apoptosis rate increased higher in down-regulated PTP4A3 cells after 1,4-BQ exposure. In addition, PI3K/AKT pathway was significantly restrained in cells with inhibited PTP4A3 after 1,4-BQ treatment. Our results indicate that HIF-1alpha may regulate PTP4A3 to be involved in benzene toxicity. Inhibition of PTP4A3 could aggravate cell proliferation suppression and apoptosis by regulating PI3K/AKT pathway after 1,4-BQ treatment.


2018 ◽  
Vol 46 (4) ◽  
pp. 1311-1325 ◽  
Author(s):  
Tao Tian ◽  
Chun-Li Li ◽  
Xiao Fu ◽  
Shu-Hong Wang ◽  
Jun Lu ◽  
...  

Objective To explore the role and mechanism of β1 integrin in the regulation of multicellular drug resistance in hepatocellular carcinoma (HCC). Methods This in vitro study used a liquid overlay technique to obtain multicellular spheroids of two human HCC cell lines, HepG2 and Bel-7402. The morphology of the spheroids was observed by optical and electron microscopy. The effects of exposure to 5-fluorouracil (5-FU) and cisplatin (CDDP) on cell proliferation and the induction of apoptosis were assessed in monolayer cells and multicellular spheroids. The levels of β1 integrin and the effects on the focal adhesion kinase (FAK)/protein kinase B (Akt) pathway were evaluated using Western blot analysis, immunofluorescence and flow cytometry. The role of β1 integrin was confirmed by using an inhibitory antibody. Results Cell proliferation inhibition and cell apoptosis induced by 5-FUl and CDDP were abrogated in multicellular spheroids compared with monolayer cells. There were high levels of β1 integrin in multicellular spheroids. β1 integrin inhibitory antibody prevented the formation of multicellular spheroids, coupled with a significant increase in proliferation inhibition and apoptosis induction. β1 integrin inhibitory antibody effectively suppressed activation of both FAK and Akt in multicellular spheroids. Conclusions β1 integrin mediated multicellular drug resistance through the FAK/Akt pathway in HCC spheroids.


2016 ◽  
Vol 47 ◽  
pp. 1-7 ◽  
Author(s):  
Delphine Manzoni ◽  
Régine Catallo ◽  
Amel Chebel ◽  
Lucile Baseggio ◽  
Anne-Sophie Michallet ◽  
...  

2017 ◽  
Author(s):  
The Journal of Applied Horticulture ◽  
K.S. Jamuna

Cruciferous vegetables have drawn a great deal of attention in cancer research because of their potential protective properties. In the present study, four vegetables viz. cabbage, cauliflower, kohlrabi and radish were procured and processed for cold extraction procedure using 70% ethanol. The extracts were subjected to the qualitative phytochemical analysis, quantitative estimation of glucosinolates content and in vitro antiproliferative activity by MTT assay on MCF7, DL and NIH-3T3 cell lines. The results of qualitative phytochemical analysis showed the presence of several bioactive compounds viz. polyphenols, flavonoids, terpenoids, steroids, glycosides and alkaloids. Quantitative estimation of glucosinolates in terms of potassium thiocyanate equivalence/5mg of extract revealed that the cabbage has highest content of glucosinolate (122.6 µg) followed by cauliflower (109 µg), kohlrabi (101.6 µg) and radish (60.2 µg). The four cruciferous vegetables registered notable cell proliferation inhibition at different concentrations (50, 100, 200, 400 and 800 µg/mL) in a dose dependent manner against three different cell lines. The results of antiproliferative activity was expressed in terms of IC50. Among the four vegetables cabbage showed considerable cytotoxicity and cell proliferation inhibition with an IC50 value of 192.5, 189.7, 589.7 µg/mL followed by cauliflower (378.7, 398.9, 597.9 µg/mL), kohlrabi (389.5, 396.9, 619.7 µg/ml) and radish (415.4, 423.3, 703.6 µg/ml) in three different cell lines MCF7, DL and NIH-3T3, respectively.. The present study underlines the epidemiological surveys that cruciferous vegetables possess anticancer effects might be due to the presence of glucosinolates augmented with other phytochemicals.


1995 ◽  
Vol 308 (1) ◽  
pp. 31-38 ◽  
Author(s):  
P A Haughan ◽  
M L Chance ◽  
L J Goad

Leishmania donovani promastigotes were cultured in the presence of an azasterol (20-piperidin-2-yl-5 alpha-pregnane-3 beta,20-diol) to determine the effects on sterol biosynthesis and cell proliferation. Inhibition of growth increased gradually with azasterol concentrations up to 5 micrograms/ml; concentrations of azasterol exceeding 5 micrograms/ml were lethal. Sterol biosynthesis was affected by the azasterol when administered at concentrations as low as 100 pg/ml. The primary site of action was the alkylation at C-24 of a delta 24-sterol precursor. The 24-alkylated sterols [ergosta-5,7,24(24(1))-trien-3 beta-ol and ergosta-5,7,22-trien-3 beta-ol] of the protozoan were replaced by delta 24-cholesta-type sterols which then accumulated in the cells. Administration of the azasterol together with a bis-triazole inhibitor of the 14 alpha-methylsterol 14-demethylase reaction, which operates in sterol biosynthesis, resulted in depletion of 24-alkylsterols and their replacement with predominantly 14 alpha-methylsterols lacking a 24-alkyl group. Continuous subculture of promastigotes in the presence of the azasterol resulted in gradual depletion of 24-alkylsterols and their complete replacement by delta 24-cholesta-type sterols. Transfer of the azasterol-treated cells to medium lacking azasterol resulted in a gradual restoration, after several subcultures, of the normal 24-alkylsterol pattern. The results indicate that, although 24-alkylsterols are normally produced by the protozoan, it can nevertheless survive with sterols possessing only the cholestane skeleton. Thus there is no absolute requirement for 24-alkylsterols to fulfil some essential ‘sparking’ role associated with cell growth in promastigotes.


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