Differential antiproliferative mechanisms of novel derivative of benzimidazo[1,2-<i>α</i>]quinoline in colon cancer cells depending on their p53 status

Sedić, Mirela; Poznic, Miroslav; Gehrig, Peter; Scott, Mike; Schlapbach, Ralph; Hranjec, Marijana; Karminski‐Zamola, Grace; Pavelić, Krešimir; Pavelić, Sandra Kraljević

doi:10.1158/1535-7163.mct-07-2261

Cited by 45 publications

(16 citation statements)

References 52 publications

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“…In addition, GTNs exhibited significantly lower expression levels of maspin and higher expression levels of m-p53 than rHMs. The results of the present study also indicated that the expression of maspin was inversely correlated with the expression of m-p53 in HMs, which was similar to the results reported for gastric cancer (29,30). Furthermore, the expression of maspin was inversely correlated, and that of m-p53 positively correlated, with a number of prognostic factors, including serum β-hCG levels, uterine size and diameter of theca-lutein cysts; however, age was not found to be associated.…”

Section: Discussionsupporting

confidence: 91%

Expression patterns of maspin and mutant p53 are associated with the development of gestational trophoblastic neoplasia

Sun¹,

Wu²,

Ruan³

et al. 2016

Oncology Letters

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Gestational trophoblastic disease (GTD) is a group of conditions that originate from the abnormal proliferation of trophoblastic cells. GTDs encompass hydatidiform moles (HMs) and gestational trophoblastic neoplasia (GTN). GTNs are a group of malignant diseases that require chemotherapy, or more aggressive treatment. There is a requirement for more tumor markers to predict the development of GTN from HMs. The current study evaluated the expression of maspin and tumor protein p53 (p53) in GTD, and their role in predicting the development of GTN. Expression of maspin and mutant p53 (m-p53) was detected by immunohistochemistry in 48 normal first trimester placentas, matched for gestational age to 49 HMs that regressed, 39 malignant HMs and 11 invasive moles or choriocarcinomas. Spearman's rank correlation analysis and logistic regression were performed on the expression patterns of maspin and m-p53, and on the clinical prognostic factors in GTD. Compared with normal placenta levels, the expression levels of maspin were decreased, whereas the expression levels of m-p53 were increased in GTDs (P<0.05). The expression levels of maspin and m-p53 in complete and partial HMs were not significantly different (P>0.05). In HMs, maspin expression was inversely correlated with serum β human chorionic gonadotropin, uterine size and diameter of theca-lutein cysts; however, m-p53 expression demonstrated a positive correlation with these factors (all P<0.05). Compared with the high-risk metastatic group (FIGO score ≥7), the low-risk group (FIGO score <7) exhibited a higher rate of positive maspin expression (P=0.041), and the frequency of positive m-p53 expression was significantly higher in patients with an advanced FIGO stages (FIGO stage ≥III) compared with patients in early stages (FIGO stage ≤II; 87.9 vs. 58.8%; P=0.019). The combination of maspin negative expression with m-p53 positive expression had an 84% specificity value, 76% positive predictive value and 70% negative predictive value for the development of GTN. In conclusion, maspin-negative and m-p53-positive expression is associated with the development of GTN in HMs.

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Section: Discussionsupporting

confidence: 91%

Expression patterns of maspin and mutant p53 are associated with the development of gestational trophoblastic neoplasia

Sun¹,

Wu²,

Ruan³

et al. 2016

Oncology Letters

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“…99,[111][112][113] Several processes were originally associated with and were then shown to be dispensable for (at least some instances of) mitotic catastrophe. These include, but are not limited to, the activation of the DNA damage-responsive protease caspase-2, 114 of the tumor suppressor TP53 109,115 and of other members of the TP53 family, including the TP73 variant TAp73. 116,117 In view of recent results from several laboratories indicating that mitotic aberrations can induce cell senescence, [118][119][120] and that cell death can be either apoptotic or necrotic, 8 we have recently proposed a novel definition and categorization of mitotic catastrophe based on purely functional considerations.…”

Section: Definition Of 'Mitotic Catastrophe'mentioning

confidence: 99%

Molecular definitions of cell death subroutines: recommendations of the Nomenclature Committee on Cell Death 2012

et al. 2011

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proposed a set of recommendations for the definition of distinct cell death morphologies and for the appropriate use of cell death-related terminology, including 'apoptosis', 'necrosis' and 'mitotic catastrophe'. In view of the substantial progress in the biochemical and genetic exploration of cell death, time has come to switch from morphological to molecular definitions of cell death modalities. Here we propose a functional classification of cell death subroutines that applies to both in vitro and in vivo settings and includes extrinsic apoptosis, caspase-dependent or -independent intrinsic apoptosis, regulated necrosis, autophagic cell death and mitotic catastrophe. Moreover, we discuss the utility of expressions indicating additional cell death modalities. On the basis of the new, revised NCCD classification, cell death subroutines are defined by a series of precise, measurable biochemical features.

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“…Even though a similar concentration-dependent antiproliferative pattern and caspase 7 activation (Figure 1B) were observed for both compounds, the cell cycle dynamics (Table 1) and percentage of apoptotic cell distribution (Table S1 in Supplementary Information) were somewhat different. The possibility of tested derivatives acting differently in the same cell line was thus studied in detail by global proteomic profiling, which proved successful in elucidating the molecular mechanisms triggered by novel antitumor compounds [17]. …”

Section: Resultsmentioning

confidence: 99%

Antitumor Mechanisms of Amino Acid Hydroxyurea Derivatives in the Metastatic Colon Cancer Model

Šaban

Stepanić

Srđan

et al. 2013

IJMS

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The paper presents a detailed study of the biological effects of two amino acid hydroxyurea derivatives that showed selective antiproliferative effects in vitro on the growth of human tumor cell line SW620. Tested compounds induced cell cycle perturbations and apoptosis. Proteins were identified by proteomics analyses using two-dimensional gel electrophoresis coupled to mass spectrometry, which provided a complete insight into the most probable mechanism of action on the protein level. Molecular targets for tested compounds were analyzed by cheminformatics tools. Zinc-dependent histone deacetylases were identified as potential targets responsible for the observed antiproliferative effect.

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Differential antiproliferative mechanisms of novel derivative of benzimidazo[1,2-α]quinoline in colon cancer cells depending on their p53 status

Cited by 45 publications

References 52 publications

Expression patterns of maspin and mutant p53 are associated with the development of gestational trophoblastic neoplasia

Expression patterns of maspin and mutant p53 are associated with the development of gestational trophoblastic neoplasia

Molecular definitions of cell death subroutines: recommendations of the Nomenclature Committee on Cell Death 2012

Antitumor Mechanisms of Amino Acid Hydroxyurea Derivatives in the Metastatic Colon Cancer Model

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