Expression of cell cycle and apoptosis-related proteins in ameloblastoma and keratocystic odontogenic tumor

Metgud, Rashmi; Gupta, Kumkum

doi:10.1016/j.anndiagpath.2013.06.006

Cited by 16 publications

(14 citation statements)

References 22 publications

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“…Several related studies have assessed cell proliferation molecules in AM and AC [ 18 – 21 ]. However, different results have been reported, likely due to the histologic features and behaviors of AM.…”

Section: Introductionmentioning

confidence: 99%

Immunoexpression of Ki-67, MCM2, and MCM3 in Ameloblastoma and Ameloblastic Carcinoma and Their Correlations with Clinical and Histopathological Patterns

et al. 2015

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Cell proliferation assays are performed using antibodies against nuclear proteins associated with DNA replication. These nuclear proteins have gained special interest to predict the biological and clinical behaviors of various tumors. The aim of this study was to analyze the presence of Ki-67 protein and the minichromosome maintenance-2 (MCM2) and maintenance-3 (MCM3) proteins in ameloblastoma. Materials and Methods. Cell proliferation marker expression levels were assessed via immunohistochemistry in 111 ameloblastoma cases (72 unicystic ameloblastoma samples, 38 solid/multicystic ameloblastoma samples, and 1 ameloblastic carcinoma). The label index was performed as described previously. Results. MCM2 and MCM3 showed higher proliferation indexes in all variants of ameloblastoma compared to the classic marker Ki-67. No correlation between the proliferation index and the clinical and protein expression data was observed. Conclusion. The results suggest that clinical features do not directly affect tumor cell proliferation. Moreover, the high levels of cellular proliferation of MCM2 and MCM3 compared with Ki-67 may indicate that MCM2 and MCM3 are more sensitive markers for predicting the growth rate and eventually might be helpful as a tool for predicting aggressive and recurrent behaviors in these tumors.

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Section: Introductionmentioning

confidence: 99%

Immunoexpression of Ki-67, MCM2, and MCM3 in Ameloblastoma and Ameloblastic Carcinoma and Their Correlations with Clinical and Histopathological Patterns

et al. 2015

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“…In addition, apoptosis is an important mechanism to maintain a stable internal environment, which is programmed cell death under regulation of multi-genes, multi-factors, and multi-signal pathways [13] . Apoptosis is regulated by apoptosis-regulating proteins, which are divided into 2 major categories: pro-apoptotic proteins (for example, Bax and p53) and anti-apoptotic proteins (for example, Bcl-2 and Bcl-xL) [14,15].…”

Section: Introductionmentioning

confidence: 99%

Tanshinone IIA Affects Autophagy and Apoptosis of Glioma Cells by Inhibiting Phosphatidylinositol 3-Kinase/Akt/Mammalian Target of Rapamycin Signaling Pathway

Ding

Wang²,

Wang³

et al. 2016

Pharmacology

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Objective: To test the effects of Tanshinone IIA (Tan IIA) on cell viability, cycle, apoptosis, and autophagy of human glioma cell U251 by regulating phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signal pathway. Methods: Tan IIA and PI3K agonist (740 Y-P) were used to treat glioma cells U251. MTT assay was used to assess cell viability and flow cytometry was used to detect cell apoptosis and cell cycle. The expressions of apoptosis-related proteins (Bcl-2 and Bax), autophagy-related proteins (LC3B and Beclin 1) and PI3K/Akt/mTOR signal pathway-associated proteins (p-PI3K, p-Akt and p-mTOR) were evaluated by Western blotting. Results: Tan IIA decreased the expression of p-PI3K and p-Akt proteins, inhibited cell viability and promoted apoptosis. Meanwhile, the expression of Bax increased, while the expression of Bcl-2 decreased. In addition, Tan IIA promoted autophagy in U251 glioma cells and raised the expression of LC3B and Beclin 1. However, 740 Y-P played a reversed role of Tan IIA in cell viability, cycle, apoptosis, and autophagy of U251 cells. Conclusion: Tan IIA could suppress the viability of U251 cells and induce cell apoptosis and autophagy, which might be related to the inhibition of the PI3K/Akt/mTOR signal pathway.

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“…Cell proliferation and apoptosis are basic events in developmental and tissue homeostasis. 27 The rate of cell proliferation may lead to local invasiveness of AB. 28 Therefore, lncRNA ENST00000512916 could regulate AB cell proliferation and apoptosis.…”

Section: Discussionmentioning

confidence: 99%

<p>A Novel lncRNA ENST00000512916 Facilitates Cell Proliferation, Migration and Cell Cycle Progression in Ameloblastoma</p>

Sun¹,

Niu²,

Wang³

et al. 2020

OTT

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Our purpose was to identify up-regulated long noncoding RNA ENST00000512916 in ameloblastoma (AB) and explore its role in the progression of AB. Methods: We analyzed lncRNA microarray expression profile between six paired AB and normal oral mucosa (NOM) tissues. An up-regulated lncRNA, ENST00000512916 was identified and validated by real-time qPCR. Cell proliferation, migration and cell cycle were detected by CCK-8 assay, transwell chamber and flow cytometry, respectively. Western blotting analysis was used to measure the expression of cell-cycle-related proteins including CyclinD1 and Cyclin-dependent kinase (CDK) 2/4/6. In addition, Xenograft tumor model was constructed to investigate tumor growth. Results: Real-time qPCR confirmed that lncRNA ENST00000512916 was up-regulated in AB tissues. ENST00000512916 knockdown significantly inhibited cell proliferation, migration and the expression of CDK2/4/6 in AM-1 cells. Moreover, ENST00000512916 knockdown suppressed tumor growth in vivo. We also found that ENST00000512916 overexpression significantly promoted the expression of HOXC13 in AM-1 cells. Overexpression of ENST00000512916 promoted cell cycle progression in AM-1 cells, which was reversed by HOXC13 knockdown. Conclusion: Our findings reveal that lncRNA ENST00000512916 promotes cell proliferation, migration and cell cycle progression of AB.

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Expression of cell cycle and apoptosis-related proteins in ameloblastoma and keratocystic odontogenic tumor

Cited by 16 publications

References 22 publications

Immunoexpression of Ki-67, MCM2, and MCM3 in Ameloblastoma and Ameloblastic Carcinoma and Their Correlations with Clinical and Histopathological Patterns

Immunoexpression of Ki-67, MCM2, and MCM3 in Ameloblastoma and Ameloblastic Carcinoma and Their Correlations with Clinical and Histopathological Patterns

Tanshinone IIA Affects Autophagy and Apoptosis of Glioma Cells by Inhibiting Phosphatidylinositol 3-Kinase/Akt/Mammalian Target of Rapamycin Signaling Pathway

<p>A Novel lncRNA ENST00000512916 Facilitates Cell Proliferation, Migration and Cell Cycle Progression in Ameloblastoma</p>

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