Cell cycle aberration in ameloblastoma and adenomatoid odontogenic tumor: As evidenced by the expression of p53 and survivin

Shaikh, Zulfin; C, Niranjan K

doi:10.4103/0970-9290.176916

Cited by 7 publications

(8 citation statements)

References 3 publications

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“…Other second messengers, such as Bcl-2 family (3,6), Survivin (15,25), APAF-1 (18), X chromosome-linked inhibitor of apoptosis protein (XIAP) have been reported, but there was not any functional study related to these molecules. (25) Therefore those molecules should be further investigated, so that a more complete strategy in inducing ameloblastoma into apoptosis could be obtained.…”

Section: Future Research Perspectivementioning

confidence: 99%

“…In accordance with the expressions of apoptotic ligand and receptor in central cells, expressions of p53 (8,15), phosphatase and tensin homolog (PTEN) (16), phosphorylated-PTEN (16), phosphorylated-Jun N-terminal kinase (JNK) (17), Bcl-2 associated X protein (Bax) (3,6), Bcl-2 homologous antagonist killer (Bak) (3,5,7), caspase 9 (18), apoptotic protease activating factor-1 (APAF-1) (18), caspase 3 (19), terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) (14,20) were observed in central cells as well. Hence, some reports suggested that central cells have higher apoptotic activity than peripheral cells.…”

Section: Introductionmentioning

confidence: 99%

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Targeting Ameloblatoma into Apoptosis

Sandra

2018

Indones Biomed J

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BACKGROUND: Generally ameloblastoma is a locally aggressive, slow growing, non-metastatic epithelial odontogenic benign tumor. However, rarely some ameloblastoma can metastasize in spite of a benign histologic appearance. Targeting ameloblastoma by inducing it into apoptosis could be a beneficial strategy, since many ameloblastoma cases were reported recurrent after surgical therapy.CONTENT: To investigate ameloblastoma in cellular aspect,cytological pattern of ameloblastoma was divided intoouter layer/peripheral and inner layer/central cells. Tumor necrosis factor (TNF)-α, Fas ligand (FasL), TNF receptor (TNFR)1/death receptor (DR)1, TNFR2/DR2, DR4, DR5andFas were highly expressed in central than peripheral cells. Despite inducing apoptosis, TNF-α can induce PI3K leading to Akt and p44/42 mitogen-activated protein kinases (MAPK) activation in AM-1 cells, which later induce cell survival and proliferation. Therefore apoptotic induction in ameloblastoma should be suggested in higher TNF-α concentration. Expression of FasL and Fas are closely associated with squamous metaplasia and granular transformation of the tumor cells, suggesting that apoptosis induced by FasL may play a role in the terminally differentiated or degenerative ameloblastoma cells. TNF-related apoptosis-inducing ligand (TRAIL) has emerged as an apoptotic inducing anticancer agent in tumor cells specifically. TRAIL induced activation of caspases, lowering mitochondrial membrane potential, high number of apoptotic cells in ameloblastoma cells. Therefore, TRAIL could be a potential agent for targeting ameloblastoma, although further study should be explored.SUMMARY: Targeting ameloblastoma by inducing it into apoptosis could be achieved effectively, although some criteria should be considered. Therefore understanding the underlying apoptosis signaling pathways are necessary for inducing ameloblasotma into apoptosis. Investigations on other apoptosis-related molecules, potential apoptosis-inducing natural products, and novel approach in reprogramming, are important in the future for a better anagement of ameloblastoma.KEYWORDS: ameloblastoma, apoptosis, TNF, Fas, TRAIL, Akt, MAPK, caspase

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Section: Future Research Perspectivementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Targeting Ameloblatoma into Apoptosis

Sandra

2018

Indones Biomed J

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“…The p53 mutation leads to promotion of the function of antiapoptotic proteins. Therefore, the importance of cell cycle aberration and uncontrolled proliferation resulting from the p53 mutation is discussed [ 27 ].…”

Section: Discussionmentioning

confidence: 99%

HIF-1α Is Associated with Resistance to Hypoxia-Induced Apoptosis in Ameloblastoma

Valladares

Balbinot

Moraes

et al. 2021

International Journal of Dentistry

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Background. Ameloblastoma (AMB) is a benign odontogenic tumour, with an aggressive local behaviour and a high rate of recurrence. Previous studies have demonstrated that hypoxia-induced factor alpha 1 (HIF-1α) and activated caspase-3 contribute to tumour invasiveness and cytogenesis in ameloblastoma. Hypoxia increases HIF-1α levels, which triggers a number of signalling pathways. This paper aimed to present data in the study of hypoxia-activated signalling pathways that modulate proapoptotic and antiapoptotic events in AMB. Methods. Twenty cases of AMB and ten cases of dental follicle (DF) were used to analyse the immunoexpression of HIF-1α, p53, BNIP3, Bcl-2, IAP-2, GLUT1, and Bax. To contribute to the study, an analysis of expression and genetic interaction was performed using the cell line AME-1. Results. AMB and DF expressed the studied proteins. These proteins showed significantly greater immunoexpression in AMB compared with the DF ( p < 0.05 ). HIF-1α showed an important association with GLUT1, and a positive correlation was observed among p53, Bcl-2, and IAP-2. Transcriptomic analysis showed the significant expression of the studied proteins, and the network generated showed a direct association of HIF-1αF with GLUT1 (SLC2A1), TP53, and LDHA. Interestingly, GLUT1 also exhibited direct interaction with TP53 and LDHA. Conclusion. In AMB tumorigenesis, hypoxia is possibly related to antiapoptotic events, which suggests an important role for HIF-1α, GLUT1, Bcl-2, IAP-2, and possibly p53.

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“…The two factors participate in the regulation of tumorigenesis by regulating cell cycle and apoptosis. [6,7] NF-κB is a key transcription factor present in the occurrence and development of tumors, and it participates in a variety of cellular biological reactions. It can enter into the nucleus after activation and regulate the expressions of encoding cytokines, growth factors, cell adhesion molecules and FAS proteins.…”

Section: Discussionmentioning

confidence: 99%

Inhibitory effect of survivin-shRNA on A431 cutaneous squamous cell carcinoma

Hao

Liu

Kang

et al. 2018

DCC

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Objective: To observe the effect of survivin-shRNA on A431 cutaneous squamous cell carcinoma (SCC) and explore the molecular biological mechanism of nuclear factor κB (NF-κB) in the inhibition of survivin-shRNA on cutaneous SCC. Methods: Survivin-shRNA adenovirus vector was constructed to screen out the best interference sequence. Nude mice were subcutaneously inoculated with the cultured A431 cell suspension to duplicate A431 transplanted tumor models. These mice were randomly divided into the blank control group, the rAd-EGFP negative control group, the rAd-survivin-shRNA transfection group and the Res positive control group, with 5 mice in each group. The corresponding reagents were injected into the tumors. All the mice were sacrificed on the 20 th day. The tumor tissues were isolated, with tumor volume and tumor weight measured, the tumor growth curves were accordingly plotted and the tumor inhibition rate was consequently calculated. Hematoxylin-eosin (HE) staining was used to observe the cellular morphology of the tumors. TUNEL was applied to the detection of cell apoptosis. Western blot was applied to the detection of the expression of Survivin, inhibitor of NF-κB (IκB), P65, P53 and Caspase-3. Results: As to the transplanted tumors, tumor volume and tumor weight were decreased in nude mice in the rAd-survivin-shRNA transfection group and the Res positive control group, in comparison with the blank control group and the rAd-EGFP negative control group, the differences were of statistical significance (p < .05); The results of TUNEL showed that the apoptosis rates were significantly increased in the rAd-survivin-shRNA transfection group and the Res positive control group, in comparison with the blank control group and the rAd-EGFP negative control group, the difference was statistically significant (p < .05); In the rAd-survivin-shRNA transfection group and the Res positive control group, the microscopic observation showed a small amount of sparsely-distributed tumor cells, degenerative liquefactive necrosis, cancer cell shrinkage and round-shape, and karyopycnosis; The expressions of Survivin and P65 proteins were decreased in the rAd-survivin-shRNA transfection group and the Res positive control group, in comparison with the blank control group and the rAd-EGFP negative control group, the differences were statistically significant (p < .05), while the expressions of IκB, P53 and Caspase-3 proteins were significantly increased, in comparison with the blank control group and the rAd-EGFP negative control group, the differences were statistically significant (p < .05). Conclusions: Survivin-shRNA can inhibit the growth of the transplanted tumors in cutaneous SCC nude mice, one of the mechanisms is to promote the apoptosis of tumor cells and inhibit the growth of SCC transplanted tumors by inhibiting the NF-κB signaling pathway and then activating the tumor suppressor gene P53.

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Cell cycle aberration in ameloblastoma and adenomatoid odontogenic tumor: As evidenced by the expression of p53 and survivin

Cited by 7 publications

References 3 publications

Targeting Ameloblatoma into Apoptosis

Targeting Ameloblatoma into Apoptosis

HIF-1α Is Associated with Resistance to Hypoxia-Induced Apoptosis in Ameloblastoma

Inhibitory effect of survivin-shRNA on A431 cutaneous squamous cell carcinoma

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