Immunohistochemical analysis of Nuclear Factor-kappa B (NF-κ	B) between follicular and plexiform ameloblastomas: A pilot study

Sivakumar, Muniapillai; Yoithapprabhunath, Thuckanaickenpalayam Ragunathan; Nirmal, R Madhavan; Veeravarmal, Veeran; Dineshshankar, Janardhanam; Amsaveni, R

doi:10.4103/jomfp.jomfp_150_20

Cited by 7 publications

(3 citation statements)

References 36 publications

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“…Survivin, B-cell lymphoma (Bcl)-2, and Bcl-X were found more frequently in ameloblastoma outer layer cells, although proapoptotic molecules such as Fas, Fas Ligand (FasL), and Caspase-3 are found in central stellate reticulum-like cells. (19)(20)(21) Akt is a 480 amino protein with a PH domain at the N-terminus, a connecting hinge region at the C-terminus, and a kinase domain. The inactive form of Akt protein can be detected in the cytoplasm of the cell.…”

Section: Akt Signaling In Ameloblastomamentioning

confidence: 99%

“…(19,28) NF-κB was initially found as a transcription factor in B-cells binding to the 11-base pair sequence enhancer element that controls the expression of immunoglobulin κ light chain. (19) It consists a group of transcription factors that promote the expressions of over 150 genes that involved in wide range of biological processes such as immune response, inflammation, bone resorption, proliferation, angiogenesis and oncogenesis. (29-32) Furthermore, NF-κB has been shown to be a positive regulator of the expression of COX-2 in stromal cells of ameloblastoma.…”

Section: Akt-nf-κb Signalingmentioning

confidence: 99%

“…NF-κB regulates the expression of downstream molecules and has an effect on the survival of tumor cells. (19,33)…”

Section: Akt-nf-κb Signalingmentioning

confidence: 99%

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Mechanism and Potential Therapy in Ameloblastoma: Akt Signaling Pathway

2022

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BACKGROUND: Ameloblastoma is the most common benign aggressive tumor. They are more prevalent in the mandible than in the maxilla, mostly observed on the posterior of the jaw. Ameloblastoma can arise at any age, however it most usually affect patients between the ages of 20 and 40. Numerous efforts have been made to develop molecular targeted therapies to treat cancers, such as Akt inhibitors. However, these drugs have not been tested for treating ameloblastoma yet, since underlying molecular factors have yet to be identified. This study was carried out to delineate possible molecular mechanisms related to the Akt signaling pathway in ameloblastoma and potential drugs for ameloblastoma treatment. CONTENT: Akt signaling pathway in ameloblastoma has been implicated in the formation and progression of tumors. Akt signaling is involved in various cellular mechanisms, such as cell cycle, apoptosis, and cytoskeletal rearrangement, which includes Phosphatidyl Inositol 3 Kinase (PI3K)-Akt signaling, Akt-Nuclear Factor (NF)-κB signaling, Akt-Mammalian Target of Rapamycin (mTOR) signaling, Akt-B-cell Lymphoma (Bcl)-2 Family signaling, Akt-Survivin signaling. Potential ways of treatments using chemical compounds and micro RNA (miRNA), and Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR) were explored as well.SUMMARY: The present review highlights various Akt signaling involved in ameloblastoma and its potential pathways for treatments, while the gold standard of ameloblastoma treatment is still surgery to remove the tumor, there are many potential agents through various means of inhibition for ameloblastoma. Therefore, understanding the underlying signaling on ameloblastoma is necessary to induce inhibition on ameloblastoma. More research in potential ways to inhibit Akt signaling in ameloblastoma will lead to a better management of ameloblastoma in the future. KEYWORDS: ameloblastoma, Akt, PI3K, NFkB, mTOR, Bcl-2, miRNA, CRISPR

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Section: Akt Signaling In Ameloblastomamentioning

confidence: 99%

Section: Akt-nf-κb Signalingmentioning

confidence: 99%

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Mechanism and Potential Therapy in Ameloblastoma: Akt Signaling Pathway

2022

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Changes of Nuclear Factor Kappa-B Pathway Activity in Hippocampus After Acute Carbon Monoxide Poisoning and Its Role in Nerve Cell Injury

Wang,

Li,

Wang

et al. 2024

Mol Neurobiol

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Protective effects of gallic acid against nickel-induced kidney injury: impact of antioxidants and transcription factor on the incidence of nephrotoxicity

Alhazmi,

El-Refaei,

Abdallah

2024

Renal Failure

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Nickel (Ni) is a common metal with a nephrotoxic effect, damaging the kidneys. This study investigated the mechanism by which gallic acid (GA) protects mice kidneys against renal damage induced by Nickel oxide nanoparticles (NiO-NPs). Forty male Swiss albino mice were randomly assigned into four groups, each consisting of ten mice ( n = 10/group): Group I the control group, received no treatment; Group II, the GA group, was administrated GA at a dosage of 110 mg/kg/day body weight; Group III, the NiO-NPs group, received injection of NiO-NPs at a concentration of 20 mg/kg body weight for 10 consecutive days; Group IV, the GA + NiO-NPs group, underwent treatment with both GA and NiO-NPs. The results showed a significant increase in serum biochemical markers and a reduction in antioxidant activities. Moreover, levels of 8-hydroxy-2’-deoxyguanosine (8-OH-dG), phosphorylated nuclear factor kappa B (p65), and protein carbonyl (PC) were significantly elevated in group III compared with group I. Furthermore, the western blot analysis revealed significant high NF-κB p65 expression, immunohistochemistry of the NF-κB and caspase-1 expression levels were significantly increased in group III compared to group I. Additionally, the histopathological inspection of the kidney in group III exhibited a substantial increase in extensive necrosis features compared with group I. In contrast, the concomitant coadministration of GA and NiO-NPs in group IV showed significant biochemical, antioxidant activities, immunohistochemical and histopathological improvements compared with group III. Gallic acid has a protective role against kidney dysfunction and renal damage in Ni-nanoparticle toxicity.

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Immunohistochemical analysis of Nuclear Factor-kappa B (NF-κ B) between follicular and plexiform ameloblastomas: A pilot study

Cited by 7 publications

References 36 publications

Mechanism and Potential Therapy in Ameloblastoma: Akt Signaling Pathway

Mechanism and Potential Therapy in Ameloblastoma: Akt Signaling Pathway

Changes of Nuclear Factor Kappa-B Pathway Activity in Hippocampus After Acute Carbon Monoxide Poisoning and Its Role in Nerve Cell Injury

Protective effects of gallic acid against nickel-induced kidney injury: impact of antioxidants and transcription factor on the incidence of nephrotoxicity

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