Expression of stem cell markers SALL4, LIN28A, and KLF4 in ameloblastoma

Abstract

Background Ameloblastoma (AME) is a benign odontogenic tumour of epithelial origin characterised by slow but aggressive growth, infiltration, and recurrence; it is capable of reaching large dimensions and invading adjacent structures. Stem cell research has proven to be significant in the sphere of tumour biology through these cells’ possible involvement in the aetiopathogenesis of this tumour. Methods Immunohistochemistry was performed on AME, dentigerous cyst (DC), and dental follicle (DF) samples, and indirect immunofluorescence was performed on the AME-hTERT cell line to determine the expression of SALL4, LIN28A, and KLF4. Results Expression of proteins related to cellular pluripotency was higher in AME cells than in DC and DF cells. The analysis revealed that the proteins in question were mainly expressed in the parenchyma of AME tissue samples and were detected in the nuclei of AME-hTERT cells. Conclusions Stem cells may be related to the origin and progression of AME.

Is the Cis-Element CACCC-Box a Master Regulatory Element during Cardiovascular Disease? A Bioinformatics Approach from the Perspective of the Krüppel-like Family of Transcription Factors

“…Regarding the interaction between SALL4 and KLFs in the heart, SALL4 interacts directly with members of the T-box family 3 and 5 and regulates the expression of Gap junction alpha-5 (GJA5) and KLF-4. This final regulation of KLF-4 is further seen in stem cells, as SALL4 has an important role in proliferation and survival, mediated by the Bmi-1 pathway [8]. Meanwhile, in cardiac development, another KLF, KLF-5, is involved in regulating TBX5, as KLF-5 absence reduces expression of TBX5 (Table 1, Table 2 and Table S2), contrasting with the interactions described between SALL4 and TBX5 in cardiac patterning [57].…”

“…Life 2024, 14, 493 2 of 16 family [4], the Specificity Protein (SP) family [5], the Wilms tumor gene (WT1) [6], Vascular Endothelial Zinc Finger 1 (VEZF1) [7], and Splat-Like Transcription Factor 4 (SALL4) [8].…”

In the Cis-Element CACCC-Box a Master Regulatory Element during Cardiovascular Disease? A Bioinformatics Approach from the Perspective of the Kruppel-Like Family of Transcription Factors

“…Regarding the interaction between SALL4 and KLFs in the heart, SALL4 interacts directly with members of the T-box family 3 and 5 and regulates the expression of Gap junction alpha-5 (GJA5) and KLF-4. This final regulation of KLF-4 is further seen in stem cells, as SALL4 has important role in proliferation and survival, mediated by the Bmi-1 pathway [48]. Meanwhile, in cardiac development, another KLF, KLF-5, is involved in regulating TBX5, as KLF-5 absence reduces expression of TBX5 (Table 1, Table 2, and supplemental Table 2), contrasting with the interactions described between SALL4 and TBX5 in cardiac patterning [49].…”