The role of <scp>SF3B1</scp> and <scp>NOTCH1</scp> in the pathogenesis of leukemia

Abolhasani, Shiva; Hejazian, Seyyed Sina; Karpisheh, Vahid; Khodakarami, Atefeh; Mohammadi, Hamed; Navashenaq, Jamshid Gholizadeh; Hojjat‐Farsangi, Mohammad; Jadidi‐Niaragh, Farhad

doi:10.1002/iub.2660

Cited by 3 publications

(1 citation statement)

References 210 publications

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“… 109 Notch 1 mutation has been reported in more than 50% of T-ALL patients but its prognosis remains unknown and appears to be associated with additional genetic lesions. 110 , 111 In hematological neoplasia, Notch 3-induced JAG1 as a paracrine stimulator facilitated leukemic cell survival, proliferative, and invasive ability and participated in the pathogenesis of T-ALL. 112 , 113 In T-cell progenitors, the Notch pathway induced LSC activity.…”

Section: Signaling Pathways Governing Lsc Maintenancementioning

confidence: 99%

Signaling pathways governing the behaviors of leukemia stem cells

Azizidoost¹,

Nasrolahi²,

Sheykhi-Sabzehpoush³

et al. 2024

Genes & Diseases

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Section: Signaling Pathways Governing Lsc Maintenancementioning

confidence: 99%

Signaling pathways governing the behaviors of leukemia stem cells

Azizidoost¹,

Nasrolahi²,

Sheykhi-Sabzehpoush³

et al. 2024

Genes & Diseases

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TMEM252 inhibits epithelial–mesenchymal transition and progression in papillary thyroid carcinoma by regulating Notch1 expression

Zhang,

Xie,

Wang

et al. 2024

Head & Neck

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BackgroundPapillary thyroid carcinoma (PTC) accounts for about 85% of thyroid cancer cases. Transmembrane protein 252 (TMEM252) is a gene encoding a transmembrane protein that has only been reported to be associated with triple‐negative breast cancer. Herein, we first elucidated the physiological roles and possible regulatory proteins of TMEM252 in PTC pathogenesis.MethodsQuantitative real‐time polymerase chain reaction, western blot, and immunohistochemical analyses were utilized to ascertain the relative TMEM252 expression in PTC and surrounding normal tissues. Functional investigations involved CCK‐8 viability assay, EdU incorporation assay for proliferation, transwell assays for migration and invasion, and an in vivo tumor development assessment to evaluate the TMEM252‐mediated regulation of tumor formation.ResultsOur results first revealed diminished TMEM252 transcript and protein expressions in PTC tissues and cell lines. TMEM252 overexpression suppressed cell proliferation through reducing p53, p21, and p16 expression. Conversely, TMEM252 depletion has opposite effects in PTC cells both in vivo. Additionally, the upregulation of TMEM252 demonstrated cell migration and invasion suppression by impeding the epithelial–mesenchymal transition (EMT) process via inhibition of the Notch pathway. Furthermore, overexpression of TMEM252 suppressed tumor growth in vivo.ConclusionOur study elucidates that TMEM252 suppresses PTC progression by modulating the Notch pathway. These findings underscore TMEM252 is a potential therapeutic target in managing PTC.

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