Correction to: B7-H3 promotes aggression and invasion of hepatocellular carcinoma by targeting epithelial-to-mesenchymal transition via JAK2/STAT3/Slug signaling pathway

Kang, Fubiao; Jia, Heng-chuan; Liu, Dong; Li, Haijun; Zhang, Yinge; Sun, Dongdong

doi:10.1186/s12935-021-02216-z

Cited by 5 publications

(1 citation statement)

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“…Tyrosine phosphorylation of STAT3 leads to dimerization followed by nuclear translocation, which regulates EMT-associated genes' transcription, such as Twist, Snail, and Slug [ 35 ]. The JAK/STAT3/Slug, JAK/STAT3/Snail, and other pathways activate EMT-related transcription factors that modulate the EMT and thus promote tumorigenesis [ 36 , 37 ]. Promoting the EMT-like processes in high-grade glioma has been linked to an aggressive phenotype and resistance to treatment, resulting in poor patient outcomes [ 38 , 39 ].…”

Section: Discussionmentioning

confidence: 99%

TCAF2 drives glioma cellular migratory/invasion properties through STAT3 signaling

Yun,

Liang,

Wang

et al. 2023

Mol Cell Biochem

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Glioma is an intracranial tumor characterized by high mortality and recurrence rates. In the present study, the association of TRPM8 channel-associated factor 2 (TCAF2) in glioma was investigated using bioinformatics, showing significant relationships with age, WHO grade, IDH, and 1p/19q status, as well as being an independent predictor of prognosis. Immunohistochemistry of a glioma sample microarray showed markedly increased TCAF2 expression in glioblastoma relative to lower-grade glioma, with elevated expression predominating in the tumor center. Raised TCAF2 levels promote glioma cell migratory/invasion properties through the epithelial-to-mesenchymal transition-like (EMT-like) process, shown by Transwell and scratch assays and western blotting. It was further found that the effects of TCAF2 were mediated by the activation of STAT3. These results suggest that TCAF2 promotes glioma cell migration and invasion, rendering it a potential drug target in glioma therapy.

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